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Exam 3 (final) Study guide

by: Puck Reeders

Exam 3 (final) Study guide PSY 425

Marketplace > University of Miami > Neuroscience > PSY 425 > Exam 3 final Study guide
Puck Reeders
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Dr. McCabe

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All the notes for test 3. Psychobiology by Professor McCabe. Last Schizophrenia lecture by guest speaker is also included.
Dr. McCabe
Study Guide
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This 44 page Study Guide was uploaded by Puck Reeders on Thursday April 23, 2015. The Study Guide belongs to PSY 425 at University of Miami taught by Dr. McCabe in Spring 2015. Since its upload, it has received 136 views. For similar materials see Psychobiology in Neuroscience at University of Miami.


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Date Created: 04/23/15
EXAM 3 STUDY GUIDE Laws of learning and the Neural Mechanisms of Learning 0 We have the ability to store any information and retrieve it in seconds 0 Learning an enduring change in mechanisms NS of behavior as a function of experience a result of our experiences I we acquire this Learning an enduring change in the mechanisms of behavior and the function of experience 0 Enduring It has to last for a period of time 0 Mechanisms of behavior in the nervous system 0 Has to be acquired Not hard wired Slide 1 laws of learning learning 2 types of learning 0 Non associative 0 Gets less attention then associative learning 0 Associative learning 1 Nonassociative learning 0 No association formed between stimuli and behavior 0 Learning something about single stimuli and behavior 0 Simple form of learning 0 Habituation response decrement to repetitive stimulus I learning that a repeated stimulus is NOT important our response to stimulus decreases O Dishabituation when a habituated stimulus changes in some way ex intensity temporal characteristics and becomes importantnovel I If you change the characteristics of the stimulus O Sensitization response increase to repetitive stimulus become hyper sensitiveaware of a particular stimulus 0 Imprinting occurs during critical periods of development I Powerful form of non associative learning I Lorenz amp Tinbergen ex young ducks follow first moving object they see after they are born this learning lasts a lifetime They form an attachment to an stimulus 2 Associative Learning learning to associate things 0 Instrumental operant conditioning O Conditioning learning 0 Learn to associate your behavior with the consequences that follow it Behavioral response with stimuli that follow 0 Likelihood that a behavior will be repeated depends on consequencesstimuli that follow that behavior reward or punishment 0 They learn a response to their behavior Do you get rewarded for it or punished O SLIDE 5 laws of learning Contingency Affective Value of the Stimulus Appetitive Aversive Stimulus Presented Positive reinforcement Punishment following emission the response of Stimulus withdrawn Omission Training Negative Reinforcement following emission the response of 0 Both and reinforcement strengthen a behavior 0 Extinction if you walk through a door and you get a doller every time you keep walking through and suddenly you aren t getting the dollar anymore you will stop going though the door This is called extinction of behavior Use successive approximations used to train animals to exhibit behaviors 0 Secondary reinforcement leads to some type of reward ex monkey s with poker chips I Slide 8 laws of learning 0 0 You can use operant conditioning clinically I Use this for behavior modification in clinical psychology 0 Classical Conditioning Pavlovian O 0 You learns to associate stimuli meaningful stimulus is associated with neutral stimulus I You learn to respond to the neutral stimulus Repetitive pairing of two stimuli causes them to be associated I the neutral stimulus then elicits learned response that was elicited by the meaningful stimuli Slide 11 I Unconditioned stimulus meaningful stimulus I Unconditioned response unleamed response I Conditioned stimulus neutral stimulus I Conditioned response learned response US unconditioned stimulus I elicits UR I unconditioned response re ex US is associated with CS by pairing them together CS I UR then UR becomes CR Pavlov dog I If you present dog food US meaningful stimulus they produce re exive response salivation UR I Neutral stimulus tone or bell conditioned stimulus normally does not produce salivation But if you do that over time and give him food after he starts salivating learned salivation Conditioned response when he hears the sound 0 Extinction Spontaneous Recovery stop pairing CS and CR stop ringing bell the dog will learn to stop salivating when he hears the bell O 0 Not decay of learning I it only takes 1 pairing of CS and CR to recover l spontaneous recovery You learn something new First the tone predicts food But now it does not anymore This is learning to NOT respond NOT forgetting Whatever he learned is still in the brain did not decay He learned not to respond suggests that there are multiple circuits that control a behavior Generalization learn to respond to stimuli that are similar tooriginal stimulus I slide 17 laws of learning baby I ex little Albert and furry white rat CS I in the beginning albert was not scared they brought the rat in make a loud noise US and the baby got scaredfearful UR Eventually he became scared CR every time he saw the rat CS He learned to become fearful of the rat But he also became fearful of other white furry things rabbit yarn etc I phobia I This could be basis of phobias or fetishes 1 r 7 f a 7431 ar39 7 J J ll ag5 I m andll minimum iWMlti l 0 X axis time 0 If you give US before the CS I backward conditioning l poor learning because you do not make the association because the CS for example tone is not predicting the US for example food 0 If you give the CS and US at the same time or if those two are overlappingdelayed conditioning robustgoodstrong learning especially delayed conditioning I When CS goes on then the US comes on El trace conditioningl medium learning Not as strong as delayed conditioning because there is a period of time in between and the animal needs to remember the tone 0 If you separate the CS and US with enough time you might not even associate the two 0 Timing is critical for this type of learning 0 There are nice control procedures that allow you to say what type or behavior is due to learning compared to something else 0 Look at drawing of paired and unpaired stimuli 0 Pseudo conditioning uses paired and unpaired conditions 0 Another way is Differential conditioning I Lo tone and hi tone I Lo tone followed by US Hi