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Integrative Neuroscience Exam 4

by: Christine Thomas

Integrative Neuroscience Exam 4 NSC 4354

Marketplace > University of Texas at Dallas > Neuroscience > NSC 4354 > Integrative Neuroscience Exam 4
Christine Thomas

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Make sure to go over his review ppt
Integrative Neuroscience
Sven Kroener
Study Guide
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This 8 page Study Guide was uploaded by Christine Thomas on Wednesday April 27, 2016. The Study Guide belongs to NSC 4354 at University of Texas at Dallas taught by Sven Kroener in Spring 2016. Since its upload, it has received 47 views. For similar materials see Integrative Neuroscience in Neuroscience at University of Texas at Dallas.


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Date Created: 04/27/16
MOTIVATION – 04.11.16  Motivation and drive states  Motivation is a catch all term that refers to a variety of neuronal and physiological factors that initiate, sustain and direct behavior DRUG ADDICTION  Prevalence of drug use  2009  8.7% age 12 or older were current ILLICIT drug users (not counting alcohol and what not)  Most prevalent is marijuana and then maybe nonmedical  Drugs lead an increase of productivity and crime  They add up to the same numbers  In one way they have taken out the loss of productivity and the other way was crime  193 billion dollars  Societal impact  Most deaths from tobacco use  438000 – tobacco  85000- alcohol  Addiction  Once addicted  Have health and other consequences  Compulsion to seek and take drug –  def of being addicted  they are aware of what they are doing  Loss of control in limiting intake  Feel like something bad is happening so go to rehab for help  emergence of neg emotional state to want to get the drug again to change that  More  Stages of addiction of drugs of abuse  Peer pressure – acute reinforcement / social drug taking  You get something out of it  Escalating/ compulsive use  Binge drinking  College drinking – over a couple of days  Increase intake  Dependence  Withdrawal – relapse  When they realize that this is bad but then something happens and then you try to drown out that feeling and relapse  Once an addict you are stuck in this cycle  Protractive withdrawal – relapse  Recovery?  Theories of addition  Animal studies done  Demonstrated that animals could be made physically dependent if forced to consume drugs but won’t consume drugs if made freely available  Humans drink or take on their own free will – believed to be only for humans  Problems  Most drugs have bitter taste and they are normally taken orally  Conditioned taste aversion – animals avoid any substance that taste like that  Motivation view : pos reinforcement  Self-administration  Animal responds on a lever to receive an IV injection of a drug  Physiological dependence is not necessary for self-administration – don’t do it cause they are addicted but cause they like it  Drug function like other reinforces  Increase the frequ or prob of the behavior that produces them  Discontinuation of drug is followed by extinction burst and decrease in responding  Realize old behavior is not working anymore but don’t forget about it  Behavior tracks location association with reinforces  Conditioned palce preference  Look at location associated with it  Animal gets a box and can move freely on either side (preference is 50/50)  After given a shot of cocaine on one side – conditions the side  Choses the same place even if they don’t get the drug cause it makes them feel good  You can measure the rewarding properties of the drug  Addiction – def and summary  Compulsive – out of control drug use, despite neg consequences  Pleasurable states or relief from distress  Drugs of abuse are both rewarding and reinforcing  Reward = interprets as intrinsically pos  Reinforces – increase probability behaviors paired with them will be repeated  Reward circuitry  Drugs hi jack brains pleasure centers  Dopamine  Abused drugs usurp brain mechanisms that have evolved to support beneficial forms of synaptic plasticity, specifically those that occur during learning and memory  Neurological bases of reinforcements  Reinforcement system  VTA  NAc  Mesolimbic dopamine – same as VTA and Nac  Motor loop  BG  Thalamus  Cortex  Learning and memory system  Hippocampus  Amygdala  Cortex  Neurological bases of reinforcements  Info from environment prcess by thalamus and cortex and is sent to the amygdala nd hippocampus  Did I do something that helped me get rid of my hunger or thirst  Incentive salience – trying to pursue  Stimulate the meso  NAc activates motor loop through BG  Motor activity that is directed toward the salient stimulus  More forging behavior  Example  Rat learning operant condition  Food deprivation  hunger  Increase homeostatic input  Motivated to do something  VTA receive signal that rat hungry  Releases DA in NAc  DA enhances NAc activity  Stimulates motor system via disinhibition of thalamus  Increase in motor activity  Thalamus receives sensory _____  Rat presses lever and gets food  Info about lever stored in learning and memory system  Info now paired with reduction in hunger  Reduction in hunger causes decerease in activity in the mesolimbic DA system  Next time rat hungry  Info about lever processed in thalamus  hippocampus/ amygdala  That stimulates the NAc  That stimulates the motor loop  Neuronal circuitry mediating goal directed behavior  NAc drives the ventral paladin to medial dorsal thalamus to initiate movement  NAc  amygdala and PFC - valuation of rewards and establishment of rewards associated memories  Habitual response aimed to rewards depends on dorsal stratum – what really worked in the past  Nucleus accumbens  Inputs  Prefrontal association corteies  Basolateral amygdala  Hippocampus  Dopamine neurons of the VTA  Outputs  Nac  VP