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Understanding Psychopathy: Costs, Characteristics, and Social Impact (Part 1)In this first episode of a two-part series, Bill Eddy and Megan Hunter explore psychopathy, its relationship to antisocial personality disorder, and its staggering $460 billion annual cost to the US criminal justice system. Drawing from recent research and their extensive experience at the High Conflict Institute, Bill and Megan break down complex psychological concepts into practical, understandable terms.The Spectrum of Antisocial BehaviorBill and Megan discuss how antisocial personality disorder manifests, its early warning signs, and its relationship to psychopathy. They explore how these traits appear in various settings — from business environments to personal relationships — and why early intervention is crucial, particularly before age 15.Understanding Psychopathy's Three Key FeaturesThe episode delves into the three main characteristics of psychopathy: disinhibition (extreme risk-taking), callousness (lack of empathy), and boldness (absence of fear). Bill and Megan examine how these traits manifest in real-world situations and their implications for relationships and society.Modern Diagnosis and AssessmentThe hosts explore the shift from viewing personality traits as fixed characteristics to understanding them as dimensions on a spectrum. This modern approach allows for more nuanced understanding and assessment of psychopathic traits.Questions we answer in this episode:What is the difference between antisocial personality disorder, sociopathy, and psychopathy?How early can antisocial behaviors be identified?Can someone with these traits change with treatment?What role does empathy play in psychopathy?How do these personalities impact everyday relationships?Key Takeaways:Psychopathy costs the US criminal justice system approximately $460 billion annuallyEarly intervention (before age 15) is crucial for changing antisocial behaviorsAntisocial personality disorder affects about 4% of adults, while psychopathy affects about 1%People with these traits often display instrumental empathy rather than genuine empathyUnderstanding these traits can help with protection and boundary-settingThis first episode in the two-part series provides invaluable insights for anyone seeking to understand psychopathy and its impact on society. Whether you're a professional working with high conflict personalities or simply interested in understanding complex human behavior, Bill and Megan's expert analysis offers practical knowledge and protective strategies. Tune in next week for Part 2, which will explore genetics, causation, and additional dimensions of psychopathy.Links & Other NotesPSYCHOPATHY ARTICLE:Berkeley Voices Psychopathy goes undetected in some people. Why?THE MOVIE BILL BROUGHT UP AS A GOOD EXAMPLE OF THIS:Catch Me If You CanBOOKSIt's All Your Fault at Work!It's All Your Fault!Our New World of Adult BulliesARTICLESLiving with High-Conflict People: Do's and Don'ts for Living with an Antisocial High Conflict PeopleThe Sociopath: Antisocial High Conflict PeopleSociopaths and Their DeceptionsManipulators in Plain Sight: Spotting Antisocial Personality Disorder OUR WEBSITE: https://www.highconflictinstitute.com/Submit a Question for Bill and MeganAll of our books can be found in our online store or anywhere books are sold, including as e-books.You can also find these show notes at our site as well.Note: We are not diagnosing anyone in our discussions, merely discussing general patterns of behavior. Nor are we providing legal of therapeutic advice. Please seek the assistance of your local professionals to seek help. (00:00) - Welcome to It's All Your Fault (01:41) - Psychopathy (02:23) - Background for the Conversation (04:11) - Antisocial vs. Psychopath vs. Sociopath (05:48) - Antisocial Personality Disorder (19:13) - Bill's Books (19:44) - Psychopathy and Sociopathy (22:18) - Disinhibition (25:37) - Callousness (29:53) - Boldness (32:08) - Personality Dimensions (35:54) - Wrap Up (36:23) - Reminders & Coming Next Week: Psychopathy Part 2 Learn more about our Conflict Influencer Class. Get started today!
In this episode, my guest is Pavel Tsatsouline, a world-renowned strength and conditioning coach, former military special forces training instructor, author, and founder of StrongFirst—an online school focused on “low-tech, high-concept” training to build strength for men and women of all fitness levels. We discuss the most effective and efficient ways to build strength, endurance, and flexibility. We cover bodyweight-only, free-weight, and machine-based protocols and describe training splits and lesser-known but highly effective ways to train, especially for people with limited time. We also discuss local versus systemic nervous system and muscle recovery, how to complete training sessions with increased energy, why training to “failure” is not advised, optimal rest-between-sets protocols to improve performance, and how to vary effort levels across each week and month to ensure regular progress. This episode brings you highly practical, science-supported, and real-world-tested training methods to build strength, endurance, and flexibility from one of the world's top experts. Show notes: https://go.hubermanlab.com/YC80Wvt Sponsors AG1: https://drinkag1.com/huberman Eight Sleep: https://eightsleep.com/huberman Levels: https://levels.link/huberman LMNT: https://drinklmnt.com/huberman Joovv: https://joovv.com/huberman Maui Nui: https://mauinuivenison.com/huberman Timestamps 00:00:00 Pavel Tsatsouline 00:02:29 Fitness, Strength, Model Athlete 00:07:19 Tool: Essential Training Movements 00:13:46 Sponsors: Eight Sleep & Levels 00:16:29 Dips, Pull-Ups, Farmer Carry, Tools: Kettle Bell Mile, Grip Strength & Longevity 00:29:57 Concentric vs Eccentric Only Movements, Isometric, Tool: Pause Reps 00:38:38 Sponsor: AG1 00:39:53 “Greasing the Groove”, Cramming Analogy, Strength is a Skill 00:48:27 Tool: Greasing the Groove Protocol 00:54:12 Tool: Movement & Motivation; Nervous System 01:00:00 Frequency & Recovery, Heterochronicity, Soviet vs American Training 01:10:25 Soviet vs American Strength Schools, Periodization, Recovery 01:20:00 Sponsors: LMNT & Joovv 01:22:45 Bell Squat, Non-Spine Compressing Leg Work, Tool: Zercher Squat 01:27:15 Machines, Beginners vs Advanced? 01:28:41 Shorter Cycles? Linear & Wave Progression, Step Loading, Variable Overload 01:32:04 Strength & Endurance, Bodybuilding, “Bro Split” 01:40:28 Endurance, Cost of Adaptation, Heart Adaptations 01:46:38 Rest Periods, Interval Training, Tool: German Interval Training 01:51:34 Tool: Cardiovascular Training, Glycolytic Power Repeats; Muscle Growth 01:57:31 Sponsor: Maui Nui 01:59:00 Rest Period Activities, Tool: Protecting Back 02:04:33 Endurance Training, Anti-Glycolytic Revolution, Specialized vs Variety 02:11:30 Not Seeking the “Pump”, Repeated Sprint Ability, Tool: Anti-Glycolytic Endurance Training 02:19:06 Seek Soreness or Pump?, Hypertrophy 02:23:05 Tool: Planning Strength & Endurance Training, Individualization 02:32:27 Training Quality, Practiced Skill 02:35:39 Non-Athletes, Strength & Endurance, Training Duration 02:40:20 Post-Exercise Fatigue, Tools: Fragmentation, Feedback, Volume 02:48:01 Pre-Workout Stimulants 02:53:51 Performance & Arousal, Breathing, Disinhibition, Emotion 03:03:42 Train to Failure?, Recovery 03:08:40 Flexibility, Range of Motion Training, Kettle Bell, Tool: Wall Squat 03:14:57 Training for Flexibility; Training as a Practice 03:17:46 Older Adults & Strength Training, Consistency Over Intensity 03:25:08 Body-Weight vs Barbell vs Kettlebell Training 03:34:06 Kettlebell Training, Swings, Power & Endurance 03:41:55 Training Choices, Tool: Simple, Consistent Program 03:47:38 Kids & Training, General vs Specialization? 03:51:21 Core Work, Abdominals, Tools: Tension & Attention; ‘Pressurize' Abs 04:03:34 Breathing, Force, Strength 04:05:02 Directing Gaze While Weightlifting 04:12:37 Zero-Cost Support, YouTube, Spotify & Apple Follow & Reviews, Sponsors, YouTube Feedback, Protocols Book, Social Media, Neural Network Newsletter