tone never followed by US I Measure responses when hi tone and when lo tone are being heard Difference in the graphs is due to associative learning 0 DRAWING Differential Conditioning Better can do with one animal Lashley 0 Engram physical representation of learning 0 didn t know wherewhat to look for 0 things in the brain that represent learning 0 problems I they thought it was localized in one place in the brain l the learning center This was not correct I In order to study learning They used very complicated paradigms rat running maze You wont find anything unless you simplify behaviors I They had no idea what an engram might be I needle in a haystack 0 Donald Hebb first person to suggest that learning was due to changes in cell synapses 0 Convergence of information information must come together in the brain to be associated 0 cells that fire together wire together 0 An axon stimulates a cell in the past becomes more succesfull in the future because there are changes in synaptic strength that make the cell more successful in the future 0 Hebbian Synapses 0 two neurons firing together and innervating same post neuron may have their synapses strengthened O neurons are strengthened by firing together and changing their synaptic strength I refer to slide 19 in laws of learning and notes in slide Model 1 0 Invertebrate Model Aplysia 0 very primitive NS 1000 neurons total 0 Eric Kandel l behavioral experiments with Aplysia I showed associative lea rning O looked for classical conditioning too I US tailshock I UR gill Withdrawal re ex I CS mantel touch I CR gill withdrawal 0 these organisms were also capable of classical conditioning 0 also capable of differential learning I CS mantle touch I CS siphon touch 0 could differentiate and learned to respond only to mantle touch 0 traced entire NS of Aplysia found circuit involved in classical conditioning 0 copy picture from slides 0 convergence of information occurs at synapse of facilitating intemeuron and sensory neuron WHAT IS HAPPENING AT SYNAPSE 0 GET PICTURE FROM NOTES 0 Coincidence detector detects coactivation of pathway 0 A cAMP l A protein kinases I block K channels 0 K ef ux causes membrane to recover the membrane potential I blocking it causes membrane to STAY depolarized I Ca continues to come in l more vesicle movement and more NT released I A EPSP I A chance of action potential 0 SYNAPSE IS STRENGTHENED How does this become more permanent 0 CAMP l nucleus I in uences transcription factors I CREB I can change physical structure of synapse I can sprout new synaptic connections 0 protein synthesis seems to be required for long term changes MODEL 2 Rabbit Nictitating Membrane Conditioning US air puff to cornea UR NMReyeblink CS tone CR NMReyeblink NMR nictitating mem response REFER TO PICTURE IN NOTES MODEL 3 0 different approach 0 measure population EPSPs 0 look to see if synapse strength changed with repeated activation of a pathway 0 found that this permanently changed synaptic strength high frequency tetinizing stimulus 0 LTP long term potentiation 0 found that it was important that synapseneuron was depolarizedactivated when strong stimulus arrived REFER TO PICTURE IN NOTES many of inputs I hippocampus use glutamate 0 2 types of glutamate receptors NMDA and non NMDA 0 non NMDA depolarize cell 0 NMDA allows Ca in ux I signal to nucleus produces proteins also activates NOS I retrograde messenger can tell presynaptic cell to also strengthen connection 3 different models but all seem to say the same thing I learning is based on synaptic changes 2 different types of memory 0 Short term memory 0 brief in duration 0 limited capacity system 0 59 chunks capacity I chunk how ever you put it together 0 need rehearsal in order to retain information 0 Long Term Memory 0 relatively permanent they are there for your entire life 0 unlimited capacity from what we know 0 structure organized knowledge I do NOT need to rehearse To convert from short to long term memory 0 Memory consolidation Slide 1 Memory Lack of memory Amnesia 0 tends to be from trauma Retrograde Amnesia lost memories from events before trauma 0 Memory slide 2 first picture Anterograde Amnesia inability to remember new information 0 Memory slide 2 second picture Patient M2 0 could recall Whole sections of books everything that was on the board at school 0 boards of insects 0 almost photographic memory Patient S 0 most famous documented by specialist named Luria synesthesia experience multiple senses when one is presented 0 see music no limit to memory had difficulty with listening to stories remembering people too many sensations at once might be easier to remember things because they have so many sensory associations with things can t forget I difficult to focus He was overwhelmed when a story was told Sound and images were evoked when the story was told Synesthesia may make it easier for you to form associations and remember things better because of the experience of multiple senses when one is presented Patient HM Henry Was studied for over 50 years passed away 4 years ago maybe most famous lived in northeast motor winder had epilepsy age 27 had surgery to correct this I removed tissue removed bilateral medial temporal lobe o palleocortex I covers hippocampus and amygdala removed hippocampus and amygdala with this developed total Anterograde amnesia other characteristics were relatively normal could not remember anything before 2 min ago asked about parents I could not tell whatwherehow they were but would tear up maybe some emotional memories could learn motor tasks eye blinks with tone etc RB O Conditioned 0 Drawing in notes Slide 3 memory 0 male postal worker 0 had coronary bypass I clot I stroke I severe anterograde amnesia I took out layer CA1 of hippocampus 0 he cant remember any facts of information 0 he does remember how to play piano Clive 0 viral encephalitis I damaged hippocampus in temporal lobe 0 super successful musician 0 Movie clip 0 His memory lasts between 730 seconds 0 His wife comes by every day but he cannot form new memories 0 all these had damage to the hippocampus Squire 0 Episodicprocedural implicit memories skills and automatic operations do not use recall are not consciously aware of it are NOT reliant on hippocampus 0 Where you were who you are with declarative exlicit memories Factsinformation accessible to conscious recollection O are stored with respect to time and place 0 hippocampally dependent l semantic 2 episodic emotional memories are not necessarily hippocampally dependent either can study this in animals by studying spatial learning 0 ex water maze I cloudy water with submerged platform I rat will remember I damage to hippocampus I won t remember hippocampal learning is relational O binds all info that happened