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Exam 2 Study Guide

by: Puck Reeders

Exam 2 Study Guide PSY 425

Puck Reeders
GPA 4.0
Dr. McCabe

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All notes needed for Final Exam 3 in McCabe's Psychobiology class. Not included: Slides and drawings.
Dr. McCabe
Study Guide
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This 39 page Study Guide was uploaded by Puck Reeders on Sunday April 19, 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 125 views. For similar materials see Psychobiology in Neuroscience at University of Miami.


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Date Created: 04/19/15
EXAM 2 MATERIALS SENSORY SYSTEMS amp VISION I If language of the NS is the same how do we get specific information from action potentials How does the information start How are action potentials integrated into real information NS is means for interacting With our enVironment I must convert environmental energy into sensory information I called TRANSDUCTION O LIGHT SOUND PRESSURE ETC I ACTION POTENTIAL Sensory receptors specialized cells used to transduce energy into action potentials these receptors have limited range of What they can detect Whether or not a stimulus is detected is based on characteristics of the sensory receptor all are electrically excitable have resting potential 70 mV receptor potentials graded potentials sensory receptors are excited by a stimulus and their graded potentials activate neurons Which then convey the signal elsewhere REFER TO PICTURE IN NOTEBOOK Adaptation sensory receptors Will adapt to constant environment 0 graded potentials will get smaller and smaller 0 they are meant to detect changes not the status quo I the receptors will respond to NOVEL STIMULI I ex When your eyes adjust to a dark room 0 NOT the same as habituation this is type of learning in nerve cells in Which neurons learn to stop responding to a stimulus How do sensory receptors differ I each type has unique properties often in membrane Coding 0 putting together action potential information to create coherent information that can be interpreted into something meaningful 1 Anatomical spatial I different pathways anatomically 2 Functional temporal I the way that the neuron is firing contains information about stimulus I ex rapid ringslow ring patterned ring neurons ring in phaseout of phase with each other synchronization I ensemble neurons many neurons firing together in or out of phase Vision 0 light electromagnetic radiation photons move in wave pattern need to be ale to detect shape color movement depth perception amplitude corresponds to the brightnessintensity of the light purity saturation is it a speci c wavelength or is it a mix of different wavelengths wavelength corresponds to the hue of the light Visible light 0 400700 nm 10quot9 m 0 ROYGBIV VIBGYOR 0 400 nm higher energy 700 nm lower energy I salmon reindeer bees scorpions some birds can induce ultraviolet light as well 0 snakes can detect infrared basically they can see heat this helps them detect prey because their vision in the visible light is not as developed Optical and Neural 0 Optical gathering in light waves and focusing them to the sensitive sight in the eye 0 Neural transduction of light and coding in the brain Parts of the eye 0 cornea protective membrane made of transparent fibrous protein no blood vessels bathed outside in tears and inside in aqueous humor 0 this is easily damaged I proteins will be denature and become opaque do not allow light to enter the eye properly 0 curved 0 aqueous humor behind the cornea 0 iris muscle that expands or contracts to change the size of the pupil allows more or less light to enter the eye 0 sclera white of the eye does have blood vessels 0 behind the pupil LENS fibrous proteins bends light to focus on the retina photosensitive surface of the inside of the eye 0 light at a distance does not need to be bent a lot 0 ciliary muscles change the shape of your lens 0 Accommodation bending the lens of the eye in order to focus light on the retina 0 fovea the center part of the retina where color vision is concentrated Focusing disorders 0 myopia near sightedness 0 when looking at a distance the light is focused in front of the retina O can occur because of non spherical eye bulging cornea 0 astigmatism part of eye is more misshapen than another part 0 concave lens is used to correct myopia 0 presbyopia far sightedness 0 lens loses its ability to focus could be from ciliary muscles losing power or from the lens becoming less elastic 0 light ends up focusing behind the retina occurs mainly in older people 0 use convex lens to correct 0 lens can fog up due to denatured proteins I cataract forms I can get surgery and get a new lens that can automatically focus 0 REFER TO PICTURES IN NOTES FOR CORRECTIVE LENSES Neural 0 retina contains photo receptors 0 I OdS slightly more sensitive to light work well in dim light scotopic related to working well in dim light little acuity achromatic 0 cones work best in bright light great visual acuity photopic related to working well in bright light chromatic 0 light falls on pit in the center of the retina 0 the FOVEA 0 density of rods and cones changes throughout the retina 0 REFER TO SLIDE 0 