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In our last episode before our mid-season break, we talk to the incredible Dr. Katya Rascovsky about some of the most heartbreaking behaviors in FTD: disinhibition, impulse control and hypersexuality. Katya is absolutely brilliant, kind, and we learned so much from her. We'll see you back here on March 5th, when we'll start to dive into the second half of Season 8. Take time to digest the first 6 episodes of our season with care. Read the blogs for more info. We want to send big love to the entire Penn FTD Center Team for jumping in feet first, to our sponsors for their support and to our guests for openly sharing their stories. Please see below for links mentioned in the show and a direct link to our informative companion blog for this episode. Each week a new episode will launch Tuesday followed by a blog that will be sent out via email to our subscribers. To sign up for our e-mail visit our website remembermeftd.com. The companion blog to this episode can be read here. Special thank you to The AFTD for their collaboration and support of these blogs! And a special thank you to Alector for their boundless work in the neurodegenerative space. Powered by innovation, exquisite science and a determination to make a difference, Alector is working on the discovery and development of potential therapeutic treatments in the hopes of improving the lives of patients, caregivers and families living with neurodegenerative diseases. Remember Me Podcast is appreciative of all your support of our work. --- Support this podcast: https://podcasters.spotify.com/pod/show/rememberme/support
The concept of sharing freely and without fear is called the disinhibition effect. There is little inhibition about vulnerability with a stranger on the train because he can't hurt you, so you believe. Of course, the possibility of being vulnerable and lacking perceived risk is part of cyberspace's bait to lure us into its net. In real-world relationships like our families or the local church, it's more challenging to “unlike” somebody. When bad things happen and hurts accumulate, we have to deal with them biblically (or not). Read Here: https://lifeovercoffee.com/what-to-do-about-disinhibition-cyber-effects-4-0/ Will you help us to continue providing free content for everyone? You can become a supporting member here https://lifeovercoffee.com/join/, or you can make a one-time or recurring donation here https://lifeovercoffee.com/donate/.
Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.08.04.552059v1?rss=1 Authors: Christie, J. M., Yang, Z., Zhang, K., Gaffield, M. A., Gross, G. G., Arnold, D. B. Abstract: Climbing fibers supervise cerebellar learning by providing signals to Purkinje cells (PCs) that instruct adaptive changes to mistakenly performed movements. Yet, climbing fibers are regularly active, even during well performed movements, suggesting that a mechanism dynamically regulates the ability of climbing fibers to induce corrective plasticity in response to motor errors. We found that molecular layer interneurons (MLIs), whose inhibition of PCs powerfully opposes climbing-fiber-mediated excitation, serve this function. Optogenetically suppressing the activity of floccular MLIs in mice during the vestibulo-ocular reflex (VOR) induces a learned increase in gain despite the absence of performance errors. Suppressing MLIs when the VOR is mistakenly underperformed reveled that their inhibitory output is necessary to orchestrate gain-increase learning by conditionally permitting climbing fibers to instruct plasticity induction during ipsiversive head turns. Ablation of an MLI circuit for PC disinhibition prevents gain-increase learning during VOR performance errors which was rescued by re-imposing PC disinhibition through MLI activity suppression. Our findings point to a decisive role for MLIs in gating climbing-fiber-mediated learning through their context-dependent inhibition of PCs. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC
Instantly download A Little Bondage Game to listen any time, without the podcast introduction. The post 4.68 The Disinhibition Hypothesis and a Little Bondage Game appeared first on Spoken By Elswyth.
Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.03.15.532773v1?rss=1 Authors: Yamaguchi, R., Ueno, S., Kawasaki, T., Chao, Z., Mitsuhashi, M., Isa, K., Takei, T., Kobayashi, K., Takahashi, J., Onoe, H., Isa, T. Abstract: The induction of large-scale plasticity in the adult brain should be key for recovery from severe damage of the central nervous system. Here, drastic motor recovery was observed after subhemisection spinal cord injury in macaques that received intensive training and cortical electrical stimulation. During recovery, movement-related activity increased in ipsilesional sensorimotor areas and functional connectivity from ipsilesional to contralesional areas was strengthened. Electrical stimulation applied widely across bilateral sensorimotor areas induced muscle twitches in affected and intact forelimbs. The interhemispheric inhibition observed before injury was switched to facilitation. Furthermore, massive re-routing occurred in corticospinal axons from the contralesional motor cortex. Such global disinhibition and massive plasticity would open the workspace for the reorganization of motor networks to recruit novel areas for recovery. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC
Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.02.16.528800v1?rss=1 Authors: Estarellas, C., Alvarez-Salvado, E., Perez-Cervera, L., Mirasso, C., Canals, S. Abstract: Cortical circuits operate in a tight excitation/inhibition balance. This balance is relaxed during learning processes, but neither the mechanism nor its impact on network operations are well understood. In the present study, we combined in-vivo and in-vitro neuronal recordings with computational modelling and demonstrated that synaptic plasticity in the afferents from the entorhinal cortex (EC) to the dentate gyrus (DG), in addition to strengthening the glutamatergic inputs into granule cells (GCs), depressed perisomatic inhibition. Computational modelling revealed a functional reorganization in the inhibitory network that explained several experimental findings, including depression of the feed-forward inhibition. In vitro results confirmed a perisomatic dominance of the inhibitory regulation with important functional consequences. It favoured GCs burst firing, improved reliability of input/output transformations and enhanced separation and transmission of temporal and spatial patterns in the EC-DG-CA3 network. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC
Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.02.14.528085v1?rss=1 Authors: Garrett, M., Groblewski, P., Piet, A., Ollerenshaw, D., Yavorska, I., Najafi, F., Amster, A., Bennett, C., Buice, M., Caldejon, S., Casal, L., D'Orazi, F., Daniel, S., de Vries, S. E., Kapner, D., Kiggins, J., Lecoq, J., Ledochowitsch, P., Manavi, S., Mei, N., Morrison, C. B., Naylor, S., Orlova, N., Perkins, J., Ponvert, N., Roll, C., Seid, S., Williams, D., Williford, A., Ahmed, R., Amine, D., Billeh, Y., Bowman, C., Cain, N., Cho, A., Dawe, T., Departee, M., Desoto, M., Feng, D., Gale, S., Gelfand, E., Gradis, N., Grasso, C., Hancock, N., Hu, B., Hytnen, R., Jia, X., Johnson, T., Kato, I., Abstract: The detection of novel stimuli is critical to learn and survive in a dynamic environment. Though novel stimuli powerfully affect brain activity, their impact on specific cell types and circuits is not well understood. Disinhibition is one candidate mechanism for novelty-induced enhancements in activity. Here we characterize the impact of stimulus novelty on disinhibitory circuit components using longitudinal 2-photon calcium imaging of Vip, Sst, and excitatory populations in the mouse visual cortex. Mice learn a behavioral task with stimuli that become highly familiar, then are tested on both familiar and novel stimuli. Mice consistently perform the task with novel stimuli, yet responses to stimulus presentations and stimulus omissions are dramatically altered. Further, we find that novelty modifies coding of visual as well as behavioral and task information. At the population level, the direction of these changes is consistent with engagement of the Vip-Sst disinhibitory circuit. At the single cell level, we identify separate clusters of Vip, Sst, and excitatory cells with unique patterns of novelty-induced coding changes. This study and the accompanying open-access dataset reveals the impact of novelty on sensory and behavioral representations in visual cortical circuits and establishes novelty as a key driver of cellular functional diversity. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC
Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2022.11.28.518253v1?rss=1 Authors: Myers-Joseph, D., Fernandez-Otero, M., Khan, A. G. Abstract: Attentional modulation of sensory processing is a key feature of cognition, yet its neural circuit basis is poorly understood. A candidate mechanism is the disinhibition of pyramidal cells through vasoactive intestinal peptide (VIP) and somatostatin (SOM) positive interneurons. However, the interaction of attentional modulation and VIP-SOM disinhibition has never been directly tested. We used all-optical methods to bi-directionally manipulate VIP interneuron activity as mice performed an attention switching task. We measured the activity of VIP, SOM and parvalbumin (PV) positive interneurons and pyramidal neurons identified in the same tissue and found that although activity in all cell classes was modulated by both attention and VIP manipulation, their effects were orthogonal. Attention and VIP-SOM disinhibition relied on distinct patterns of changes in activity and reorganisation of interactions between inhibitory and excitatory cells. These results reveal the remarkable ability of cortical circuits to multiplex strong yet non-interacting modulations in the same neural population. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC
Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2022.11.09.515872v1?rss=1 Authors: Whitebirch, A. C., Barnett, A., Santoro, B., Scharfman, H. E., Siegelbaum, S. A. Abstract: A significant proportion of temporal lobe epilepsy (TLE) patients experience drug-resistant seizures associated with mesial temporal sclerosis, in which there is extensive cell loss in the hippocampal CA1 and CA3 subfields, with a relative sparing of dentate gyrus granule cells and the CA2 pyramidal neurons. A role for CA2 in seizure generation was suggested based on findings of a reduction in synaptic inhibition (Williamson & Spencer, 1994) and the presence of interictal-like spike activity in resected hippocampal tissue from TLE patients (Wittner et al., 2009). We recently found that in the pilocarpine-induced status epilepticus mouse model of TLE there was an increase in CA2 intrinsic excitability associated with a loss of CA2 synaptic inhibition. Furthermore, chemogenetic silencing of CA2 significantly reduced seizure frequency, consistent with a role of CA2 in promoting seizure generation and/or propagation (Whitebirch et al., 2022). In the present study we explored the basis of this inhibitory deficit using immunohistochemical and electrophysiological approaches. We report a widespread decrease in the density of pro-cholecystokinin-immunopositive interneurons and a functional impairment of cholecystokinin-expressing interneuron-mediated inhibition of CA2 pyramidal neurons. We also found a decrease in the density of CA2 parvalbumin-immunopositive interneurons and disruption to the pyramidal neuron-associated perisomatic perineuronal net in the CA2 subfield. These data reveal a set of pathological alterations that may disrupt inhibition of CA2 pyramidal neurons and their downstream targets in epileptic mice. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC
Aleks Krotoski explores whether disinhibition, often associated with toxic online behaviours such as trolling, may also have benefits in our digital world? Since the early days of the internet, research into disinhibition, including John Suler's much-cited paper on the ‘online disinhibition effect' has recognised that benign disinhibition not only exists alongside toxic but deserves equal consideration. Yet somehow, our fascination with the negative often drowns out more nuanced perspectives. In this episode of the Digital Human, Aleks investigates scenarios where disinhibition might be helpful, examines factors which positively facilitate it and asks whether assumptions that aggressive online behaviours are a result of disinhibition might be a misdiagnosis of the problem. Producer: Lynsey Moyes Researcher: Juliet Conway Contributor Biographies: Ani de la Prida is a psychotherapist and creative arts counsellor and teaches at the University of East London, where she did her master's degree research on the use of digital media in arts therapy. Ani also the founder and course director of the Association for Person-Centred Creative Arts. Tom Postmes is professor of Social Psychology at the University of Groningen. He completed his PhD at the University of Amsterdam. In his research Postmes shows how everyday interactions can lead to such collective behaviour. Judith Donath is a writer, designer and artist whose work examines how new technologies transform the social world. Author of The Social Machine (MIT Press, 2014), she is currently writing a book about technology, trust and deception. Caitlin McGrane is a feminist activist, researcher and academic based in Melbourne, Australia. She works for Gender Equity Victoria leading a project enhancing online safety for women working in the media. Catherine Renton is a freelance writer and culture reviewer based in Edinburgh.
Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2022.09.08.507205v1?rss=1 Authors: Wadsley, C. G., Cirillo, J., Nieuwenhuys, A., Byblow, W. D. Abstract: Response inhibition is essential for terminating inappropriate actions. A substantial delay may occur in the response of the non-stopped effector when only part of a multi-effector action is terminated. This stopping-interference effect has been attributed to nonselective response inhibition processes and can be reduced with proactive cueing. This study aimed to elucidate the role of interhemispheric primary motor cortex (M1-M1) influences during selective stopping with proactive cueing. We hypothesized that stopping-interference would be reduced as stopping certainty increased, owing to proactive recruitment of interhemispheric facilitation or interhemispheric inhibition when cued to respond or stop, respectively. Twenty-three healthy human participants performed a bimanual anticipatory response inhibition paradigm with cues signaling the likelihood of a stop-signal occurring. Dual-coil transcranial magnetic stimulation was used to determine corticomotor excitability (CME), interhemispheric inhibition (IHI), and interhemispheric facilitation (IHF) in the left hand at rest and during response preparation. Response times slowed and stopping-interference decreased with cues signaling increased stopping certainty. Proactive response inhibition was marked by a reduced rate of rise and faster cancel time in electromyographical bursts during stopping. There was a nonselective release of IHI but not CME from rest to in-task response preparation, while IHF was not observed in either context. An effector-specific CME but not IHF or IHI reduction was observed when the left hand was cued to stop. These findings indicate that the stopping-interference effect can be reduced through proactive suppression. Interhemispheric M1-M1 channels modulate inhibitory tone that supports responding, but not selective stopping, in a proactive response inhibition context. Copy rights belong to original authors. Visit the link for more info Podcast created by PaperPlayer
Chapter 17 of Sloterdijk's Critique of Cynical Reason. Conspirators and Dissimulators. Political Cynicisms IV: Conviction as Disinhibition.
Hvad former vores adfærd på de sociale medier? Er vi mere kyniske og aggresive online end vi er, når vi mødes ansigt til ansigt. I denne uge fortæller vi i vores nye koncept “Kort sagt” om the online disinhibition effect. Vi diskuterer, hvorvidt man burde lave et kørekort til internettet.
Author Michael Wiley discusses his new series starring Private Investigator Sam Kelson. The most recent installment is Lucky Bones, book #2 in the series. Sam Kelson is not your typical PI. He suffers from disinhibition, and his inability to keep his mouth shut is not a helpful trait for a private investigator. However, it does make for some very interesting storylines. Michael found inspiration for his character's affliction from his teenage kids' embarrassment at almost everything he said and did.
