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83 Cards in this Set
- Front
- Back
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PD is characterized by four principal symptoms:
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Rigidity: Stiffness of the flexor and extensor muscles where movement is short and jerk “cogwheel rigidity”.
Resting Tremor: Prominent in the hands. Disappears during sleep. Postural tremor is also common during postural maintenance. As soon as movement becomes purposeful, tremor will go away. Bradykinesia: Difficulty initiating movement, slowness in movement, and paucity or incompleteness of speech. Postural Instability: abnormal righting or postural reflexes such that when PD patients trip, they are unable to stop falling, or ease their fall–resulting in injury. Shuffling gate |
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The MPTP Story
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1982 – a backstreet chemist in an attempt to synthesize synthetic Demerol, mistakenly created the compound MPTP.
Several opiate addicts injected the toxic substance and within hours were in the hospital with severe paralysis. Langston (a neurologist) noticed that the symptoms resembled Parkinson’s. He treated them with a Parkinson’s drug, and symptoms subsided. The tainted drug was identified and synthesized. When injected into non-human primates, they too developed Parkinson’s. due primarily to : metabolite of MPTP seems to selectively destroy Dopamine Neurons in the Substantia Nigra (tegmentum of the Midbrain mesencephalon.) |
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Cause of PD
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Loss of Dopaminergic Neurons in the Substantia Nigra (tegmentum of the Midbrain mesencephalon.)
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Disinhibition & Partial Anatomy of the Basal Ganglia
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“Inhibiting an inhibitor” with the net effect being excitation
**Review Pathway of Basal Ganglia substantia nigra--> caudate/putamen-->globus pallidus--> VA/VL complex of thalamus--> premotor cortex |
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PD Drug Treatments
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Levodopa*precursor for dopamine synthesis
deprenyl other drugs that increase dopamine production: MAO inhibitors (also for depression) |
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PD Surgery: Invasive Techniques
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cryothalamotomy, destroys the thalamic brain area that produces tremors
deep brain stimulation pallidotomy interrupts the neural pathway between the globus pallidus and the striatum or thalamus transplant stem cells |
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Huntington's Disease
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inherited
symptoms dont usually develop until age 35 (most have already had children by the time they realize they have the disease) characterized by: involuntary movements (chorea) and sometimes rigidity progressive dementia, irritability, moodiness weight loss from constant movement death 15-20 years after onset profound progressive destruction of GABA and Acetylcholine neurons in basal ganglia |
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Schizophrenia Prevalence
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1% of population
more than 2million americans a year affects men and women with similar frequency, but develops earlier in men all races and cultures onset sudden and intense-can begin with acute psychotic phase can be brought on by drug use or life stressor(anything that changes homeostasis like a drug) can be successfully treated with drugs, but the long term prognosis is poor |
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Symptoms of Schizophrenia
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positive symptoms: disorders of thought, hallucinations, delusions (false beliefs)
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Causes of Schizophrenia
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10% likelihood of developing the disease if a biological relative has it (even if adopted by a healthy family)
concordance rate in identical twins 45% concordance rate in fraternal twins 10% genetic regions on chromosomes 6 and 13 have been associated with the disease can inherit suceptibility-but just because it is in lineage does NOT mean you will definitely have the disease also due to enlargement of ventricles in the brain due to loss of neurons decreased cortical volume |
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Major Breakthrough in Schizophrenia Treatment
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Chlorpromazine-first developed as an antihistamine, shown to have calming effects, alleviate symptoms, is a Dopamine antagonist
prolonged use of these drugs produced Parkinson's-like symptoms |
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the dopamine hypothesis of Schizophrenia
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antipsychotic drugs like chlorpromazine block DA receptors: long term usage of phenothiazines often develops parkinsonian-like symptoms (tardive dyskinesia)
Amphetamine psychosis resembles schizophrenia: amphetamine blocks DA transporters, raising DA levels. Amphetamine exacerbates schizophrenia. |
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Evidence for the Dopamine Theory of Schizophrenia
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drugs that block dopamine reduce schizophrenic symptoms
-->most effective antipsychotic drugs block D2 receptors drugs that block dopamine have side effects similar to PD (caused by a lack of dopa in basal ganglia) best drugs to treat schizophrenia resemble dopamine and COMPLETELY BLOCK dopa receptors high doses of amphetamines cause schizophrenic-like symptoms "amphetamine psychosis", a model for schizophrenia b/c drugs that block amphet psychosis also reduce schizophrenic symptoms. Amphets also make symptoms of Schizo WORSE |
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Chlorpromazine
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first antipsychotic medication developed (for Schizo)
trade name Thorazine |
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Questioning the Dopamine Theory of Schizo