cones are mostly distributed on the foveanear the fovea O sharp detail and color is apparent when you look directly at something 0 rods are not at the fovea density increases outside of the fovea 0 at night use the periphery to see Retina has layers of cells 1 photoreceptors 0 horizontal cells in outer plexiform later allow cells to communicate horizontally 2 Bipolar cells 0 amacrine cells in inner plexiform layer 3 Ganglion cells At the Fovea the ganglion and bipolar cells are pulled back I forms the pitgroove I reason for great visual acuity at the fovea light is able to go directly to the photoreceptorscones they do not have to pass through the other layers of cells remember that the fovea has sort of backwards organization of cell layers what is this called Light stimulating a rod light hits RHODOPSIN activates retinal opsin a gprotein coupled receptor this activates an enzyme phosphodiesterase which metabolizes cGMP metabolization of cGMP causes Na in ux to stop which basically HYPERPOLARIZES the cell cell does not re we perceive light Absence of light on a rod 0 NO light hits rhodopsin 0 cGMP is NOT metabolized cGMP causes Na to enter the cell Na depolarizes cell THIS IS CALLED THE DARK CURRENT cell releases NT ex glutamate the rod excites the connecting bipolar cell bipolar cell sends out inhibitory NT ex GABA the ganglion cell does NOT re I we perceive darkness This process turns light into an action potential I TRANSDUCTION Iodopsin the receptor found in cones 130 million rods and cones connect to only 1 million ganglion cells 0 receptive eld all the rods and cones that project to a single ganglion cell The ratio of rodcone to ganglion cell is responsible for the different characteristics of the two receptors 0 Basically a 11 ratio of cones to ganglion cells 0 greater Visual acuity O fewer cones 0 Rods have to share ganglion manyzl ratio 0 lots of rods 0 less spatial resolution for a group of rods because they are all connected to the same ganglion cell 0 more sensitive to dim lighting because the graded potentials of the many rods connected to a single ganglion cell can summate and produce an action potential cones are not able to do this Contour 0 Lateral inhibition the areas that are stimulated will inhibit adjacent areas adjacent receptive fields of ganglion cells so that the shape is more apparent 0 this will cause the edges of objects to appear darker than they really are because our eyes are trying to make it easier for us to distinguish between different objects 0 REFER TO PICTURE IN NOTES Changes in Illumination 0 Refer to slide 0 Oncenterof39fsurround O on response light falling on center on response 0 off response light falling on surround off response 0 Offcenteronsurround O on response light falling on surround on response 0 off response light falling on center off response 0 these detect illumination 0 retina also has the ability to code for movement 0 REFER TO PICTURE IN NOTES Ganglion converge into optic nerve I exits eye I blind spot no rods or cones Binocular overlap Refer to slide Monocular crescents different depending on nose size Optic nerve comes together to form partial crossing at optic chiasm I go into brain and form optic tract in the brain 0 REFER TO PICTURE IN NOTES Suprachiasmatic Nucleus SCN brains clockpacemaker 0 works on 2526 hour cycle Wout stimulus 0 light cycle helps keep these cells on proper schedule Superior colliculus 0 control muscles of eye neck and trunk so that your body can track visual stimulus Lateral Geniculate 0 part of thalamus first place where visual stimuli are perceived Visuotopic 0 Visual map of world I lateral geniculate and retina have this Laminar organization 0 Refer to slide 0 layers get input from different sides some from contralateral and some from ipsilateral Layers 1 and 2 O Magnocellular cells 0 gross form and movement layers 0 send information through Mchannel magnocellular pathway to cortex Layers 36 0 Parvocellular cells 0 fine detail and color 0 send information through Pchannel parvocellular pathway to cortex Calcarine Fissure location of primary Visual cortex Visual Cortex 0 Visuotopically organized 0 REFER TO SLIDE Hubel amp Wiesel 0 cells in cortex favor line stimulus contours between light and dark Primary Visual Cortex Striate cortex Area 17 1 Simple cells 0 respond to lines at particular orientation favor one orientation over others 2 Complex cells 0 detect moving lines at particular orientation and direction of movement 0 connected to several simple cells 0 REFER TO SLIDE 3 Hypercomplex cells 0 only respond to lines at speci c angles I two lines and their orientations 0 these types of cells are set up in columns COLUMNAR ORGANIZATION o ORIENTATION COLUMNS o REFER TO PICTURE IN NOTES Ocular dominance columns columns that distinguish cells that respond to input from the right or left eye 0 cells are very specific to 0 which eye left or right 0 orientation of stimulus 0 location in space where the stimulus is located within the visual eld Modules 0 one modulecluster of cells tells us everything we would need to know about a specific area in our visual field each cylinder of the module codes for a different wavelength color these cylinders are called blobs analyzes Visual world into line segments contours Visual cortex