in one timeplace cortex holds the memories Spatial learning type of declarative memory 0 Ex Water maze tank of water Make the water opague cant see through it somewhere there is a platform submerged Rat swims around till they find the platform When they climb up the platform they look around and form a spatial map So the next trials they go find the platform They learn Medial temporal lobe gets info from neo cortex and puts into hippocampus Hippocampus I fornixl part of hypothalamus mamilari bodies interior thalamus I cingulate cortexl medial temporal lobe 0 Similar to papez circuit Medial dorso thalamus CHECK DRAWING Hebb thought stimuli thoughts memories went through loop of neurons I cell assembly 0 can be strengthened by strengthening the synapses I as information strengthens circuit U reverberating circuit I continues through circuit short term memory as this is repeated long term changes occur long term memory called consolidation 0 cells that fire together wire together 0 Check drawing takes time for these changes to occur 0 one cell assembly can activate another cell assembly I chain of activation this might be neurological basis of thought 0 memories are stored THROUGHOUT the circuit in the whole assembly basically I engram is NOT stored in a single cell 0 you can use same circuits for memory and for other purposes sensation learning etc 0 One cell assembly can actually activate another cell assembly which can activate another Neurobasis of Thought 0 Memories can be stored in any circuit in the brain as long u can facilitate those synapses O CEREBRAL CORTEX LANGUAGE AND FUNCTIONAL ASYMMETRIES IA inch thick 0 surface area is huge I must be tucked and folded to fit into skull 0 groovesulcus largedeep fissure 0 bumps gyrus 0 4 major lobes division cortex slide 2 0 occipital lobe back of brain contains Visual cortex 0 parietal lobe back half contains somatosensory cortex info from body and face and posterior parietal lobe coding for spatial relationships 0 temporal lobe side contains auditory hearing and olfactory cortex smelling medial temporal cortex 0 frontal lobe front motor cortex Broca s area speech prefrontal cortex 0 back half of brain cortex is mostly sensory functions 0 parietal occipital and temporal 0 front half is mostly motor functionsbehaviors I motor unit 0 Controlling behaVior and regulating motor function 0 frontal lobe large in humans 0 Sensory Motor Integration sensory to motor 0 Brain does the same as What the spinal cord does but at a more complex level 0 if you cut open brain there is a lot of cortex hidden on the medial surface 0 interior singulate cortex in medial frontal lobe O Insular cortex hidden behind the temporal lobe polysensory taste cortex 0 Cortex Where sense of taste is processed Sulcus and Gyri they make up different areas of the brain and all have a different name slide 4 cortex 2 types of cortex 0 Neocortex O O O 90 of the cortex newer evolutionarily 6 cell layers Each layer has a different function 0 Paleocortex 0 0000 0 Critical for memory and emotional behavior 3 or 5 cell layers part of limbic system We share this with a lot of other creatures orbitofrontal cortex front stippeled region slide 7 I eyes part of limbic system cingulate cortex emotion the loop around the corpus callosum I part of limbic system medial temporal cortex memory I aka entorhinal cortex parahippocampal cortex I feeds input into hippocampus I it surrounds the hippocampus Brodmann 0 Primary somatosensory cortex 0 studied architecture of brain and found anatomical distinctions within the brain l Brodmann areas found that they had functional distinctions as well 0 Areas know 0 000000 0 1 2 3 somatosensory cortex 6 SMA supplementary motor cortex and PMA pre motor area 8 frontal eye fields 57 posterior parietal lobe coding of space 17 primary Visual cortex 18 19 secondary and tertiary Visual cortex 41 42 primary and secondary auditory cortex 45 Broca to send info to cortex usually u go through thalamus Relay Nuclei in Thalamus project to cortex slide 10 cortex 0 Regulates activity in cortical areas 0 00000 0 Lateral Geniculate Visual cortex Medial Geniculate audition VPL somatosensory body below neck VPM somatosensory above neck headface VL motor cortex Anterior thalamus cingulate cortex orbitofrontal projects to Paleocortexlimbic system PulVinar occipitalparietaltemporal O Dorsomedial thalamus prefrontal cortex thalamus also has intrinsic nuclei l fan out and activate millions of cortical cells I reticular formation in uences this related to electrical cortical activation 0 they get info from reticular formation and terminate in the thalamus in intrinsic nuclei 0 Non specific they can regulate the excitability in the cortex I They regulate the electrocorticol excitability Slide 11 People think that info ows from thalamus to the primary neocortex then 2ndary and 3ary and then goes to the motor area The brain is an example of Parrallel processing 0 Simultaneously process separating different pathways and the same time ammonia salts Parallel processing vs traditional hierarchical model Slide 12 parallel allows for very complex processing Diffuse modulatory systems Other way of getting info in cortex without necessarily using the Thalamus Ex Serotonin system norepinephrine dopamine acetylcholine single neurons that branch to 100000s of cells in cortex I send out broadcast message sprinkling neurotransmitter in the cortex abnormalities in these systems lead to attentional issues schizophrenia depression ocd anxiety etc Cell Layers slide 3 cortex NEOCORTEX 0 LAYER 2 CorticoCortical Connections INPUT layer 0 LAYER 3 CorticoCortical projections OUTPUT layer 0 LAYER 4 BLUE input from thalamus gate keeper to cortex in sensory this area is large in motor it is small 0 LAYER 5 OUTPUT LAYER projection layer I Out of the cortex down into rest of the brain to brain stemspinal cord 0 large in motor red 0 LAYER 6 transition layer to White matter 0 Glial cells aligodendricytes that myelinate the axons going in or our the cortex 0 layer of White matter myelinated axons 0 organization of cortex is very specific not random 0 Every cell layer has its specific function Major fiber bundles travel right under cortex slide 14 Smaller fiber bundles connect neighboring gyri Axons that travel sideways connecting 2 hemispheres 0 Corpus Callosum largest commissure Primary cortex first area that processes information from the thalamus Association not purely sensory or motor combination of both Different animals have different primary cortex association cortex ratios 0 rat 901 91 0 90 of brain is primary cortex sensation and movement 0 10 higher level processing of information association cortex 0 cat 5050 11 0 monkey 2575 13 0 human 1090 19 0 Association cortex Not