In this episode of, Philosophy of the Nerd, Keoni, and Logan attempt to understand the dynamics that make some online videogame communities unpleasant and toxic. From specific examples experienced personally to philosophical theories, this a broad topic but nonetheless essential to discuss. Music by Rutger Muller - https://freesound.org/people/RutgerMuller/Edited by: Keoni EckingerFollow us on Twitter Philosophy of The Nerd (@Polygonbois) / TwitterCheck out Logan's writing at https://ldbwriting.comCheck out Keoni's writing at https://keck60.medium.com
Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2020.11.04.367722v1?rss=1 Authors: Gazea, M., Furdan, S., Sere, P., Oesch, L., Molnár, B., Di Giovanni, G. D., Adamantidis, A. R., Lorincz, M. L. Abstract: The lateral hypothalamus (LH), together with multiple neuromodulatory systems of the brain, such as the dorsal raphe nucleus (DR), is implicated in arousal, yet interactions between these systems are just beginning to be explored. Using a combination of viral tracing, circuit mapping, electrophysiological recordings from identified neurons and combinatorial optogenetics, we show that GABAergic neurons in the LH selectively inhibit GABAergic neurons in the DR resulting in disinhibition of a substantial fraction of its neurons that ultimately promotes arousal. These DR GABAergic neurons are wake active and project to multiple brain areas involved in the control of arousal including the LH, where their specific activation potently influences local network activity leading to arousal from sleep. Our results show how mutual inhibitory projections between the LH and the DR promote wakefulness through disinhibitory mechanisms and suggest a complex arousal control by intimate interactions between long-range connections and local circuit dynamics. Copy rights belong to original authors. Visit the link for more info
Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2020.10.13.337188v1?rss=1 Authors: Guerreiro, I., Gu, Z., Yakel, J., Gutkin, B. Abstract: Hippocampal synaptic plasticity, particularly in the Schaffer collateral (SC) to CA1 pyramidal excitatory transmission, is considered as the cellular mechanism underlying learning. The CA1 pyramidal neurons are embedded in an intricate local circuitry that contains a variety of interneurons. The roles these interneurons play in the regulation of the excitatory synaptic plasticity remains largely understudied. Our recent experiments showed that repeated cholinergic activation of 7 nACh receptors expressed in oriens-lacunosum-moleculare (OLM2) interneurons could induce LTP in SC-CA1 synapses, likely through disinhibition by inhibiting stratum radiatum (s.r.) interneurons that provide feedforward inhibition onto CA1 pyramidal neurons, revealing a potential mechanism for local interneurons to regulate SC-CA1 synaptic plasticity. Here, we pair in vitro studies with biophysically-based modeling to uncover the mechanisms through which cholinergic-activated GABAergic interneurons can disinhibit CA1 pyramidal cells, and how repeated disinhibition modulates hippocampal plasticity at the excitatory synapses. We found that 7 nAChR activation increases OLM activity. OLM neurons, in turn inhibit the fast-spiking interneurons that provide feedforward inhibition onto CA1 pyramidal neurons. This disinhibition, paired with tightly timed SC stimulation, can induce potentiation at the excitatory synapses of CA1 pyramidal neurons. Our work further describes the pairing of disinhibition with SC stimulation as a general mechanism for the induction of hippocampal synaptic plasticity. Disinhibition of the excitatory synapses, paired with SC stimulation, leads to increased NMDAR activation and intracellular calcium concentration sufficient to upregulate AMPAR permeability and potentiate the synapse. Repeated paired disinhibition of the excitatory synapse leads to larger and longer lasting increases of the AMPAR permeability. Our study thus provides a novel mechanism for inhibitory interneurons to directly modify glutamatergic synaptic plasticity. In particular, we show how cholinergic action on OLM interneurons can down-regulate the GABAergic signaling onto CA1 pyramidal cells, and how this shapes local plasticity rules. We identify paired disinhibition with SC stimulation as a general mechanism for the induction of hippocampal synaptic plasticity. Copy rights belong to original authors. Visit the link for more info
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TITLE High Sensation Seeking & The Highly Sensitive Person—You May Be Surprised! GUEST Tracy Cooper, Ph.D. EPISODE OVERVIEW Author, Tracy Cooper, Ph.D defines how High Sensation Seeking (HSS) shows up in the Highly Sensitive Person, and the 4 core aspects of Sensation Seeking. Dr. Cooper talks about ADHD vs. HSS, and the role dopamine plays in sensation seeking. We talk about being in flow, and the relationship between anxiety, depression. Dr. Cooper says HSPs are wired for creativity (so are sensation seekers). We explore how HSPs are impacted by social media. Dr. Cooper talks about what we can do when we’re overactivated, and how boundaries can help the HSP. HIGHLIGHTS In the 1960’s Marvin Zuckerman was doing research on sensory deprivation using deprivation tanks Those people that became restless fairly quickly and were thought to need stimulation, leading Zuckerman and his colleagues to develop Sensation Seeking as a personality trait. 30% of Highly Sensitive People are High Sensation Seekers (HSS) It is presumed that of that 30 % of HSS/HSPs, 30% are extroverts and 70% are introverts The 4 core aspects of Sensation Seeking are 1. Thrill and adventure seeking—bungee jumping, parachuting, adrenaline rush type activities. It can also mean driving fast, exciting TV shows, anything that provides a physical rush. Most HSPs are not this type 2. Experience and novelty seeking—travelling, foodies, reading new books. They are not satisfied with ordinary things and will seek out unusual or different experiences for the sake of having them. Boredom susceptibility—want stimulation, boredom can be physically painful, and boredom is their worst enemy, their capacities are begging to be engaged 4. Disinhibition—willingness to exceed normal bounds of behavior for the thrill of having an experience. They may not be concerned with legal, financial, relational or personal repercussions, which can lead to disastrous results. Can experiment with drugs, sexual behavior, parties, may go before the light turns green or doesn’t stop fully at stop signs. May exceed speed limits or tailgate, use cars and driving to seek thrills. Sensation seeking is a general trait that is seen in the larger population Any extreme expression of a trait is never a good thing. The moderate to moderate-high expression is where the advantages are realized. You can imagine a bell-shaped curve for the expression of sensation seeking where the majority will fall in the middle, comparatively fewer at the extreme on both ends. There is a crossover in HSPs between novelty & new experiences and boredom susceptibility, but you don’t typically see a crossover with thrill & adventure and disinhibition because Sensory Processing Sensitivity is about pausing think first before doing. All humans are sensation seeking to some degree. Men more than women. Experience and novelty seeking can be a powerful drive We get a “hit” of dopamine (a neurotransmitter involved in the brain’s pleasure pathway) when we engage in sensation seeking. This feel-good rush entices us to do more to get another rush. There is a tension between the HSP and the HSS. If the HSS wins out it can lead to burn out for the HSP quite easily. One must learn to balance the two traits by understanding the giftedness inherent in both traits. ADHD vs. HSS They share some components The HSS focuses on stimulation. Once they get the stimulation, they can still focus The ADHD brain can’t get the stimulation it needs (when it gets even a small amount it wants more until it is overloaded) If the person doesn’t get stimulation they don’t function as well, or they don’t function and isolate (like playing video games to excess) HSPs and HSS/HSPs may seek stimulation through other people We absorb energy from other people and through social interactions, and we get a dopamine hit from the interaction if it is positive. When the HSS side rules out, it takes the HSP along for the ride, which can leave the HSP exhausted afterward When we block things out (HSS side), we can become less patient, less sensitive and less empathetic We don’t want to lose the HSP trait because we want to maintain the traits of patience, sensitivity and empathy It’s about learning to balance our HSP and HSS parts We can get addicted to sensation seeking if we are not aware of this risk. Boredom susceptibility—we have to do things to stay in our optimal range of arousal since that is the preference When are we in entropy, depression, and anxiety This is a natural state, according to psychologist Mihaly