codes for form and movement and contours and depth 1st time combining info from both eyes I 3D Color Vision I REFER TO SLIDE LOOK THIS UP IN BOOK cones w iodopsin I responds to blue cones w iodopsin I responds to red last set of cones respond to green there is some overlap so that we do not have gaps in our ability to perceive color 0 This led to the trichromatic theory Ganglion cells respond to pairs of color redgreen blueyellow 0 OPPONENT PROCESS THEORY Yellow light falls between red and green I activates both I they contribute to the blue yellow ganglion and inhibit blue input color Vision deficiency is generally sexlinked I common in men 0 generally partial color blindness I especially redgreen I blueyellow is much more rare Brain takes color information and segregates it form other visual information almost immediately amount of focusing that lens uses gives us information about how far away a stimulus is Primary Visual CortexArea 17 0 sends information to areas 18 and 19 0 secondary Visual cortex VII Area 18 0 tertiary Visual cortex VIII Area 19 0 VII and VIII analyze more complex aspects of visual stimuli 0 information does not ow through a single pathway but rather through ascending parallel pathways 0 not linear hierarchical model 0 PARALLEL PROCESSING 0 pathways interact I leads to complexity 0 adding complexity to Visual stimulus leads to recruitment of higher level cells in areas 18 and 19 Pathway 1 AKA VENTRAL STREAM 0 travels to inferior temporal lobe from areas 18 and 29 0 object vision I the what pathway Pathway 2 AKA DORSAL STREAM 0 travels to posterior parietal lobe from areas 18 and 19 0 spatial vision I the where pathway REFER TO SLIDE FOR SPECIFIC REGIONS WITHIN PATHWAY Hierachrical coding O certain cells require the activation of several other cells before it can be stimulated 0 REFER TO SLIDE Gnostic cell 0 know depends on position the network of cells allows higher cells to only respond to speci c complex stimuli Fusiform Area 0 part of ventral stream 0 there are cells in this area that ONLY re when you see a speci c person at a speci c angle Grandmother cells 0 there may be cells that only respond to grandma s face 0 this idea seems too simple to really be true there are an infinite number of potential objects but not an infinite number of cells to be assigned to each object Feature detector systems 0 this is a more likely possibility 0 Ensemble coding cells that together recognize a specific stimuluscomplex feature Prosopagnosia failure to recognize faces can describe all features but cannot put the pieces together problem with the ventral stream DORSAL STREAM 0 MT aka V5 RESPOND TO DIRECTION OF MOVEMENT OF VISUAL STIMULUS AND SPEEDACCELERATION OF STIMULUS Place C6118 know where you are in relation to everything else in your visual eld your physical position 0 Damage can t mentally rotate and recognize objects can t do incomplete figure tasks draw a complete picture Posterior parietal lobe codes for spatial information from all senses not just Visual Astereoagnosia inability to feel something and recognize it When you are imagining things you use some of the same pathways that are used during sensation ATTENTION Attention and sensation are closely related Although we can process lots of information at the same time we do need to focus on specific stimuli I the important relevant facts stimulation we pay attention to important novel interesting things attention can be involuntary externally driven attention can also pay attention to things within yourself memory thoughts I internally driven attention REFER TO SLIDE FOR GLOBAL AND SELECTIVE STATES 0 cycle through states of consciousness O cocktail party effect I we can selectively choose to attend to certain stimuli and ignoreblock out other stimuli Broadbent limited capacity system somewhere in brain there is a gate this only allows some info through Early selection lter out uninteresting infostimuli before it is perceivedprocesses I blocked at source I can be problem because you don t fully perceiveunderstand stimuli Late selection fully perceive all stimuli I then focus attention on most important stimuli Refer to notes Orienting Re ex re ex designed to put you in contact with suddendrastic stimuli What is it O Involved with the colliculi brainstem re ex Voluntary attentionl kind of like a search light search and select where you would like to focus EEG can see events occurring in the brain as they occur I GREAT temporal resolution 0 however not very specific I bad spatial resolution looking at summation of electrical activity from LOTS of cells Spontaneous EEG recording from neurons without specific task Synchronous activity will get nice regular waves when cell activity is synchronous 0 814 Hz Alpha 0 47 Hz Theta 0 lt1 Hz Delta Dysynchronous activityEEG while awake doing something 0 gt 25 Hz Beta 0 will occur during dreaming paradoxical sleep Event Related Potential ERPEvoked Potentials 0 giving stimuli and looking to see how brain is responding 0 to get rid of noise add many trials I the response will amplify and noise will decrease O summation of lots of trials 0 P1 first positive wave of the evoked potential 0 REFER TO PICTURE 0 information enters the eye 0 travels to the LGN 0 travels to VI 0 travels to VII or