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Amphetamines do more than increase dopa levels, they also alter other neurotransmitter levels
drugs that block dopa receptors act on receptors quickly, however these drugs sometimes take many days to change the behavior of people with schizo effects of dopa blockers may be indirect, may influence other systems that have more impact on schizo symptoms new drugs for schizo, like chlozapine, block receptors of serotonine and dopamine structural abnormalities in the brains of schizos outside the dopamine system most likely a collection of problems that cause Schizo-not just too much dopa being produced |
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Neural Degeneration
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degeneration: anterograde (cell body to synapse)
retrograde (synapse to cell body) transneuronal:( anterograde/retrograde transneuronal) from a higher to a lower form, especially change of tissue to a lower or less functionally active form Apoptosis: active, programmed cell death Necrosis: passive cell death when cells arent used normally they die |
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Apoptosis
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triggered by variety of conditions
activation of apoptosis associated with chromatin condensation |
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Neural Regeneration
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proceeds readily in lower animals, especially invertebrates
ability to accurately grow axons is all but lost in adult humans "successful" regeneration depends on the extent of the damage and distance the regenerating axons must travel PNS neurons more capable of regeneration than CNS schwann cells: growth factors, cell adhesion molecules |
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Neural Reorganization
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Stregthening of existing connections
"sprouting" of new connections |
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"New" Neurons in the CNS
How is BrDu Used? |
dividing cells can be marked with BrDu
BrDu positive cells have been seen in hippocampus of adult rats, mice, humans |
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what is neurogenesis?
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growth of new neurons
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sensation
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process of detecting and encoding environmental energy
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perception
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result of organization and integration of sensations into an awareness of objects and environmental events
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sensory receptors
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specialized neurons that change energy into neural signals
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receptor potential
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local depolarization or hyperpolarization of receptor membrane
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transduction
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process by which energy is transferred into neural signals
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Mullers Law of specific nerve energies
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any activity by a particular nerve always conveys the same kind of information to the brain
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Structures of the Eye to know
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Pupil, Fovea, Blind Spot, Retina, Optic Nerve
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retina
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rear surface of the eye, lined with visual receptors
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photoreceptors
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specialized neurons that transduce light information
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bipolar cells
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receive information from photoreceptors and send it to ganglion
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ganglion cells
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receive information from bipolar cells. Axons make up optic nerve
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ID cell types of the optic nerve
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Horizontal/Amacrine
Ganglion Bipolar |
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fovea
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tiny area specialized for acute, detailed vision. ganglion cell axons, no blood vessels, each receptor connects to a single bipolar cell which in turn connect to a single ganglion cell (1:1:1) for better acuity
in peripheral retina, several receptors converge onto bipolar and ganglion cells (several photoreceptors can activate a ganglion cell) hence the periphery of your eye is more sensitive in dim light |
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Rods and Cones
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rods: respond to faint light, abundant in periphery
cones: essential for color vision (3 types of cones, sensitive to one of three different wavelengths of light) not active in faint light |
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photopigments
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chemicals that release energy when struck by light
human rod can contain 10 million molecules consisting of two parts: opsin and retinal, bound together. when exposed to light, break apart |
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when transduction occurs, what cell types produce action potentials?
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GANGLION cells produce action potentials
in the dark, photoreceptors are depolarized when light breaks apart opsin and retinal, cascade of events hyperpolarizes the photoreceptor, which normally inhibits bipolar cell, light causes DEpolarization of bipolar cell, which excites Ganglion to produce and Action Potential |
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what does light do to photoreceptors? bipolar cells? ganglion cells?