purely sensory or purely motor Association allows us to speak inhibit behavior think etc Association areas 1 Prefrontal Association cortex 2 Limbic Association cortex parts of temporal and frontal lobes and on medial surface 3 Parietaltemporaloccipital association cortex border between parietal occipital and temporal lobe REFER TO SLIDE FOR CHART 0 Prefrontal cortex is the main area that makes our decisions 0 most functions have input from both sides 0 language is only controlled by left side 0 asymmetry Partial lobe 0 S1 Striped strip cortex primary somato sensory cortex slide 18 0 S1 1 secondary somatosensory cortex 0 Slide 19 cortex Homunculus Cells in sometosenory cortex also line up in columns according to function 0 Slide 20 of Cortex 0 Columnar organization is a feauture of the somatosensory and visual cortex Damage Parietal Lobe 0 Somatosneosry perceptual problems asterio agnosia inability to know what something is by feeling it slide 21 0 You cant spacially recognize something from 2 different angles slide 22 what is this called 0 Attentional problems neglect syndrome the person develops attentional problem where they ignore half of their world slide 23 Occipital lobe 0 Major feature visual cortex most on medial cortex 0 Visual cortex is organized visiotopically 0 Map of your visual world 0 Anatomical coding Slide 25 0 Columnar organization ocular dominance columns 0 Visual info leaves primary visual cortex goes to higher projects then goed to 2 different pathways dorsa and ventral What and Where pathways 0 You can recognize a visual space grandmother cells Temporal lobe 0 Auditory cortex 0 Part goes down in temporal lobe in fissure 0 There is an Asymmetry 0 The auditory cortex is laid out in a map slide 30 0 It maps the frequency of sound Medial temporal cortex 0 Inner surface of medial temporal lobe O Surrounds hippocampus and it s the input to hippocampus I Memory and declarative memories 1860 Broca I Broca s area Broca s aphasia Language is asymmetry in the brain Left hemisphere Aphasia lack of speech Patient named Ta that was all he could say 0 Ta had a problem with articulation Analyzed patients brains when they died who had aphasia I most had damage in Broca s area Area 45 0 have trouble with articulating getting the soundswords out speech production 0 expressive aphasia WemickeGeschwind Model Info is processed in left hemisphere Auditory info comes into the auditory cortes and visual language comes in the brain through visual cortex They come together in information feeds into angular gyrus area 39 polysensory area this receives visual and auditory information and sends it to Wernicke s area I changes it to phonetic representations to language I Arcuate fasciculus I goes to Broca s area contains memories of how to produce sounds grammer I motor cortex 0 both spoken and written language goes in this system model has some holes I too simple 0 thalamus is also involved O basal ganglia 0 visual cortex can send info directly to Wemickes area I without going through other areas and turns it into sounds 0 there may be parallel pathways phonetic and semantic pathways for the processing for the phonetic meaning and semantic Sounds 0 Language is not just a cortico phenomenon Left thalamus and left caudate nucleus are also involved in language Brains of Asians might be less lateralized language may be more distributed throughout both hemispheres 0 Asian languages are very pictoral and not purely symentic I right brain is spatial which is needed to process these pictoral representations 0 We have an alphabet they have thousands of symbols Language is somewhat plastic Damage in older individuals is basically permanent but in a child the other hemisphere tends to take over I PLASTICITY There are ways to test which side of the brain has language processing 0 WADA I use short acting barbiturate I inject in carotid artery I anesthetize one side of brain l if they can still speak or not tells you which side has language Dominant Hemisphere 0 determines handedness 0 left dominant right handed 100 0 right dominant left handed 13 0 left dominant left handed 23 0 left hemisphere dominant 97 of all people 0 dominant hemisphere is generally language hemisphere 97 of people Minor Hemisphere generally right slide 8 in assym and split Left hemisphere Right hemisphere Language basic language Math spatial activity Logicanalytical reasoning relational activity science art sculpture writing dance music appreciation perceptual emotional fantasy 0 The two hemispheres work together as a unit and communicate very quick 0 There are bridges commissure that communicate with eachother From now on dominant hemisphere is the left hemisphere 0 corpus callosum axons that connect 2 hemispheres commissure how the hemispheres communicate 0 split brain patients sperry 0 communication through one Visual field 0 language is controlled by left hemisphere I left will say what it saw 0 split brain will cheat to try to figure out what is going on I cross cueing I makes a guess I right brain communicates if it is correct 0 Seizures can go from one hemisphere to the other Therefore if u cut the corpus callosum the seizure can only stay in one hemisphere 0 Lateralized stimuli and choice stimuli 0 Refer to slide slide 10 and 11 0 use this to determine how each hemisphere processes stimuli 0 he can see the spoon on ths screen goes to right hemisphere uses left hand to feel for the objects 0 w corpus callosum our brain works as a unit and share information immediately with both sides 0 Word ring and key The person will see ring because the langage is on the left hemisphere What you see to the right that goes to your left hemisphere 0 Vickie the split brain patient 0 When she is talking to you you only hear the opinion of the left hemisphere since language is there 0 Vickie saw pic on the left Went to right hemisphere Could not understand picture but only said woman With her left hand she wrote telephone When she read the word she could connect that to woman and could connect women speaking on the telephone 0 Google this 0 Slide 13 0 If u show a picture in the left side goes to the right brain They do not have language on that side The right side does know it is the picture and can signal the right side with a slap or something else 0 They use behavioral compensation slap I somatosensory 0 Prosscueing is this type of behavioral compensation 0 Slide 14 0 Project choice stimulus to one hemisphere 0 Them u give them a choice Which one is more similar I Analytical Left functional to eat a cake I Right brain will choose the cake because it looks more like the cake More engaged in appearance I Left Scissors I needle and thread Functional I Right Scissors spoon and fork because it looks like the the scissors 