VIII I dorsal stream goes to RP posterior parietal 0 travels to prefrontal cortex I travels to pulvinar nucleus in thalamus LATE SELECTION 0 travels back to V1 I ventral stream goes to IT whuuut I some input goes from VII and VIII to the reticular nucleus of the thalamus an inhibitory network super early selection gets rid of very irrelevant info Attention involves many parts of the brain 0 similar systems are found in other sensory pathways Executive attention focuses attentionenergy on one attentional system Supervisory Attentional System not sure function I anterior cingulate cortex I receives input and monitors performance and error detection connected to attentional systems Dopaminergic systems Neglect system will only do things on one side I Attentional disorder I they can perceive but they do not attend to one half of their world 0 they also have problems attending to thoughts and imagining things Motor SystemsSpinal and Peripheral Mechanisms I the outputbehavior of our bodyN S 0 gross bodily movement organ control lip movement 0 encompasses many behaviors 1 Simple Re exes stereotypic unlearned responses to stimuli 0 ex coughing swallowing sneezing kneejerk 2 PosturePostural changes 0 all these require motor activity to support body 0 tonic activity sustained contraction of muscle I muscle tone also unlearned I hard wired properties of the NS Locomotion 03 hard wired motor programs are present even in new born babies they cannot walk because they have not developed enough yet 1 Sensory Orientation body orients itself to react to a stimulus 0 stimuli come into colliculi I causes body to turn towards incoming stimuli ORIENTING REFLEX O hardwired O a little more complex than other re exes Fixed action patterns hardwired motor programs to control behavior 0 reproductivemating behavior grooming nest building weaver birds spider web 0 ex preying mantis 6 Acquired Skills 0 learned motor skills U 0 ex playing sports speaking have to learn how to make all the different sounds involved in speaking Muscle Movement cardiac muscle heart does not fatigue easily smooth muscle found in organs of body skeletalstriated muscle used in voluntary behavior 0 connected by tendons to the bones I allows skeleton to move 0 muscles can contract shortening and relax lengthening all muscles pull contraction antagonistic muscles allow us to move bones in both directions 0 extensors ex tricep O exors ex bicep antagonistic muscles cannot both be activated at once I inhibitory re ex reciprocal control 0 REFER TO SLIDE Neural Aspects of Muscle Activity skeletal muscle is innervated by motor neurons 0 alpha motor neurons in ventral horn I final pathway to muscle I can innervate many muscle fibers I innervation ratio I 13 lgood control hands face etc II 1150 I not speci c gross crude legs back butt etc 0 motor unit single alpha motor neuron and the muscle fibers that it innervates 0 motor neuron pool several motor units Neuromuscular junction synapse between motor neuron and muscle 0 acetylcholine nicotinic receptors 0 end plate location where neuron contacts muscle 0 Ach causes Na in ux I small depolarization 0 CALLED end plate potential EPP 0 if there is enough Na comes pouring in I muscle action potential Drugs 0 Nicotine agonist 0 Venoms black widow cobra toxin 0 botulism toxic ricin 0 nerve gases serin Diseases 0 Myaesthenia gravis 0 immune system produces antibodies for aceylcholine receptors I blocks them Action potential now must be paired with contraction 0 release of intracellular calcium 0 triggers biochemical series of events produces energy 0 within muscle fibers are fibrils I thick filament myosin and thin lament actin proteins 0 muscle relaxed I thin and thick are apart 0 contraction causes filaments to come together shortening the muscle Autoregulation of Muscle Tone 0 embedded in muscle are spindle organs 0 extrafusal muscle fiber 0 spindle organs have extrafusal with intrafusal attached 0 intrafusal has a stretch sensor I tells intemeuron whats up I goes from dorsal to ventral horn alpha and gamma motor neurons in ventral horn 0 alpha I extrafusal 0 gamma I intrafusal I interneuron tells these to adjust muscle tension 0 REFER TO SLIDE 0 muscles can work with spinal cord to do most of this I brain doesn t have to work 0 for voluntary changes brain uses SAME system 0 send descending info to gamma I fire I intra becomes taut I activates stretch receptor I sensory neuron I activates interneuron I gamma and alpha contract the fibers 0 shows how brain evolved 0 higher parts of brain utilize existing pathways Proprioception Golgi tendon organs I detect stretch in series with muscle fibers I break mechanism to prevent muscle from contracting too stronglyforcefully Recurrent inhibition 0 Renshaw cell inhibits the alpha motor neuron causes recurrent inhibition or periods of silence O prevents muscle from over firing fatiguing and over contracting O REFER TO PICTURE Motor Systems 11 0 Central Motor Systems 0 can be seen as hierarchy 1 association cortex basal ganglia motor strategy goal of movement 2 Motor cortex cerebellum motor tactics spatial and temporal sequence required to smoothly and accurately achieve the goal 3 Brainstem spinal cord execution activation of motor neurons and neuron pools interneurons activate