Csikszentmihalyi, when we’re NOT in flow We spend too much time in our heads, and our capacities are begging to be engaged It’s important to break out of our rut by getting in touch with our curiosity and sense of wonder We may need to push ourselves to do new things Our natural tendency as HSPs is to be positive and open but cautious You can get a friend to go with you or meet you if it’s challenging to try new things You can remind yourself that if you try something new, you can always leave if you don’t like it Analysis/paralysis—if we had a bad experience or got overstimulated, and we have an opportunity to engage in a similar activity, we decline based on past experience due to overthinking. If we do this repeatedly, we can get stuck in a rut, and our world can become too small We can use mindfulness when this happens We can know that we can only experience 1 moment at a time and be open to each new moment Flow state—our skills are matched to the task, and we are fully engaged and absorbed in that state (we don’t experience anxiety or depression) If the task is too hard, we experience anxiety; if the task is not challenging enough, we experience boredom Being in flow is the best play experience HSPs are wired for creativity We traditionally thing of creativity in terms of an artistic end-product HSPs are naturally predisposed to creativity and creative thinking HSPs engage in creative thinking naturally but need to build their ability to think rationally and critically to complement creative thinking, they are synergistic and interdependent. HSPs noticed more things when shown visual scenes—they were more empathetic, and showed a broader emotional range, psychologically androgynous. Boundaries HSPs can set boundaries that limit overstimulation HSPs can practice anticipating what they will do if a boundary is crossed When we’re overstimulated/overactivated Enforcing boundaries is most important We need to know where the boundary is—often we find the boundary only when we hit a limit If you’re overstimulated (aversive state) Withdraw—take time away Allow your body to relax, dispel the pent-up energy Use self-compassion and be kind to yourself Reframe—that wasn’t so bad; it was temporary; I recovered Social media/electronics/boredom and addiction HSSs seek stimulation through people as much as through external sources With electronics we tend to gravitate to people like us (confirmation bias—values/people similar to you), ignore information that disagrees with current beliefs. Technology can be an addiction We do better when we’re outside, moving around, and being sedentary and indoors can be highly detrimental to HSPs Anxiety isn’t always a negative—it asks you to think about what you’re doing. Anxiety will usually dissipate once you are engaged We’ve got to learn to develop self-care practices If you struggle with overthinking Take a class that uses your hands/body/mind Learn when to put the brakes on thinking Allow a specific amount of time (15 minutes a day) to worry/think Getting outside, taking a walk, time in nature, or talking it over with a trusted friend are all ways to shift out of overthinking QUOTES Any extreme expression of a trait is never a good thing. The moderate to moderate-high expression is where the potential of the trait is realized best. All humans are sensation seeking to some degree Novelty is a powerful drive We prefer to do things that keep us in our optimal range of arousal We spend too much time in our heads, and our capacities are begging to be engaged HSPs and HSS/HSPs are wired for creativity GUEST BIO Tracy Cooper, Ph.D. is an expert in the areas of highly sensitive people and career, the high sensation seeking highly sensitive person, the highly sensitive man, and highly sensitive people and creativity. He has written two books, Thrive: The Highly Sensitive Person and Career and Thrill: The High Sensation Seeking Highly Sensitive Person. His forthcoming book is titled Empowering the Sensitive Male Soul. Dr. Cooper appeared in the 2015 documentary film, Sensitive-The Untold Story. He is the Department Chairman for Baker University’s Master of Liberal Arts program and a faculty member. Dr. Cooper regularly works with individuals in career crisis and transition, as well as corporations interested in diversity and inclusion initiatives for HSPs, innovation and HSS/HSPs, and frequently speaks on subjects related to sensory processing sensitivity and sensation seeking. PODCAST HOST Patricia Young works with Highly Sensitive People (HSPs) helping them to understand their HSP traits, and turning their perceived shortcomings into superpowers. Patricia is a Licensed Clinical Social Worker, who is passionate about providing education to help HSPs and non-HSPs understand and truly appreciate the amazing gifts they have to offer. Patricia works globally online with HSPs providing coaching. Patricia also facilitates online groups for HSPs that focus on building community and developing skills (identifying your superpowers, boundaries, perfectionism, dealing with conflict, mindfulness, embracing emotions, creating a lifestyle that supports the HSP, communication and more). LINKS Dr. Tracy Cooper’s links drtracycooper.wordpress.com @tracycooperphd (FaceBook) @sensitivemalesoul (FaceBook) tracycooperphd (LinkedIn) tracycooperphd (Instagram) Flow by Mihaly Cziksventmihalyi Man’s Search for Meaning by Viktor Frankl Patricia’s Links HSP Online Course--https://unapologeticallysensitive.com/hsp-online-groups/ To write a review in itunes: click on this link https://itunes.apple.com/us/podcast/unapologetically-sensitive/id1440433481?mt=2 select “listen on Apple Podcasts” chose “open in itunes” choose “ratings and reviews” click to rate the number of starts click “write a review” Website--www.unapologeticallysensitive.com Facebook-- https://www.facebook.com/Unapologetically-Sensitive-2296688923985657/ Closed/Private Facebook group Unapologetically Sensitive-- https://www.facebook.com/groups/2099705880047619/ Instagram-- https://www.instagram.com/unapologeticallysensitive/ Youtube-- https://www.youtube.com/channel/UCOE6fodj7RBdO3Iw0NrAllg/videos?view_as=subscriber e-mail-- unapologeticallysensitive@gmail.com Show hashtag--#unapologeticallysensitive Music-- Gravel Dance by Andy Robinson www.andyrobinson.com
Rachel & Neil discuss the psychological phenomenon of the online disinhibition effect, known more commonly as trolling in relation to the case of Conrad Roy.
Without order, there is chaos. And our diminished self consciousness and self control has damaging impacts on our community. If we do not restore restraint and discipline to our language and behavior, how can we grow? How can our families be successful? And how will our communities improve? If you would like to engage with the Nurah Speaks podcast, submit your listener questions to info@NurahSpeaks.com. Listeners can also learn more about Nurah by visiting her website: NurahSpeaks.com or reading her blog by clicking this link. Follow Nurah Speaks @NurahSpeaksPodcast on Facebook, Twitter and Instagram. To bring Nurah as a speaker at your next event, email info@NurahSpeaks.com Remember, don't just Join the Movement, Be the Movement!
Chad Gailey of Necrot, Vastum, Mortuous, Atrament, and Disinhibition calls into the hole! Voicemail : 631-837-3274 Music Featured: Necrot - Blood Offerings Mortuous - Through Wilderness Vastum - Reveries in Autophagia Harm's Way - Become a Machine Karnarium - The Glory Of Necrolatry Gender Fluids - Licking the Palms Clean Noose Rot - The Creeping Unknown Coffin Mulch - Demo Sekkusu - Satyromania Burial Temple - Mortal Scum Antigama - Discomfort Meshuggah - Chaosphere Mastic Scum - Tilt 7"
SSD Podcast brings you part II of this epic convo with Lyle McDonald! After discussing the state of Flexible dieting and some of the issues surrounding it (as well as the benefits), now we'll discuss some of the more important implications of dietary adherence. - How do binges happen? - The What the Hell effect - What kind of dietary strategies are better for certian personality types - Rapid vs Slow weight loss. Time Stamps: 01:33 - The what the hell effect: 10:34 - Personality types and diet success 15:06 - Changing your habits for diet success 21:08 - Slow vs Rapid Weight Loss 35:50 - Starting the diet aggressively and then slow it doen 44:10 - Life after dieting - finding goals and purpose once you're done with fat loss 52:20 - Summary Check out Lyle's stuff: www.bodyrecomposition.com
In today's podcast we hear about patching: the good, the bad, and the ugly. But mostly the good. Dridex is back. Brussels airport hacker turns out to be a literal script-kiddie, with the emphasis on the "kiddie." Moscow treason trials shut down Russian cooperation with Western law enforcement. Robert Lord from Protenus returns to share their Breach Barometer Report results. Ben Yelin from the University of Maryland Center for Health and Homeland Security revisits the Playpen case. Industry notes, a look ahead to RSA, and some Valentine's Day advice.