0 It looks like there are 2 brains interconnected by networks of axons They rapidly communicate 0 Do we have a split personality because the left and right brains are fighting Logic vs emotion I You can take one mind and turn it into two minds Doesn t this say that the mind is all brain chemistry l mind brain dualism December 31 d 0 executive processesfunctions regulate behavior 0 modulate other processes in the brain with exibility and goal directed fashion 0 ability to regulate and control automatic behavior inhibitory control O association cortex not purely motor or sensory 0 Area 4 primary motor cortex 0 Area 6 premotor supplementary cortex secondary motor 0 Area 8 frontal eye fields voluntary eye control 0 Area 45 Broca s Area 0 orbitofrontal cortex 0 principal sulcus and principal sulcus regionlateral prefrontal cortex I used in memory I REFER TO SLIDE 0 medial prefrontal cortex anterior cingulate cortex 0 Area 25 I stimulate this I decreases depression 0 VL thalamus I 4 6 0 anterior thalamus projects to anterior cingulate and orbitofrontal 0 dorsomedial thalamus I PFC 0 other projections into frontal are from diffuse modulatory systems serotonin dopamine norepinephrine etc o acetylcholine I cognitive impairments and Alzheimers 0 Primary motor cortex is essentially the final output of the cortex 0 posterior parietal lobe I space sensory information Where your body is located limbic 100p motivation and emotion disrupted I poor impulsivity control Frontal Lobes Part of the cortex that is thought to plan and control behavior executive brain 0 It oversees the activities of the organism and decides how to behave Frontol lobe can be seen as a motor element Frontal lobe has subredions with subthalamis inputs and corticocortical connections Broadman map Slide 3 frontal lobes Regions 0 Broadman area 4 6 8 45 Orange slide 4 broadman area 4 redorange broadman area 6 Broadman area 8 eye fields Slide 5 red to the left broadman area 45 Broca Slide 6 0 The eyes sit Whitin the orbit 0 The cortec above the orbit orbital frontal cortex ventral medial prefrontal cortex I Area of paleocortex Slide 7 dark spot on the left upper pisture principle sulcus 0 Area around principal sulcus doral lateral prefrontal cortex or principal sulcus area Slide 8 Medical prefrontal cortex 0 Infront of area 4 and 6 0 Including singulate cortex 0 Includes Anterior singulate cortes which is limbic cortex and connected to the limbic system Area 4 and 6 get motor input from ventro lateral thalamus Dorsal lateral prefrontal cortex gets input from medial dorsal thalamus blue on slide 9 Anterior thalamus goes to the cingulate cortex and orbital prontal cortex which are both paleo cortex and are part of the limbic system 0 This structure plays large roles in limbic systems Frontal lobe activities are fed info by the thalamus Thalamus is gate keeper of info check Kats notes Disregulation of dopamine input to the frontal lobe has to do with schizophrenia Disorcers like ADHD has also been linked to the dopaminergic inputs to the prefrontal cortex Mood disorders depression and impulse disorders serotonergic systems Memory problems and other cognitive impairments alzheimers l cholinergic cells Regulation of F L is critical for cognitive functioning O Dopamine serotonine and acetylcholine Anatomy Broadman area 4 slide 10 0 Primary motor cortex all the info ultimately goes to broadman area 4 0 Gets send down to the spinal cord slide 11 0 Last stop Everything eventually goes through here Broadman area 6 slide 12 O Receives input from parietal lobe O Sesory info 0 Info in prefrontal cortex goes to Area 6 then to area 4 then to cortical spinal tracts and that produces movement Loops slide 14 0 go signal that does the goal selected movements 0 Motor cortex to putamen to globus pallidus to thalamus sends to prefrontal cortex this says GO Slide 15 0 Timing and accurately 0 Motor guidance 0 Cerebellum brings that into to the prefrontal cortex Which then again decides the behavior Slide 16 0 1st 100p skeletal motor loop 0 parietal lobe I basal ganglia I area 6 0 CHECK SLIDE 0 2nd 100p Occular loop 0 controls eye movement in a goal direction fashion 0 3rd100p cognitive or association loop 0 memory and cognitive functions 0 impairments memory impairments 0 4th 100p Limbic loop 0 limbic cortex I structures adjacent to Basal ganglia I thalamus I limbic cortex anterior cingulate and orbital frontal cortex I motivated behavior and emotional regulation I Impairment cant regulate their behavior in a normal way I Turrets grunt uncivil behavior they do not have control over that behavior 0 Each of these loops is regulating the frontal loop in some way 0 They have similar pathways but are anatomically separate and distinct 0 Each pathway goes to a different region anatomically 0 Loop 1 target is B area 6 0 Loop 2 ocular motor loop eye fields 0 Loop 3 target principal sulcus 0 Loop 4 target anterior cingulate and orbital frontal lobe 0 Damage in basal ganglia or in thalamus you will have frontal lobe problems You will have problems with motivations and emotions Prefrontal cortex Executive Functions supervisory or regulatory role 0 Regulates other brain functions 0 Activities that are regulated are goal directed 0 Important in overcoming behaviors that are normally overcome automatically 4 different groups of the prefrontal cortex 1 Inhibition and task switching 2 Working memory 3 Actions in social domain appropriate decision making simulation and empathy 4 Planning and coordinating complex behavior and selecting an action 1 Inhibition and task switching Humans have ability to inhibit behavior before you do it Damage to frontal lobe I trouble with inhibition Poor inhibitory control Can test this with Wisconsin card sorting 0 Tell them to sort cards based on one aspect then ask to switch to sorting by a different aspect O Deck of cards with symbols on it and they can vary in different aspects triangles stars etc They can have different number of symbols and can be in different colors The task is sort the cards into piles according to a certain rule all stars together or by number of symbols or by color Most of us have a exible anough brain to do this This is called Switching set People with inhibition problems have errors of perseberation I they continue using old preVious rules They cannot inhibit their behaVior and do not have the exibility to switch to a different rule also use stroop task inhibit and switch set 0 frontal lobe is filter allowing you to focus on the task at hand 0 frontal lobe can inhbit behaVior and allow us to switch to a new set of rules 2 Working Memory special kind of short term memory I lateral prefrontal Short term memory buffer l allows you to focus on one aspect of your memory slide 1920 Holds