muscles Sensory information gives feedback to alter the motor movement appropriately Ballistic Movements 0 very fast movement cannot be altered once it has started I sensory information cannot alter this action but can in uence subsequent movements based on initial outcome Sensorymotor systems closely linked in uence each other 0 1 0 2 sensory info yields memory of outcomes 0 3 sensory feedback is used to adjust posture muscle tension etc Bundlestracts bring info descending through spine 0 Lateral pathway voluntary control of movements of distal musculature limbs arms and legs under direct control of cerebral cortex 0 Ventromedial pathway 4 pathways control posture balance locomotion control proximal muscles trunk and hips axial and girdle muscles large core muscles under brainstem and spinal control LATERAL PATHWAY 2 TRACTS 0 1 CORTICOSPINAL TRACT originates in motor cortex ends in spinal cord AKA pyramidal tract 0 in medulla pyramidal decussation crossing over some fiber switch sides 0 Betz cells large pyramidal neurons 0 fibers are uninterrupted until synapse in the spinal cord very direct pathway 0 2 Rubrospinal Tract parallel to corticospinal tract 0 red nucleus synapse between cortex and brainstem O deemphasized because of corticospinal tract if the cortico tract is damaged the rubrospinal tract can help compensate somewhat 0 PATHWAY cortex I red nucleus I ventral horn LOOK UP THIS VENTROMEDIAL TRACT 4 TRACTS 0 all originate in brainstem I spinal cord synapse on gamma motor neurons I controls muscle tone and tension 0 control muscles of axial and girdlecore and some large leg muscles 0 1 tectalspinal tract I tectum colliculi I neurons originate in colliculi and go to spinal cord I orienting re ex controls core chest hips I track things in space 0 2 Vestibulospinal tract I balance acceleration I come down from inner ear pons I synapse on lateral vestibular nucleus I go down spinal cord and help with balance and posture 0 3 Pontine reticulospinal tract I important for controlling antigravity muscles I used to maintain posture and balance while moving 0 4 Medullary reticulospinal tract liberates muscles from antigravity I so that you can walk etc I also used to maintain posture and balance While moving CEREBRAL CORTEX PLANNING MOVEMENT back of frontal lobe primary motor cortex Area 4 0 map of body premotor cortex PMA area 6 supplementary motor cortex SMA area 6 frontal eye fields area 8 0 controls muscle of eyes I voluntary visual tracking high level control prefrontal cortex large area of association cortex primary somatosensory cortex areas 1 2 and 3 0 front of parietal lobe secondary somatosensory cortex areas 1 2 and 3 posterior parietal lobe areas 5 amp 7 Area prefrontal I 6 I 4 look at slide Ready set go I Where does this signal come from Set in Area 6 before you are ready to move neurons are holding info Go signal BASAL GANGLIA BASAL GANGLIA 0 caudate putamen striatum globus pallidus pallidum 0 interacts with cortex through loops 0 descending projects I striatum I globus pallidum 0 gp can directly or indirectly go to thalamus ventrolateral thalamus projects back up into area 6 makes loop and gives go signal 0 I acts like funnel with lots of info from cortex I goes to fewer cells in area 6 when there is enough stimulation in 6 the go signal is sent to area 4 0 problems with basal ganglia I issues with voluntary movement I Parkinson s O akinesia lack of movement I trouble moving because the funnel is shut I the go signal is gone because dopaminergic cells are dead from substantia nigra 0 Huntington S Korea destroys basal ganglia similar motor disorders Map of body within the motor cortex 0 homunculus CEREBELLUM 0 critical for motor behavior 0 balance posture I damage will disrupt this 0 damage also causes fractionated movements muscles are not really working together 0 dysmetria inability to measure your movements FUNCTIONAL AREAS OF CEREBELLUM 0 vermisSpinocerebellum interact with brainstem control posture O vestibulocerebellum oculus and nodules regulates balance 0 cerebrocerebellum lateral hemispheres interacts with cerebral cortex through loop REFER TO SLIDE I provides info to cortex about direction timing and force motor guidance 0 slow movements can be controlled in real time O ballistic movements provides predictions of what it should do based on past motor learning EMOTIONS STRESS amp COPING 0 emotions are difficult to study I so many different types how do you categorize them or distinguish them also difficult because emotions do not correlate with physical changes the way other things do 0 1 Bodily Response expression physical bodily changes ex skin tingling sweating heart racing etc 0 2 Feelings subjective expression the thoughts that go along with those feelings the mental experience Motivated states emotions drive humans toward goal or away from danger I evolutionarily adaptive 0 ex attack from predator I anger aggression fear anxiety 0 these are a defense against costly events I ex sadness I can show others in group that there is something wrong we are social creatures I it is beneficial to be able to communicate that there is a problem 39 cognitive reappraisal saddness can cause us to reevaluate our behaviors to adapt III Neural Basis of Emotion 0 hypothalamus O pissed cat