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U of M PSY 3061 - Exam 3 Study Guide

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PSY 3061 1st Edition Exam # 3 Study GuideNeurodevelopmentI. Neuronal deatha. Necrosis: caused by brain trauma or other pathologyb. Apoptosis: genetic programs that tell the cell to self destructi. Already fulfilled cellular functionsii. Lack of nutrientsiii. Neurotrophic factors: chemicals released by postsynaptic cells that help maintain the survival of presynaptic cellsII. Brain reshapinga. Young brain is overconnected because it does not know which connections it will need mostb. Synaptic pruning makes way for strengthening of used synapsesIII. Postnatal brain maturationa. White matter increasesb. Gray matter decreasesc. Primary motor and somatosensory areas develop first, followed by reasoning, language, and complex spatial areas of the brain in more anterior and posterior regionsIV. Sensitive periods in brain developmenta. Childhood and adolescence encompass sensitive periods, windows in time where the brain is more malleable to experiencesb. During a sensitive period, one’s experiences may cause long term effects on the brainc. Before or after a sensitive window, one’s experiences affect the brain less, and these effects tend to last a shorter durationd. Critical period: windows where the developing organism must be exposed to a particular experience in order for a brain structure to appropriately develope. Excitation of retinal ganglion cells for their survival; some language during early childhoodf. For the most part, critical periods are more rare than sensitive periods, and problems during critical periods may lead to serious disorderV. Neurogenesisa. Can postnatal brain generate new cells?b. Until recent years, it was largely assumed that all neuron one has at birth is all the individual is going to get  i.e. neurons only die and don’t come backc. Neurogenesis: growth of new neurons  may happen in adultsd. Rats raised in the exercise condition had more new neurons than did rats raised in no exercise environment regardless of enrichmentNeurodegenerationI. Phantom limb syndromea. Sensation that a missing limb is still attached to the bodyb. Neuromas hypothesisi. Scar tissue caused by removal of the limb has severed nerve endings and these nerves send a cacophonous signal to the brain that “this limb is in pain”ii. Lead to additional surgeries to remove more of the limb or sensory nerves  rarely any improvement in clinical condition; pain often gets worsec. Somatosensory plasticityi. Some patients with phantom limbs can actually feel the limb by touching other parts of the bodyii. VS Ramachandran: axons from phantom arm may connect to neighboring area (e.g. face)  areas are closely situated in the somatosensory homunculus iii. Mirror box therapy: subject inserts intact arm into a box with a mirror  doctor tells patient to move hands/arms in synchrony1. Mechanism still largely unknown2. Visual feedback probably has an important roleII. Multiple sclerosisa. Typical onset in early adulthoodb. Symptoms range broadly in effect and severity c. Physical  muscle spasms/weakness, tingles, pain, ataxia, sensory dysfunctiond. Fatigue, sluggish cognition, depression/mood swingse. Sclerosis refers to a hardening of body tissue as a result of scarringf. In MS, tissue damage occurs via demyelinationg. MS is known to be an autoimmune diseaseIII. Parkinsonsa. Primarily considered a movement disorderb. Some mental functions are also affectedc. Second most common neurodegenerative disorderd. Symptomsi. Tremorsii. Slowness, rigidity of movement iii. Difficulty initiating and changing physical/mental activitye. Death of dopamine releasing cells in the substantia nigraf. Basil ganglia modulates motor commandsi. Initiates new movements and stops ongoing movements via the thalamusii. 3 major divisions of the basal ganglia connect the thalamus and motor cortex (remember that basal ganglia relate to substantia nigra)g. Substantia nigra produces dopamineh. Chain reaction takes place for the basal ganglia to either start or stop a movementi. Start depends on dopamine input from substantia nigraii. Without an input of dopamine, the basal ganglia has an inhibitory hold on motor commandsiii. To start/stop a movement, this hold must be releasedi. Most treatments for parkinson’s attempt to replace the death of dopamine producing neurons of the substantia nigrai. L-DOPA  precursor to dopamineii. Deep brain stimulationIV. Huntington’s diseasea. Excessive involuntary movementb. Gradual and extensive damage to the basal gangliac. Inhibitory control over the thalamus by the basal ganglia slowly deteriorates causing randomly occurring, unwanted movementsd. Dominant genetic diseasei. C-A-G repeats code for a protein (Huntingtin) which has many neurotoxic effects ii. C-A-G repeats can predict likelihood of developing Huntington’siii. Can also predict when the disorder may begine. No curef. About a 20 year life expectancy after the onset of Huntington’s, but most of the later years are marked by cognitive decline V. Learning and memorya. Learning: process of acquiring new infob. Memory: ability to store and retrieve learned informationc. In ways, a “memory” is evidence that one has experienced somethingVI. HMa. Famous case of anterograde explicit amnesiab. Suffered from medicine intractable seizuresc. Bilateral temporal lobectomyd. Seizures dramatically reduced but got anterograde explicit amnesia e. Primacy: tendency to remember things first exposedf. Because HM could remember some things as they were presently happening, we say that his short-term memory was mostly intactg. Explicit (declarative): memory that we usually think of as memory, we can declare this kind of memory (e.g. I remember meeting you yesterday)Long term potentiation I. Parkinsonsa. Primarily considered a movement disorderb. Some mental functions are also affectedc. Second most common neurodegenerative disorderd. Symptomsi. Tremorsii. Slowness, rigidity of movement iii. Difficulty initiating and changing physical/mental activitye. Death of dopamine releasing cells in the substantia nigraf. Basil ganglia modulates motor commandsi. Initiates new movements and stops ongoing movements via the thalamusii. 3 major divisions of the basal ganglia connect the thalamus and motor cortex (remember that basal ganglia relate to substantia nigra)g. Substantia nigra produces dopamineh. Chain reaction takes place for the


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