information for brief period of time while you perform a task Monkey experiment slide 20 O Other species then monkeys and humans don t have a lot of prfrontal cortex 0 Delay alteration memory task 0 Monkey sits in case Infron of him are two wells He puts food in one and coveres both up A window goes down for a minute Monkey need to remember where the food is 00 Monkey needs to remember an mental image of where the food is If she lesioned the prefrontal cortex in the sulcus area animals would perform by chance 0 Animals with an intact PF cortex could do this perfectly 0 PF cortex has the working memory 0 Similar task with symbols The mnkeys with the lesioned PFC can do this task this means that the PFC is not involved very much in associative learning 0 PFC is involved in working memory buffer not with associative learning 3 Action in social domain Damage in frontal lobe causes impulsive antisocial behaviors lack of embarrassment with sexual or excretory functions do NOT regulate behavior based on social rules and morals normally you can determine and weigh consequences of actions before you do something May be related to emotional markers as you grow up you have experiences that you associate with emotions 0 ex schizophrenics sociopaths psychotics children teenagers etc Social cognition simulation 0 We have the ability to simulate in our brain what is going to happen to us before it plays out We can evaluate the consequences of our actions 0 Slide 29 she has emotional markers Empathy appreciating other people s feelings and needs understanding that other s needs are as important as their own needs 0 Theory of Mind understanding that others have thoughtsfeelings too Mirror Neurons neurons mirror actions of other organism They fire when someone else performs You understand the actions of others 0 important for social cognition O Autism lack of these mirror neurons Limbic and orbitofrontal and ventro medial areas are important in these social issues 4 Planning complex behavior develop action plans 00000 O 0 Set a goal and maybe subgoal slid 30 anticipate consequences of that action determine What is required to reach goal People with frontal lobe problems are bad at these tasks with multiple steps executive attention is REQUIRED for this I monitors different parts of brain and helps focus sources on task at hand can detect errors and shift resources to complete task I this relates to ADHD NOT sure Where this system is but the anterior cingulate might be involved look at slide maybe really all of this is about regulating behavior in exible goaldirected fashion I high level sensory motor integration 0 Sustained attention is critical for complex tasks 0 Ppl with frontal lobe damage Attentional problems Supervisory attention executive attention Brain Damage Recovery of Function and Epilepsy 1 Brain Damage and Recovery of Function 0 Events associated with brain damage tumors drug use stroke surgery trauma 0 O O 0 What happens at the site of damage What functions are lost What can you do to enhance recovery of function Closed head injury I can have rupture of vessels outside the dura extradural hematoma this will displace brain tissue and will cause increased intracranial pressure this can cause cell death O I can also occur under the dura on the surface of the brain subdural hematoma causes increased intracranial pressure also can have affects because brain is exposed to blood I spinal cord injury U compressed fracture causes the spinal cord to stretch U actual fracture of spine can cause transection of cord U damage will depend upon extent of damage compression transection stretching etc and the location of the damage U Depends upon the extend of injury and the location of the injury 0 In the neck you are going to separate the brain from the neck down You will effect the upper limbs and lower limbs Quadriplegic 0 Chest or below you will spare the upper limbs paraplegic penetrating injury I like a bullet causes tissue damage bleeding open head wound opportunity for infection to enter the head Aneurism slide 5 of Damage and recovery I Weakness in vessel pressure causes the vessel to balloon sometimes not even weakness just chronic high blood pressure causes it to burst and then you get a hemorrhage U Hemorrhage slide 6 Stroke occlusion of blood vessels to the brain Cardiac arrest cerebrovascular I Your brain does not get any blood Microvascular occlusion I Mini clots can pass through large blood vessels but get stuck in smaller blood vessels transient ischemic attack global ischemia within 710 min you get cell death can have small or large vessel occlusions causes infarctions O remember circle of Willis can cause occlusion to have no affect 0 stroke can cause major injury 0 hydrocephalus slide 10 during development csf cerebral spinal uid travels through ventricles occlusion can cause ow to stop causes increased pressure inside ventricles ventricles increase in size and in children will cause the head to swell because their skulls have not fused yet It compressed tissue all around the brain Kids have soft skulls and they expand csf has a normal ow normally through the ventricles Was fatal But now with imaging techniques this can be diagnosed early Surgery can prevent it Put shunt in ventricles to heart Some children who had hydrocephalus actually turned out relatively normal despite their tissue being compressed 0 Events occurring at the site of injury Cellular changes at site of damage Necrosis area of dead or dying cells at the site of injury U Slide 11 Hippocampus U Decrease in blood ow to that area D Decrease in Gluco utilization U Metabolically inactive Gliosis glial cells proliferate and go to site of injury reactive astrocytes and microglia these cells will also fill in area and can form scar tissue that actually block area from healing can also multiply out of control and cause a tumor U Micro glia tiny glial cells D Astrocytes phagocytosis U Phagocytosis glial cells become phagocytes and engulf deaddying cells and remove them Help In the healing process Those Astrocytes are called phagocytes U Sometimes they are overproduced and clog up D Nerve cells general don t reproduce Gliar cells do U Many brain tumors are due to glial cells growing out of control Area can lose blood ow and oxygen I Edema uid build up in response to injury U increases intracranial pressure can change the extracellular uid composition U Can cause healthy cells to malfunction bc of the electrolyte balance U Hallmark of Neuronal injury Neuronal Injury happens over time D You need to control this kind of swelling in the nervous system I These things take time to occur neurological injuries evolve over time 0 Cellular changes away from site of damage remote effects somewhat paradoxical I