pictureslide 0 If u electrically stimulate a part of the hypothalamus you can stimulate this behavior 0 Periaqueductal Gray PAG 0 can both elicit species specific emotional behavior when stimulated I innatehardwired emotional behavior re exive 0 we can also LEARN emotional behavior 0 able to assess emotions and situations require higher level processing Broca 0 along midline there is a circle of tissue 0 lobe limbic I thought this was involved in emotion I limbic is border 0 On slide dotted area McLean 0 tiune brain 0 3 parts of brain 0 Reptilian brain basically brainstem stereotypic behaviors 0 Old Mammalian brain evolved on top of brain stem gt made up of limbic system experience emotions learned emotional behavior 0 New Mammalian brain neocortex problem solving and rational thought Limbic System 0 hippocampus amygdala septal nucleus fornix cingulate cortex hypothalamus thalamus olfactory system James Papez 0 expression is regulated by hypothalamus 0 REFER TO SLIDE 0 Singular cortex is the main thing in experience in emotion cognition 0 Neocortex Where emotional emmories are stored that color your emotional experiences 0 this leaves out the amygdala and prefrontal cortex Problems with the amygdala I KluverBucy syndrome 0 oral fixations strange increased sexual behaviors complete lack of fear and anxiety at affect don t show much emotion 0 prefrontal regulates emotional behavior and limbic system through inhibitory control 0 without this you have emotional lability large uctuations in emotion COULD THIS SINGLE CIRCUIT BE RESPONSIBLE FOR ALL EMOTIONS 0 No there are other sub circuits Phineas Gage 0 Railroad worker They had to blowup mountains and tracks His job was to take explosive charges and with an iron rod tamp them One day the explosive went off the rod went through his nose and through his head 0 They went to the dr He survived 0 Dr documented his recovery 0 Her had a personality change FACIAL EXPRESSIONS 0 nonverbal communication 0 facial expression is universal 0 2 circuit that are responsible 0 the ability to read other peoples emotion is important 0 U need to be adaptive to mask your emotions VII facial nerve 0 voluntary facial expressions can mask emotions 0 circuit in the basal ganglia I projects to brainstem and in uences facial nerve I spontaneous facial expression 0 damage to basal ganglia causes lack of normal expression I seen in Parkinson s patients Appetitive Motivation 0 makes you feel good when you are trying to do something positive I euphoria happiness pleasure 0 ex eating drinking 0 involved in ascending dopaminergic pathway 0 Nucleus accumbens IDopamine is released at this synapse limbic system I frontal cortex motivational system 0 cocaine activates this pathway Anhedonia problems in the dopamine system linked to depression Aggression Pathway 0 PFC I amygdala I hypothalamus I PAG 0 serotinergic system controls this I problems with this cause aggression issues Fear and Anxiety 0 pavlovian fear conditioning I experimental model to induce fear 0 testing learned emotional behavior and how they express it Method 0 aversive unconditioned stimulus leads to 0 unconditioned response 0 behavioral freeze potentiated startle O cardiovascular decreased heart rate increased blood pressure 0 pupillary dilation O hormonal 0 Pair the aversive stimulus with conditioned stimulus like tone CS Stress 0 tone elicits same response I conditioned response CR 0 now that you have control you can look at what circuits in the brain are being utilized 0 conditioned stimulus and unconditioned stimulus I thalamus I amygdala which is responsible for 0 hormonal response 0 autonomic response 0 behaVioral response 0 Amygdala is responsible for learned fear if you get rid of the amygdala these responses are GONE 0 the entire circuit is subcortical information has not yet reached the cortex 0 we can be and become afraid of things subconsciously phobias we don t even know why we are afraid LedouX and DaVis 0 REFER TO SLIDE FOR THE FLOW CHART PTSD 0 Fear memories and learning do not go away easily 0 they are stored in cortex and stimulate amygdala Stressor 0 stimulus that demands adaptation 0 response to the stressor 0 can have stress without distress it is not necessarily bad I it causes adaptation 0 REFER TO SLIDE for stressors and points 0 death of spouse 0 marriage 0 Good stress Stress Without distress Life event stress scale 0 1 death of spouse 2 divorce 0 heart blood disease arthritis High BP Cancer CANNON 0 fight or ight syndrome 0 sypatho adreno medullary system SAM 0 increase muscle activity mobilize muscles 0 Increase energy production 0 increase blood ow to muscles shut down blood ow to internal organs shunted to muscles 0 increase heart rate and cardiac output 0 increase respiration 0 mobilizes energy stores 0 Slide of guy in Fight or ight Selye O body s response to stressors occurs in stages I General Adaptation Syndrome GAS 0 in GAS we respond in phases 0 1 Alarm reaction immediate response SAM 0 2 Resistance phase I hypothalamic pituitary adrenocortical system HPA 0 google HCTH I produces CORTISOL U cortisol glucocortisol I helps producesynthesize glucose 0 3 Exhaustion Phase when stressor occur for too long we lose abilities to resist I this is when disease occurs I wen you are most susceptible I