along the GP  mediodorsal thalamus  prefrontal cortex/ striatum  Called a limbic loop  Intrinsic circuitry and outputs of BG  Learn the pathway  Intra cranial self stimulation  Very powerful …. Animals do till they basically die of exhaustion 04.13.16  Cortex  Everything in blue is higher cortex – inputs from several areas in adjacent to it – spreads out but as soon as it goes out it gets input from other areas  Cortical areas  Where and what info  Limbic corticies toward the bottom – connections to amygdala and hippocampus  Association cortex  They all have functions that are more complicated that simple input and output  Whatever on the slide is important to what defines this (memory and what not)  Parietal  Space  Attention  To generate action  Temporal  High order visual and auditory processing  Language  Located in regions below the ________  Frontal  Executive functions  Largest summary of what they do  Plan behavior  Working memory  Inhibit prepotent responses  Neocortex – 6 layers  Different from isocortex which includes the hippocampus  They consist of 3 layers  Some regions don’t have a 4 layer but in this case they do  White layer is the fiber – connection of the axons  Subcortical structures  Cortex needs to be connected among each other  Much more space taken up by axons – myelinated fibers (white matter)  Grey matter – six layers and beneath that is the fibers that connect them  Cortical module  How inputs come in  Layer 4 is where most of the thalamic inputs come in  Cortical connections 0afferents  Shows you (second row) macack brain  Area 20  area 21  to area in front of the prefrontal cortex  Have a parallel and hierarchical  Prefrontal cortex can modulate the type of input it receive (same for hierarchy)  Same for somatic and auditory  Almost always reciprocal  Projections from sensory cortices…  Thalamic connections  Inputs come from  Mediodorsal thalamus  frontal cortex  Puvinar  parietal cortex  Ventral anterior nucleus  Nuclei not primary recipients of sensory or motor  Cortical and subcortical efferents  They are interconnected – to motor cortex or BG  Mostly connections are reciprocal  Inputs and outputs of BG  Cortex caudate putamen  Limbic system  Hippocampus and amygdala are reciprocally connected to association cortex  partically the prefrontal cortex  cerebellar inputs  inputs from motor, premotor cortex and AC  pontine nuclei  cerebrocerebellum  cerebello cortical out put – deep cerebellar nuclei  projection to cortex   posterior parietal cortex  major sub divisions  broadmanns areas and economo  large over lap  major lobes – don’t need to remember them all or anything  organization and function of the frontal  1,2,3 of the Brodmann  Part of parietal cortex is a part of primary somatic sensory cortex  The posterior zone integrates somatic and visual info form the control of movement  Spatial info – obj recognition/ guidance of movement  Where are things  Anterior zone  Lesions / disruptions that mess with accuracy of movements = apraxia and contralateral neglect  Function of the posterior partial cortex  Spatial location – where are things  Body image – where are my own parts – limbs  Attention  Use info to the motor  Flow of visual info in cortex – parietal (where) and temporal (what)  Temporal lobe –  ventral pathway  object recognition  what?  Parietal lobe  Dorsal pathway  Spatial vision  Where  The parietal association cortex mediates attention  Lesions in parietal cortex: contralateral neglect syndrome  They miss half the world – only draw half of the picture  Attention shifted to one side of the stimulus and the other side neglected  Contralateral neglect syndrome  Typical by right side lesion  Right hemi dominates attention for both sides  Left side lesions compensates  Left side for language  Attention in parietal cortex  Right side bias – normal control subjections FI  Attention neurons in parietal cortex  Pays attention – luminance drive paying attention or instruction make them more important  Visual info / auditory triggers this in the thalamus that goes to the temporal lobe  Neurons fire much more when they do pay attention – found more in prefrontal cortex  Guidance of movement  Parietal cortex sends visual info to premotor cortex to primary motor cortex to guide movements  What direction are they moving  Apraxia  Ideomotor apraxia  Inability to copy movements when asked to do so  Difficulty demonstrating hammering – cant visualize the movement  Actual control of muscle is fine though  Constructional apraxia  Spatial organization is disordered  Can’t put together a puzzle or draw a picture or copy a series of facial movements  Temporal cortex  Ventral steams comes in  Amygdala and hippocampus involved  Hippocampus – declarative memory  cortex  Amygdala – emotional / fear  Not really cortex  Temporal cortex  Auditory and unimodal and visual  Wenickes area – border of temporal and parietal lobes  Recognition neurons  Further you go down the more complex the integration what neurons become  Neurons only respond to face- combination feature that see a face  Strong response to monkey face, less to human and not at all to the hand  If you scramble the feature the cells doesn’t really respond  Columns for complex objects and or orientations of faces  Get blobs of activations which allows you to map it across the cortical surface  Changing columns  Faces are special  Not obvious when upside down  Cause we want to see a face even if it is messed up  Configuration – mouth is where it should be  Grandmother cells  Increased level of complexity lead to this  Push cells enough that they respond only to seeing your grandmother  Did in recoding of an awake patient – found neurons that were specific to certain ppl  Language  Wernickes area – understanding written and spoken language  Brocas area – production  Prefrontal cortex 


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