Delta-Notch's weekly mix, featuring some of the most enjoyable, entertaining, and innovative music in the electronic dance world. This week features the guest mix I made for the Beatdown Krew's podcast. I worked a long time getting it exactly how I liked and I'm very proud of how it turned out. It's 29 tracks in 55 minutes and I made sure to include some of my favorite DnB bangers and a few of my own live remixes and mash-ups. The mix has everything from light and atmospheric to dark and heavy so you're sure to find something that fits your taste. For those interested to see this mix performed in a penguin suit... http://www.youtube.com/watch?v=eRnyfVhlX0s "A Penguin's Drum & Bass" tracklist: Rido -- Exoplanet Noisia feat. Amon Tobin -- Sunhammer Phace & Noisia -- Micro Organism Andrew Bayer & Matt Lange vs. Dub Phizix & Skeptical & Calyx & Teebee -- In and Out of Marka (Delta-Notch Mashup) Blu Mar Ten -- Sweet Little Supernova Black Sun Empire -- Are You There? Rockwell vs. Breakage -- Stowaway Temper (Delta-Notch Mashup) Netsky vs. Gridlok -- Mellow Insecticide (Delta-Notch Mashup) Rawthang -- Beautiful Morning (Gein Bootleg) Body & Soul & Fourward -- Authority VIP The Upbeats -- Undertaker Mark Knight -- Nothing Matters (Noisia Remix) Bad Company vs. Kosheen -- The Nine Will Hide U (Delta-Notch Mashup) Spor, Ewun, & Evol Intent -- Levitate Hardwell -- Spaceman (Carnage Festival Trap Remix) Tasha -- Journey (Culprate & Twist Remix) Gemini -- Elevate Phace & Misanthrop -- Energie Noisia & Foreign Beggars -- Soul Purge (Current Value Remix) The Qemists -- Your Revolution (Reso Remix) Cause4Concern -- Dream Killer (Teknian Remix) Noisia & Phace -- Program (Chainsaw Police Remix) Noisia -- Friendly Intentions Hazard vs. DJ Fresh -- Bust Kryptonite (Delta-Notch Mashup) Spontaneous Activity: Ry & Frank Weidemann -- Howling (Ame Remix) http://facebook.com/DeltaNotch
Delta-Notch's weekly mix, featuring some of the most enjoyable, entertaining, and innovative music in the electronic dance world. Looking for love? You found it! Focusing on the fire that brings two people together and the passion that keeps them there, this hour-long mix features some of trance music's greatest love songs. Tracklist: BT -- Every Other Way (Armin van Buuren Remix)Eco -- Love (Dub Mix)Laura Jansen -- Use Somebody (Armin van Buuren Remix)Dash Berlin -- Better Half of MeFilo & Perri -- This Night (Dash Berlin Remix)Fedde le Grand -- So Much LoveOrjan Nilsen -- Lovers LaneKaren Overton -- Your Loving Arms (Club Mix)Andrew Bayer -- You (Original Mix)BT -- Mercury & Solace (BT 12" Mastermix)Deadmau5 -- Alone with You (Original Mix)Paul Van Dyk -- I Don't Deserve You Spontaneous Activity: Armin van Buuren -- Virtual Friend http://www.facebook.com/DeltaNotch
Delta-Notch's weekly mix, featuring some of the most enjoyable, entertaining, and innovative music in the electronic dance world. "Climax" takes the calm and meditative energy of the previous mix, "Presence," increases its intensity throughout the first few warmup tracks, then unleashes it in a fury of all-encompassing soundscapes to create a very heavy yet very beautiful conclusion to the two-part Tantra series--appropriate for any time a good energy release is required. Tracklist: Shogun -- Skyfire (Original Mix Edit) Tiesto -- Speed Rail Kyau & Albert -- Made of Sun (Stoneface & Terminal Remix) A*S*Y*S -- Acid Glitch Noisia -- Tommy's Theme Ellie Goulding -- Lights (Bassnectar Remix) Gemini -- Elevate Phace & Misanthrop -- Energie Loadstar -- Link to the Past Body & Soul & Fourward -- Authority VIP Excision & Downlink -- The Underground Smoothiesforme -- Forbidden (System Remix) The Bloody Beetroots -- Warp (Dirtyphonics Remix) Gemini -- Blue Arkasia -- Pandemonium Spontaneous Activity: Ladytron -- Destroy Everything You Touch (Sasha Invol2ver Remix) http://facebook.com/DeltaNotch
Delta-Notch's weekly mix, featuring some of the most enjoyable, entertaining, and innovative music in the electronic dance world. Some friends of mine are Tantrikas (followers of Tantra) and asked me to make a mix to facilitate the act of finding "presence," disregarding either past or future. This ecclectic mix of vocal, instrumental, ambient, and atmospheric tunes may just have you reaching enlightenment sooner than you thought. Tracklist: Roland Conil -- Malibu Beach Andrew Bayer, Kaskade & Adam K -- Counting the Raining Points (Simon Dawn Mash-Up) Motorcitysoul -- Space Katzle (Jerome Syndenham Remix) Spor -- Pacifica (Kito & Reija Remix) Omnia & The Blizzard -- Closer Clouded Leopard -- Hua-Hin Irrelevant -- Grains (Myrkur Remix) DJ Hooligan -- Hear You Now (Grand Chillas Remix) Deadmau5 -- Faxing Berlin Banyan Tree -- Feel the Sun Rise Lung -- Afterlife (Kryptic Minds Remix) Blu Mar Ten -- Sweet Little Supernova Sensa & Haste -- The Place Pink Elephant -- Lax Kulture -- Mako Energy Phaeleh -- Afterglow Spontaneous Activity: Orjan Nilsen -- Viking http://facebook.com/DeltaNotch
Delta-Notch's weekly mix, featuring some of the most enjoyable, entertaining, and innovative music in the electronic dance world. This week's show is designed for the dance floor with a mix that is guaranteed to get you moving. A Penny Saved... tracklist: Omni & IRA -- The Fusion (Armin van Buuren Intro Edit) Kaskade -- Room for Happiness (Mysto & Pizzi Remix) Knife Party -- Destroy Them with Lazers Robyn -- Call Your Girlfriend (Feed Me Remix) Zedd -- Shave It (Inphinity's Electrostep Edit) Avicii -- Two Million Martin Solveig -- The Night Out (Madeon & A-Trak Remix) Sander Van Doorn -- Slap My Pitch Up Sander Kleinenberg -- This is Our Night (Dj Groovy Remix) Boys Will Be Boys -- We Rock W&W -- Nowhere to Go Steve Aoki -- Steve Jobs Silvio Ecomo & Chuckie -- Moombah! (Afrojack Remix) Jacob Plant -- Jump Up Big Sean -- Dance A$$ (DaGo Booty Dutch Bootleg) Chris Lake & Nelski -- Minimal Life Tiesto -- Bend It Like You Don't Care Above & Beyond -- Sun & Moon (Club Mix) Deadmau5 -- City in Florida Avicii -- My Feelings for You David Guetta -- Dreams Gareth Emery -- Concrete Angel Dash Berlin & ATB -- Apollo Road Haddaway -- What is Love (Krunk! Bootleg) Fun. -- We Are Young (Revolvr Remix) Fun. vs. Knife Party -- We Are On You (Share Mash-Up) Spontaneous Activity Track: Andy Moor -- Elysian Fields