diseases of adaptation 1 Active coping 0 increase motor activity 0 increase SAM 0 increase co 0 increase glucose utilization 0 increase blood ow to muscles 2 Passive coping aversive vigilance 0 monitoring situation and waiting for opportunity to act 0 decrease in motor activity 0 decrease heart rate 0 increase blood pressure increase total peripheral resistance 0 increase SAM and HPA cortisol Differences in coping styles causes different diseases of adaptation Not all physiological coping is the same 3 Conservation withdrawal helplessnesshopelessness 0 when an organism totally gives up trying to cope with a situation I they stop shut down mode conserve energy Seligman 0 prisoner of war coping well with being a prisoner because he was promised to be released soon actively coping well 0 When he was about to released he found out he was not leaving 0 He turned into a funk stopped eating and drinking and died Richter 0 looked at how rats used whiskers cut them off 0 swimming mechanisms of rats 39 would sink to the bottom and die I if he took them out and then put them back in water they would swim I before they had totally given up trying to cope HOW DOES THIS RELATE TO HEALTH 0 heart disease 0 sudden cardiac death 0 hypertension 0 stroke 0 asthma 0 ulcer 0 migraine 0 colitis 0 infectious diseases 0 cancer 0 emotional upset can trigger onset of disease or accelerate it 0 physical problems accompany emotions 0 people Who are physically ill commonly have emotional responses 0 physical ailments can cause mental disturbances Major causes of diseases 0 REFER TO SLIDE 0 1900 infectious diseases very low life expectancy 0 development of antibiotics and sanitation movements 0 1973 heart disease cancer stroke accidents 0 causes of death are related to behavioral and psychological behaviors REVER TO SLIDE FOR BEHAVIORS ASSOCIATED WITH LEADING CAUSES OF DEATH Psychosocial behavior I drives up blood pressure Behavioral Medicine 0 interdisciplinary field dealing With integration of biomedical 0 REFER TO SLIDE 0 application of this science I disease prevention diagnosis treatment rehabilitation health promotion Behavioral suspects 0 health damaging behaviors 0 stress I can you work with people to reduce stress or do things medicinally to prevent effects of stress What do biological mechanisms link behavior to disease 0 coronary heart disease 0 leading cause of death in the US 0 due to atherosclerosis in coronary arteries which occuludes the vessels leading to angina myocardial infarction and sudden death REFER TO SLIDE 0 endothelial cells are innermost layer 0 cells invade wall I plaque and fat buildup I occlusion I platelets form clots 0 if you block vessel I ischemia lack of blood ow 0 chest pain Angina 0 when blood ow shuts off and tissue starts to die you get myocardial infaction O vessel that is completely occluded the part of the heart that gets blood from that vessel dies and is called a myocardial infarction 0 Heart pumps less efficient 0 If its small you can live with it but you will be more tired etc because your heart needs to work harder 0 If it s a big infarct you get scar tissue and the electrical current in your heart is not going smooth anymore and the pumping or the different ventricles and atriums might be off 0 electrical disturbances Arrhythmias 0 there are beneign ones Everyone has them at some point 0 also dangerous ones I called ventricular brillation I can cause SUDDEN CARDIAC DEATH l the ventricular fibrirllation are lethal 0 myocardial infarction I arrhythmias I death 0 happens over time due to atherosclerosis Pathophysiology of Atherosclerosis 0 response to vascular injury I hypertension toxic chemical in blood infections 0 response to retention of LDL cholesterol and oxidative stress 0 response to in ammation SLIDE of layers of cells in vessels 0 2 weeks of increased dose of adrenalin damage to blood vessels How to get atherosclerosis 0 LDL cholesterol bad cholesterol goes into the vessels There has to be a dysfunction Within the endotheloim for this to happen 0 LDL once inside gets oxidized by NADPH and turns into Oxidized LDL This is called OXIDATIVE STRESS 0 One of the things it does is it causes the expression in a protein MCPl monocyte chemo attractive protein 0 Monocytes are undifferentiated cells in blood that circulate through blood and bounce against endothelium They stick to adhesion molecules on the endothelium 0 Then MCPl draws these monocytes through the endothelium in the intima 0 When monocytes are in the vessel wall they get signals from oxidized LDL and become macrophage O Macrophages produce cytokines Many of these are in ammatory molecules IL6 etc 0 They stimulate the further production of adhesion molecules Then more monocytes are trapped O This is a vicious circle 0 This is called INFLAMATION I Macrophages suck up oxidized LDL and become foam cells But they continue to secrete cytokines and enzymes 0 Because the foam cells produce cytokines growth factors metalloproteinases and what happens I Further in ammation cell proliferation and matrix degradation 0 REMEMBER the two processes I OXIDATIVE STRESS I INFLAMMATION REFER TO PICTURE IN NOTES PROCESS OF INFLAMMATION monocytes adhere to adhesion molecules on endothelial cells I go into intima I turn into macrophages I