degeneration U lose connections and cells this could cause effects in areas that are not in the original site of injury D Slide 13 I transneuronal degeneration cell death can jump synapses U Sometimes not the cell that is damage dies degeneration But also the cells next to it die U Sensory and motor loss and cognitive impairment that do not have anything to do with the site of injury because of these remote effects Effects from a site away from the injury I diaschesis kind of a shock wave that travels through NS temporary stunning of tissue that causes normal functions to stop U Spinal shock when spinal cord is injured bc breing neck U Tissue is stunned temporarily U NY Jets football player broke his neck was paralysed Over the course of 6 weeks he gradually regained function His paralyse was probably due to this remote effect 0 Recovery of Function 0 You can resolve remote effect I Things that you think are gone but the tissue starts to recover Over the course of weeks you slowly recover O Mechanisms underlying recovery behavioral compensation use other behaviors to compensate for loss of function if you lose sight in one eye you can move your head to use the other eye to see that area of visual field not true recovery of function El El El El El Not actual recovery but looks like recovery You use good parts of your brain to compensate for the loss Take out parts of hippocampus and have memory loss You write things down Split brain one hand was slapping the other There is no actual healing of the neural tissue Reorganization of surviving tissue Slide 14 it would be great if neurons could regenerate or grow back but this doesn t really happen sometimes neighboring tissue will take on functions that have been lost El Why don t we grow new cells makes brain less stable less efficient neurons require very specific environment to proliferate regeneration of neurons or fixing damaged neurons can occur in PNS 0 Amphibeans can grow legs and tails back 0 Slide 15 Damage nerve cell and regenerates But this does not occur in our nervous system What does occur is sprouting Sprouting slide 15 will make new connections to try to make up for damage 0 collateral sprouting done by the remaining healthy neurons or 0 Proximal Sprouting damaged neurons will sprout and connect to the healthy ones 0 Nerve cells try to do something but they are not really good at healing themselves denervation supersensitivity if a nerve is not being stimulated it will increase the number of receptors on its synapse so that it is more likely to be activated this is a kind of plasticity 0 The cells become super sensitive 0 Brain is trying to heal itself 0 Slide 16 disinhibition some pathways are not often used but damage to an inhibitory neuron will cause pathway to be active Some pathways are always inhibited by a inhibitory neuron But if there is brain injury and that inhibiting neuron is taken out the pathways become disinhibited and start working 0 Variables affecting recovery age sex Neuronal injury in the young not as devastating as in the elderly Cotard damage to certain areas in children causes less issues than same damage in adults studied speech Kennard looked at brain lesions in monkeys causing motor impairments in old and young monkeys U became known as the Kennard principle the young brain deals with brain injury better than old brain more compensation and plasticity gender some evidence that the same injury in females produces less impairments than male why might be because the female brain is less lateralized so it may be more possible for the female brain to compensate 0 Therapeutic approaches to brain damage Behavioral rehabilitation U Soldiers coming back from Iraq with head injuries They try to behaviorally rehabilitate them They are trying to force them to use the limb that is paralyzed U Sometimes if cortico spinal tract is damaged the rubro spinal tracts will take over this could happen D You have to overcome depression If they are depressed they are less likely to actively be open to behavioral rehabilitation pharmacological treatmentsinnerventions B When the brain is injured they dump glutamate into the brain and excited cells to death 0 You need to protect the brain for further injury 0 You cant just block glutamate because it is everywhere They only want to bock the glutamate cascade U Neurotrhophins NGF amp BDNF stimulates neuronal cell growth and survival U Hypothermia cooling the brain and spinal cord Brain is vulnerable lack of blood ow glutamate cascade ischemia edema etc cooling will slow this down Brain tissue transplants U Putting cells in the brain and spinal cord to heal the brain or spinal cord Problem is that they use embryonic stem cells D Use of other kind of stem cells but they are not as good at embryonic stem cells D You can change 4 genes in a cell and create stemcells U Even if we do have stemcells if you put them in an adult brain the environment is so different you cannot expect these stemcells to become the right kind of You need to figure out how to program them so they make the right connections and become the right type of neurons I neurotrophins NGF BDNF I glutamate cascade this occurs during brain injury this starts killing off nerve cells I hypothermia might just give a window of slowed down progression of damage I stem cell therapy a little controversial embryonic vs adult stem cells they don t seem to act quite the same they are also trying to convert skin cells to stem cells by altering their DNA sequence Epilepsy Most common neurological disorder Sudden and Uncontrollable electrical excitability storm of electrical activity seizure Nerve cells start to fire out of control Most are idiopathic We do not know what causes them 0 Symptomatic we know what caused them Leads to muscular contractions that cause convulsions A person who is predisposed to epilepsy will have an episode when their excitability reaches a certain threshold lots of variability in epilepsy sometimes we know what caused it like a tumor other times we do not know common factors 0 Aura warning of an impending seizure could be sensory seeing hearing smelling something or just general weird feeling 0 Temporary loss of consciousness I Amnesia O movements motor component twitching blinking body shaking Types 0 Focal epilepsy originates from a specific site hot spot spreads to other regions will reach the motor cortex this activates motor neurons and leads to the motor symptoms that are characteristic generally starts with the face and moves down the body as it moves through the motor cortex called J acksonian march I It can happen very fast I If the seizure spreads and goes to the motor cortex you will see this in movement I Hotspot is temporal lobe They reach the region at the cortex