Delta-Notch's weekly mix, featuring some of the most enjoyable, entertaining, and innovative music in the electronic dance world. This week's show starts the semester off right with a mix intended to listen to while you study. Trance to Study By tracklist: Sasha -- Magnetic North Armin van Buuren -- Minack Rex Mundi -- Sandstone (Original Mix Edit) Orjan Nilsen -- Le Tour de Trance TyDi -- Out in the Cold Cressida -- No More Lies Arnej -- The Strings that Bind Us JayTech -- New Vibe Zoo Brazil -- Crossroads Tiesto -- Green Sky Danilo Ercole -- Water that Birds don't Drink (Original Mix) Motorcitysoul -- Space Kaztle (Jerome Syndenham Remix) W & W -- Based on a True Story Paul Van Dyk -- Symmetries Deadmau5 -- Brazil Spontaneous Activity: Phace & Misanthrop -- Energie
Medizinische Fakultät - Digitale Hochschulschriften der LMU - Teil 07/19
Zahlreiche Befunde deuten auf eine Störung der interhemisphärischen Konnektivität bei Patienten mit Schizophrenie. Funktionell wurden beispielsweise Veränderungen der interhemisphärischen Kohärenz gefunden. Die Kohärenz gilt als ein Indikator für funktionelle Verbindungen zwischen den entsprechenden Hirnregionen und ist in ihrer interhemisphärischen Variante ein Maß für die Synchronisation des EEG zwischen den korrespondierenden bilateralen Regionen. Für die interhemisphärische Kohärenz und die interhemisphärische Konnektivität kommt dem Corpus Callosum (CC) als wichtigster kommissuraler Verbindung der Hemisphären eine entscheidende Bedeutung zu. Gleichzeitig ist bei CC-Pathologien einerseits die Prävalenz der Schizophrenie erhöht und es findet sich andererseits bei Patienten mit Schizophrenie ein erhöhtes Vorkommen von CC-Pathologien. Strukturelle MRT-Befunde deuten auf ein leicht verkleinertes CC bei Patienten mit Schizophrenie. Zusätzlich finden sich pathologische Veränderungen in der Lamina III des präfrontalen Kortex von Patienten mit Schizophrenie, dem Ursprungsort der kallosalen Projektionen. Auch Entwicklungshypothesen finden Bezug zu einer Pathologie des CC bei Patienten mit Schizophrenie: seine Entwicklung, bei der die Elimination von Axonen mit zunehmender Myelinisierung und Vergrößerung einhergeht, zieht sich bis in die dritte Lebensdekade hin und zeigt damit Parallelen zur späten klinischen Manifestation der Erkrankung. Aufgrund der Heterogenität der Befunde ist allerdings nicht klar, welcher Art die Störung der interhemisphärischen Konnektivität bei Patienten mit Schizophrenie ist. Eine Hypokonnektivität würde z.B. die Assoziation zwischen CC-Agenesien und Schizophrenie vermuten lassen, neuro- und psychophysiologische Experimente deuten eher in Richtung einer Hyperkonnektivität. Ziel der Arbeit war die explorative Untersuchung der Frage, ob eine Störung der interhemisphärischen Konnektivität bei Patienten mit Schizophrenie vorliegt und welcher Art diese interhemisphärische Konnektivitätsstörung sein könnte. Methode: Es wurden 27 männliche Patienten mit chronischer Schizophrenie und 25 gematchte Kontrollen untersucht. Anhand des Ruhe-EEGs wurden fünf interhemisphärische Kohärenzen bipolarer Verschaltungen berechnet. Mittels MRT wurde die CC-Größe durch Vermessung der midsagittalen Fläche des CC ermittelt und in fünf Unterabschnitte unterteilt. Neben der Analyse auf Unterschiede bezüglich der Kohärenzen und der CC-Größe, wurden die interhemisphärischen Kohärenzen mit der CC-Größe korreliert, um über die Verbindung von strukturellen und funktionellen Parametern Hinweise über die Integrität der interhemisphärischen Konnektivität zu erhalten. Zusätzlich wurde der Einfluss der neuroleptischen Medikation und die Abhängigkeit der Kohärenzen und der CC-Größe von klinischen Parametern anhand der PANSS-Skala untersucht. Ergebnisse: Die Mittelwerte frontozentraler interhemisphärischer Kohärenzen waren im Beta-Frequenzbereich signifikant bei den Patienten mit Schizophrenie gegenüber den Kontrollpersonen erhöht. Dabei zeigte sich eine negative Korrelation zwischen der Neuroleptika-Dosis und der Höhe der Kohärenzen. Für die CC-Größe zeigten sich keine signifikanten Unterschiede. Klinisch korrelierten frontale und frontotemporale Theta-Kohärenzen mit der Psychopathologischen Globalskala, aber nicht mit der Positiv- oder Negativsymptomatik. Die Pearson-Korrelationen der interhemisphärischen Kohärenzen mit der CC-Größe zeigten bei den Patienten für alle Frequenzbereiche signifikant positive Korrelationen zwischen den interhemisphärischen Kohärenzen besonders in mittleren Segmenten des CC. Nach Berücksichtigung des Neuroleptika-Einflusses waren diese Korrelationen noch deutlicher. Dagegen wiesen die Gesunden negative Korrelationen zwischen allen interhemisphärischen Kohärenzen im Delta- und Beta-Frequenzbereich ebenfalls besonders in mittleren CC-Segmenten auf. Diskussion: Damit bestehen Hinweise für eine interhemisphärische Hyperkonnektivität bei Patienten mit Schizophrenie. Während bei Gesunden mit steigender CC-Größe die interhemisphärische Konnektivität abnimmt, nimmt sie bei den Patienten mit Schizophrenie zu. Im Rahmen einer Entwicklungshypothese mit gestörter kallosaler Entwicklung könnte die in der Literatur gefundene Tendenz einer CC-Verkleinerung für eine vermehrte Anzahl an Axonen, mit verminderter Myelinisierung sprechen, da in der kallosalen Entwicklung die Größenzunahme und zunehmende Myelinisierung mit der massiven Elimination von Axonen einhergeht. Eine verminderte Elimination von Axonen könnte somit die Grundlage einer interhemisphärischen Hyperkonnektivität sein. Verkleinerungen von Pyramidenzellen in Lamina III des präfrontalen Kortex, den Ursprüngen der kallosalen Axone scheinen dies zu bestätigen. Auch psychophysiologische Experimente unterstützen eine interhemisphärische Hyperkonnektivitäts-Hypothese. Ähnlich wird sie durch das Modell einer verminderten Lateralisierung bei Patienten mit Schizophrenie unterstützt, welche mit einer Hyperkonnektivität einhergeht. Ein weiterer Aspekt der interhemisphärischen Hyperkonnektivität ist eine verminderte Inhibition auf kortikaler Ebene, welche durch eine Funktionsabschwächung inhibitorischer GABAerger Interneuronen in Lamina III des präfrontalen Kortex erklärt wird. Die GABAergen Interneuronen werden ihrerseits durch dopaminerge Afferenzen inhibiert, welche bei Patienten mit Schizophrenie pathologisch vermehrt sind. Es resultiert daher eine Disinhibition der Pyramidenzellen, den Ursprungsorten kortikaler Projektionen. Neuroleptika als Dopamin-Antagonisten würden damit diese Hyperkonnektivität reduzieren. Die signifikante Korrelation der Kohärenzen mit der globalen Psychopathologie, aber nicht mit den jeweiligen Positiv- oder Negativ-Skalen spricht eher für die Einheit dieser Symptomkonstellationen, unter dem Vollbild der Schizophrenie.