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light hyperpolarizes the photoreceptor. because photoreceptor normally inhibits bipolar cell, light causes a depolarization in bipolar cell, which excites ganglion to produce action potentials
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neurotransmitter released by photoreceptors
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glutamate
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trichromatic theory
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Young-Hemoltz: the preception of color from the relative responding of three kinds of cones, each maximally sensitive to a different set of wavelengths
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afterimage
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optical illusion, image continues to appear in ones vision even after image removed
negative color afterimage: see the opposite colors |
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opponent process theory
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we perceive color in terms of paired opposites, red-green, black-white, yellow-blue
BUT perception of color also depends on higher-level processing in visual cortex (retinex theory), this also does not account for color constancy |
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most common cause of color blindness
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lack of one or two cone types, or abnormal cone development
most common where long (red) and medium (green) wavelength cones have same photo pigment --> cant see red or green as well X chromosomal trait affecting more men than women |
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lateral inhibition
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reduction of activity in one neuron by activity in neighboring neuron
sharpens contrasts to emphasize borders one receptor is excited by sensory input, cells next to are inhibited |
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receptive field
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part of the visual field that excites or inhibits neurons in visual system
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once visual information leaves the retina...
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ganglion cell axons make up the optic nerve, which exits the eye, crosses midline at the optic chiasm, goes to the lateral geniculate nucleus in the thalamus.
Information then passed to visual cortex. info from right ends up in left visual cortex |
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magnocellular and parvocellular layers in the LGN
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Magno: large neurons, receive input largely from rods, respond to movement
parvo: small neurons, receive input fron cones and respond to color, detail, shlow or non-moving objects |
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primary visual cortex
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=V1, area of cortex that is the first stage of visual processing, responsible for conscious vision.
imaging a visual scene will increase activity of V1 |
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blindsight
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people with extensive damage in V1 can sometimes still react to visual information that they report not seeing (may orient to flash of light)
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visual association cortex
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area of cortex that further processes visual information, qualities such as shape, movement, brightness, color etc..
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processing of visual information once it gets to the brain
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neurons in visual cortex may be "feature detectors", they respond to particular features of visual stimuli, shape, depth, movement. As visual information processed, cells may respond selectively to more and more complex shapes so you might have a circle detector or triangle detector
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selective adaption
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support for the idea that some neurons respond best to specific type of stimulus
when we view a stimulus with specific property (like movement) for a long time, neurons that respond to that property adapt by: 1. decreasing firing rate 2. less immediate firing rate upon re-presentation of stimulus |
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simple cells
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found in primary visual cortex, have fixed excitatory and inhibitory zones in their receptive field
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complex cells
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do not have fixed inhibitory and excitatory zones, but do respond to light of a particular orientation anywhere in its large receptive field
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response to complex shapes and faces
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Inferior Temporal Cortex: neurons have large receptive fields which always include information from the fovea. they often respond to complex shapes.
face recognition is processed in the Fuisform Gyrus , which is part of the inferior temporal cortex Damage can cause visual agnosia |
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prosopagnosia
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inability to recognize faces
difficulty determining wether two clas model of faces are different, even using touch, but can describe wether the face is young, old, female, male, but cannot identify the person |
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Stress
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any deviation of the body from HomeostasiS
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Hans Selye
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first person to systematically study stress
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HPA axis
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Hypothalamic Pituitary Axis
Hypothalamus (CRF) Anterior Pituitary (Adrenocorticotropic Hormone) Adrenal Cortex end product: cortisol, a glucocorticoid which feed back INHIBITS HPA axis, and help body release stores of FAT for E (stress response activates 2 systems: Endocrine and autonomic) HPA part of the endocrine |
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Effects of Cortisol (Glucocorticoid)
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stimulate glucose synthesis
inhibit uptake glucose into fat and muscle stimulate breakdown of fat suppress immune system (anti-inflamm) affects behaviors like fear as well |
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Cushings Syndrome
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hypercortisolism
caused by tumor of pituitary gland caused by increased production of cortisol or excessive use of cortisol or other steroid hormones |
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Stress Response Systems
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1. Endocrine: HPA Axis
Glucocorticoids like cortisol in blood help relase stores of fat for E and feedback inhibit HPA axis 2. Autonomic: The Sympathetic Nervous System: Fight/Flight see 4 effects: increase blood flow to muscles increase HR increase blood sugar piloerection (hair stands up) Also effects BEHAVIOR |
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Why are endocrine and autonomic nervous systems catabolic?