Where the facial features are J acksonian March I If the seizure does not reach motor cortex no motor movement I If seizure reaches reticular formation The Whole brain goes up A focal seizure will turn into generalized seizure 0 generalized epilepsy I Gran mal seizure tonic clonic B First Aura then brain goes into a full seizure the motor cortex is activated Then the tonic phase happens Where the body stiffens This results in that all the air goes out of the lungs They Scream Then you get the J acksonian March D If you see this keep them from hitting their head to the oor and turn them on their side They will not swallow there tongue so don t put your hand in their mouth 0 Why do these seizures stop only have so much neurotransmitter fatigue or inhibitory processes start The neurons get tired I Inhibitory neurons kick in O Treatments I Can surgically remove the area D cut corpus callosum don t do that so much anymore I Can also give certain drugs U Dilantin anti seizure valproic acid Depakote U Barbiturates used to be used U GABA Agonists 0 They stimulate inhibitory processes Schizophrenia Guest Speaker Dopamine is not directly involved in schizophrenia at all What is schizophrenia 0 Disturbance of cognition and information processing 0 Dissociated and fragmented thoughts 0 Flow of thoughts interrupted O Involuntary ideaton 0 Impairs ability to 0 Reason 0 Concentrate 0 Focus attention or purpose 0 Result observed vagueness illogicality and bizarreness of thinking 0 Not progressive disorder 0 ALS Parkinsons alzheimers are progressive diseases Symptoms 0 The symptoms of schizophrenia can be divided into positive and negative symptoms 0 Negative symptoms deficit symptoms 0 Loss of the abilities and motivation a person once had 0 Social withdrawal 0 Difficulty concentrating 0 Poverty of speechthought 0 Positive symtoms active distortion of normal function O Hallucinations changes in the senses such as hearing voices or seeing unusual things that are not there I Auditory hallucinations most common very typical 0 Delusions Bizarre fixed beliefs that are not based in reality 0 Paranoia feeling fearful that others are plotting against you O Disorganization changes in thought processes such as having trouble thinking clearly or becoming easily confused 0 First symptoms that show up are the negative symptoms then the positive 0 Positive symptoms are very visible Onset of the disease 0 Schizophrenia is a disorder late adolescence early adulthood around 20 years 0 This is the time that the last developmental processes in the brain are occurring Natural history of schizophrenia 0 A lot of kids are at risk for schizophrenia Pathophysiology Dopamine Hypothesis 0 Drugs that increase dopamine activity can include paranoid psychosis similar to schizophrenia O Amphetamines O Cocaine O Methylphenidate O L dopa 0 Drugs that block dopamine activity tend to lesson symptoms Dopamine pathways 0 Nigrostriatal track substantia nigra I basal ganglia movement 0 Parkinson s 0 Function extrapyramidal system movement 0 Blockade produce movement disorders 0 Mesolimbis tegmentum nucleus accumbens amygdala hippocampus 0 Is thought to be intergral to behaviors such as euphoria of drug abuse and sensations of please involved in the formation of delusions and hallucinations of psychosis symptoms 0 Limbic system controlling emotions 0 Function Arousal memory stimulus processing 0 Blockade Relief of positive symptoms 0 Mesocortical Tegmentum I frontal cortex 0 Thought to mediate positive and negative symtoms of psychosi 0 Last part of the brain to develop 0 Function Cognition communication social function response to stress 0 Blockade exacerbation of negative symptoms 0 Tuberoinfundibular hypothalamus I anterior pituitary gland secretion of prolactin Other Transmitters 0 Serotonin LSD blocks serotonin receptors can cause hallucinations 0 Glutamate phencyclidine PCP can producte effects similar to positive and negative symptoms ketamine blocks glutamate receptor subtype NMDA causes psychotic symptoms 0 Excitatory and everywhere in the brain 0 GABA in pre frontal cortex inhibits normal activity in limbic structures 0 Gamma Amine Butyric Acid Brain structure and function 0 Ventricular enlargement nearhippocmpmjtmctures O a quot 39 Huhd FM t isquot mm mm malt udmh 23 in WIquot 7 If Temporal lobe auditory 0 Hypofrontality O 0 Associated With negative symptoms Frontal lobe has a decreased activity in patients With schizophrenia 0 Changes in grey matter 0 0 Grey matter loss in adolescents With schizophrenia Temporal lobe and frontal lobe 0 Cellular level 0 Risk Factor 0 Genetic component 0 Developmental factors 0 O O Prenatal factor infection in mother eg In uenza Maternal malnutrition Perinatal risk factor Accidents Hypoxia limbic structures hippocampus very sensitive Children at risk for schizophrenia show subtle changes psychological and neurological functioning Changes observed are irreversible but not progressive early developmental changes Late stage of brain maturation involves a careful calibration of excitatory inhibitory balance in the cortex With the prefrontal cortex the last region to mature 0 As one potentially relevant modulator of this balance dopamine innervation of the prefrontal cortex increases markedly during adolescence I Dopamine can show the same symptoms or loss of symptoms But the actual lesion in the brain has nothing to do with dopamine it is a developmental process that went wrong A theory 0 Early insults genetic external alter normal brain development creating vulnerability to schizophrenia 0 Disease manifests later in life when new demands placed on brain systems in adolescence and early adulthood O Puberty further brain development changes increased psychological challenges 0 Damage in frontal cortex 0 I Decreased frontal cortex activity produces negative symptoms 0 I Decreased release of GABA inhibitory NT 0 I Decrease inhibition of limbic structures produces positive symptoms Neurodevelopmental model schizophrenia 0 Glutamate in the frontal cortex that makes synapses to GABA which are inhibitory The Glutamate gets fucked up and doesn t activate the GABA which then stops the inhibition to the limbic system 0 Schizophrenia is a developmental disorder Traditional neuroleptics 0 Developed in 1950 s and 1960 s chlorpromazine 0 Action through dopamine receptor D2 blockade 0 Effect on symptoms not on negative symptoms 0 Significant side effects 0 Extrapyramidal O Tardive dyskinesia similar to cerebral palsy Atypical antipsychotics 0 Developed in the 1970 s and 1980 s clozapine risperidone olanzapine 0 Action primarily through dopamine receptor D2 and serotonin 5HT2 blockade 0 Effective on positive and negative symptoms


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