Medizinische Fakultät - Digitale Hochschulschriften der LMU - Teil 01/19
Spiegelbildliche Mitbewegungen bei Kindern und Jugendlichen mit infantiler Zerebralparese Spiegelbildliche Mitbewegungen sind Mitbewegungen homologer Muskelgruppen der Gegenseite bei einseitigen Willkürbewegungen, die sowohl bei gesunden Individuen, als auch bei Patienten mit zerebralen Läsionen beobachtet werden. Spiegelbewegungen gel-ten als Ausdruck von Reorganisationsprozessen im Zentralnervensystem; über ihre Häufigkeit, Phänomenologie und ihre Grundlagen ist aber immer noch wenig bekannt. Bei Patienten mit infantiler Zerebralparese wurden spiegelbildliche Mitbewegungen mehrfach berichtet. Zur Erklärung werden unter anderem eine durch die Hirnläsion be-dingte Disinhibition vorbestehender ipsilateral deszendierender Anteile der motorischen Bahnen diskutiert, ferner das Aussprossen neuer Bahnen. In der vorliegenden Arbeit wurden 52 Patienten mit infantiler Zerebralparese (weiblich: 13; männlich: 39) im Alter von 6 bis 41 Jahren (davon 11 Patienten mit Hemiparese, 37 Patienten mit bilateraler, seitenbetonter Schädigung und 4 Patienten mit Zerebralparese ohne feinmotorisches Defizit) sowohl klinisch als auch apparativ auf das Vorkommen und die Phänomenologie von Spiegelbewegungen bei infantiler Zerebralparese untersucht und mit den Befunden einer Kontrollgruppe verglichen. Die klinische Prüfung bestand aus vier Aufgaben (sequenzielle Fingeropposition, Finger schnipsen, Faust öffnen, Finger spreizen gegen Widerstand); danach wurde apparativ, computergestützt die maximale Frequenz der Kraftwechsel im Präzisionsgriff zwischen Daumen und Zeigefinger simultan in beiden Händen aufgezeichnet, wobei eine Hand willkürliche Kraftwechsel mit höchstmöglicher Frequenz ausführen sollte, während die andere ruhig gehalten werden sollte. In der klinischen Untersuchung variierte der Ausprägungsgrad von Spiegelbewegungen zwischen vollständigem Fehlen bis hin zur maximal möglichen Ausprägung. Die Spiegel-bewegungen waren bei 40% der Patienten pathologisch, d.h. stärker ausgeprägt als das von den altersentsprechenden gesunden Kontrollpersonen erreichte Maximum. In der apparativen Untersuchung variierten die Verhältnisse der Kräfte zwischen „Spie-gelhand" und willkürlich bewegter Hand von Mittelwerten von 0,51% bis hin zu 207% zwischen den einzelnen Patienten. Gemessen an den Höchstwerten der altersentspre-chenden Kontrollpersonen war diese Aktivität bei 56% der Patienten pathologisch. Klinisch traten Spiegelbewegungen eher bei Willkürbewegung der betroffenen Hand auf, insbesondere bei Hemiparese. In den experimentellen Untersuchungen fand sich eben-falls eine ausgeprägte Seitendifferenz bei den Patienten mit unilateraler Beeinträchtigung. Pathologische Spiegelaktivität fand sich bei den Patienten mit Hemiparese tendenziell häufiger in der gesunden Hand (also bei Willkürbewegung der betroffenen Hand), bei den Patienten mit bilateraler Schädigung eher in der stärker betroffenen Hand. Eine Korrelation mit dem Schweregrad des neurologischen Befundes zeigte sich in der klinischen Untersuchung nicht. In den apparativen Untersuchungen hingegen zeigte sich eine deutliche Korrelation: pathologische Spiegelaktivität trat umso häufiger auf, je aus-geprägter das feinmotorische Defizit war. Es fand sich kein Hinweis für einen Einfluß der Seite der Läsion auf das Auftreten und den Ausprägungsgrad von Spiegelbewegun-gen. Zusammenfassend bestätigen die Ergebnisse, daß pathologische Spiegelbewegungen bei Zerebralparese häufig sind. Eine regelhafte Beziehung hinsichtlich ihres Ausprägungs-grades oder ihrer Lokalisation (ipsi-/kontraläsional) war in dieser Untersuchung aber nicht erkennbar. Zur Erklärung bei Hemiparese kommen insbesondere die „Disinhibiti-onshypothese" und die „Hypothese der neuen kortikospinalen Bahnen" in Frage, da sie das Auftreten von Spiegelbewegungen in der gesunden Hand voraussagen. Eine Ent-scheidung zwischen den unterschiedlichen Erklärungsmöglichkeiten ist aber aufgrund des hier verfolgten rein phänomenologischen Ansatzes nicht möglich. Zudem sind vermut-lich je nach Zeitpunkt der Hirnschädigung unterschiedliche Mechanismen für den ätiolo-gisch heterogenen Befund abnormer Spiegelbewegungen verantwortlich.
Intracellular recordings were performed on hippocampal CA3 neuronsin vitro to investigate the inhibitory tonus generated by endogenously produced adenosine in this brain region. Bath application of the highly selective adenosine A1 receptor antagonist 1,3-dipropyl-8-cyclopentylxanthine at concentrations up to 100 nM induced both spontaneous and stimulus-evoked epileptiform burst discharges. Once induced, the 1,3-dipropyl-8-cyclopentylxanthine-evoked epileptiform activity was apparently irreversible even after prolonged superfusion with drug-free solution. The blockade of glutamatergic excitatory synaptic transmission by preincubation of the slices with the amino-3-hydroxy-5-methyl-4-isoxazolpropionic acid receptor antagonist 6-cyano-7-nitroquinoxaline-2,3-dione (10 μM), but not with theN-methyl-d-aspartate receptor antagonistd-2-amino-5-phosphonovaleric acid (50/μM), prevented the induction of epileptiform activity by 1,3-dipropyl-8-cyclopentylxanthine. The generation of the burst discharges was independent of the membrane potential, and the amplitude of the slow component of the paroxysmal depolarization shift increased with hyperpolarization, indicating that the 1,3-dipropyl-8-cyclopentylxanthine-induced bursts were synaptically mediated events. Recordings from tetrodotoxin-treated CA3 neurons revealed a strong postsynaptic component of endogenous adenosinergic inhibition. Both 1,3-dipropyl-8-cyclopentylxanthine and the adenosine-degrading enzyme adenosine deaminase produced an apparently irreversible depolarization of the membrane potential by about 20 mV. Sometimes, this depolarization attained the threshold for the generation of putative calcium spikes, but no potential changes resembling paroxysmal depolarization shift-like events were observed.