release cytokines I create more adhesion molecules I REPEAT PROCESS macrophages suck up oxidized LDL I turns into foam cells secrete more cytokines growth factors and metalloproteinases these cause further in ammation cell proliferation and matrix degradation understand in ammation and oxidative stress smooth muscles will grow over the mound FIBROUS CAP Lesion vulnerability advanced lesions plaque can become vulnerable to rupture especially those with thin caps lack of collagen structural protein and laden with lipids O rupture of vulnerable plaque can lead to sudden cardiac events due to thrombi including sudden cardiac death What role does behavior have in this process RISK FACTORS for CHD 1 smoking 2 HBP high blood pressure 3 high cholesterol serum 0 particularly low density lipoproteins LDL 4 Family history of CHD 5 Sex being male I after menopause risk for female male 6 Diabetes metabolic syndrome 7 Age starts to show up late 308 El 8 Type A behavior pattern smoking and HPB are the primary risk factors If u control these you control over half of the cases There are behavioral treatments for this Women are more protected when they have their eggs when they go through menopause that protection stops Type A 0 Aggresice hard driving hostile loud impatient irritable time pressured compulsively striving psychomotor mannerisms unusually competitive excessively job involved Age 0 We build up atherosclerosis 0 Obesity will cause atherosclerosis 0 Genetics can start atherosclerosis early in life Profile of hypothetical Type A Individual 0 aggressive harddriving hostile loud impatient irritable timepressure compulsively striving psychomotor mannerisms constant foot tapping ex 0 refer to slides Western collaborative group study 0 controlled risk factors statistically removed 0 Type A had 2X the risk as type B 0 Not all studies have found a significant relationship between global type A behavior and CHD 0 Hostility 0 is a component of type A that is associated With CHD even When global type A is not Sympathetic Hypothesis 0 It has been suggested that type A behavior and particularly hostily leads to chronic sympathetic nervous system activation 0 Sympathetic activation may initiate or accelerate disease processes What is the physiological link Behavioral stressors alone do not induce disease 0 interactions between biobehavioral and other variables may lead to cardiovascular pathology I diet genetic predisposition Emotional stress and diet appear to interact to promote atherogenesis Kaplan Manuck male monkeys repeated social organization groups of cynomolgus monkeys accelerates artheogenesis in animals fed an atherogenic diet social stressors rearrange monkeys to socially reorganize create unstable social colony compare with stable social colony high fat and low fat groups 0 within each there were unstable and stable social environments and within each of those there were dominant and subordinate the males developed 2X as much HD as any other group in the high fat unstable setting type A females the highest group with HD was high fat unstable subordinate monkeys are expensive and takes a long time Dominant monkeys with fat diet in unstable groups get more stress than subordinate or domants liVing in stable groups Cynomologous Monkeys Beta blockers stopped disease differences in groups stopped behaVioral difference Refer to slide Wantanabe Heritable Hyperlipidemic Rabbit WHHL model for human familial hypercholesterolemia slide 0 assigned to one of 3 social condtions I High stress unstable paired with unfamiliar rabbit rearranged each week 39 Stable paired with littermate they stayed with them the entire study I Individually caged housed alone no contact the entire study lab rabbits from Japan this happens in humans too develop atherosclerosis as early as 2 months old genetically wired to develop heart disease unstable agonistic behaviors with unfamiliar rabbit individually caged increases atherosclerosis very advanced lesions fast progression stable decreases atherosclerosis YAY friendship unstable and individually caged have much more atherosclerosis then bunnies with their littermate bunnies Stable Social Environment It has been shown in rodents that affiliative social behaviors maternal behavior pair bonding affiliative grooming cuddling are related to peptide systems in the brain oxytocin vasopressin CNS oxytocin has also been shown to attenuate peripheral stress responses HPA and sympathetic Plasma peripheral oxytocin Stable Social group exhibited elevated plasma oxytocin relative to the other groups 0 Oxytocin receptors have been identified on cardiac and vascular cells particularly on vascular endothelial cells 0 Oxytocin reduces oxidative stress it is anti oxygen 0 Oxytocin is anti in ammatory Summary 0 Oxytocin receptors are expressed on endothelial cells smooth muscle cells and macrophages In vitro studies suggest that Oxytocin has antiin ammatory and antioxidant effects on vascular cells These actions may explain the relationship between a stable social environment and atherosclerosis in the WHHL model How your body deals with stress Aminohistochemistry innervation of sym nerve terminals in blood vessels NOT hormonal plasticity refer to slide


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