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help mobilize energy sources in the body (breakdown to use E)
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Real Stress Hormone
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CRF/CRH
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Manipulation in Learned Helplessness Experiments
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Controllability
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Paradigm of Learned Helplessness
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two groups of rats receive tail shock from same source. the escapable shock (ES) group can terminate the shock by turning a wheel. The inescapable shock (IS) group receives the same shock but unable to terminate
in order to study stressor: uncontrollability NOT shock |
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Effects of Learned Helplessness
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decrease in : food, water, aggression, social dominance, social interaction
increase in: ulcers, conditioned fear behavior |
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what evidence suggests that learned helplessness is a good animal model of depression?
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more evidence that LH rats are depressed: Chronic treatment with antidepressant drugs before LH treatment blocks the behavioral effects associated with LH
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potential flaws of learned helplessness model
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behavioral effects last only a few days, whereas DSM requires symptoms to be present for two weeks (however you cannot prolong LH by re-exposing animals to treatment)
antidepressant drugs are only effective as profilactics(low dose, preventative). the experimental design doesnt allow us to administer these drugs after an animal is already helpless, because effects didnt last long enough |
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what do Maier and colleagues suggest that LH is modeling?
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one aspect that is common to depression and many anxiety disorders: uncontrollability of environmental stressors
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uncontrollability and the fight/flight response, as well as the fear and anxiety behavior
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LH is associated with deficits in escape behavior, assoicated with fight flight
LH also assoc. with increased fear conditioning and anxiety |
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autoreceptor
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presynaptic receptor that binds the neurotransmitter released by a given neuron, inhibiting further release
a mechanism for feedback inhibition, help maintain homeostasis Paradoxically, less norepinephrine in the locus coerulus=more norepinephrine elsewhere |
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Evidence that the DRN is critical for LH
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DRN is a region containing serotonin, also called 5-HT
inhibition of DRN serotonin blocks LH (proving its necessary) Stimulation of DRN serotonin produces LH (sufficient) LH mediated by activation of serotonergic neurons in DRN increased 5-HT activation also associated with increase extracellular 5HT |
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DRN Hypothesis of LH
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inescapable shock activated DRN 5HT neurons more than equivalent escapable shock
this leads to increased 5HT release in DRN and projection areas increased 5HT release sensitizes DRN 5HT neurons for a period of time after inescapable shock |
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role of medial prefrontal cortex in LH
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executive control
inhibit lower brain regions emotion regulation shutting off the medial prefrontal cortex during stress produces LH, even if animal has control over stressor! |
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Kluver-Bucy Syndrome
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Damage to Medial Temporal Lobe produces:
Emotional blunting: flat effect, no appropriate response to stimuli Hyperphagia: extreme weight gain with out strictly monitored diet, tendency to put inedible objects in mouth Inappropriate Sexual Behavior: mounting inanimate objects Visual Agnosia: "psychic blindness" inability to visually recognize objects |
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Part of Brain Assoc with Urbach-Weithe Disease
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Amygdala
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Darwin on Emotional Expression
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expression of emotion evolve from behaviors that indicate what an animal might do next
if signals provided by behaviors enhance animals ability to survive, they will be retained opposite messages are revealed through opposite behaviors |
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James-Lange vs Cannon-Bard
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J-L: emotional stimuli activate physiological reactions that are then interpreted as emotional experiences
C-B: emotional stimuli simultaneously activate physiological reactions and emotional feelings |
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What part of the brain is activated by masked faces?
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eyes of faces masked, activation of amygdala
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Low and High Road fear responding
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Ledoux's Idea: brain is wired to learn to associate a fear with a visual image, sound, smell, tactal sensation without mediate by cerebral cortex
low road: fear of stimulus before you even know it high road: when you realize you are afraid |
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how is fear in rodents observed
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freezing= fear response
change in HR decreased appetite increase startle defecation decrease pain activity change in motor activity |
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what structure mediates conditioned fear?
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damage to amygdala interferes with fear, conditioned fear
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