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PSYD35H3 (12)
Chapter 3

Chapter 3 notes- detailed (neuroanatomy).docx

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Department
Psychology
Course
PSYD35H3
Professor
Nussbaum D
Semester
Winter

Description
PSYD35- A Primer of Drug Action, 12 Edition CHAPTER 3—NEUROANATOMY & TRANSMISSION  90 billion neurons (10x glial cells)  Three primary divisions: hindbrain, midbrain, forebrain  Spinal cord: carry sensory info from body to brain  Organizes/modulates motor outflow to muscles  Modulate sensory input (pain)  Autonomic control of vital body function  Brain stem: medulla, pons midbrain (sleep/wake, bp, heart rate, breathing, intestinal functioning)  Barbiturates depress brain stem—giving hypnotic action  Cerebellum: movement ,posture, mood  Diencephalon (thalamus, hypothalamus, subthalamus, pituitary) Subthalamus: together with Substantia nigra, and basal ganglia constitute the motor system of extrapyramidal system Basal ganglia: caudate, putamen, goblus pallidus---PD patients have deficiency in DA which is located in SN and released onto BG Hypothalamus: ANS control, sleep, eat, drinking, hormones, water balance, emotion Limbic system: amygdala and hippocampus (reward, beh, emotion, memory) Dopamine rich reward centers: VTA, MFB, nucleus acumens located in hypothalamic/limbic areas NEURON  Axon varies in length from short as few mm to long as meter  Neurogenesis: new formation of neurons  Synaptic plasticity: reshaping and remodeling of neurons  Mitochondria are located in body, fibers, and terminals  Presynaptic terminal onsiste of vesicles that contain different NT (first messengers)  Exocytosis: influx in Ca ions cause vesicles to fuse with membrane and NT are released into left  Synaptic transmission: time span from release to receptor attachment and activation (on post) can be 1ms TERMINATION  Transmitter removal occurs 1 of 3 ways: Enzyme in cleft breaks down NT NT reuptake into presynaptic by transporter In GLU transmission, after release GLU taken up into adjacent glial cells reprocessed, and returned to presynaptic terminal  NT removed by reuptake: NE reuptake is blocked by tricyclic antidepressant and atomoxetine 5H reuptake blocked by SSRI Dopamine reuptake is blocked by bupropion (Wellbutrin) and cocaine Ach (process 1+2) enzyme Ache breaks down Ach into acetate and choline, then reuptaken  See Table on page 71 SOMA  Has nucleus that has DNA  DNA is expresses a subset of genes that encode structures, enzyme proteins that determine size, shape, location, and other characteristics  Mitochonria provide biological energy (ATP)  DNA in nucleus is transcribed into RNA (hnRNA) which is then edited and exported to the cytoplasm. The edited RNA is called messenger RNA and this is then translated into aa sequence of protein that’s to be expressed  Expression/translation occurs on endoplasmic reticulum where NA are synthesized and transported (in vesicles) in microtubules down axon Quaternary Amine NEUROTRANS  Ach: deficits associated with cognitive dysfunction seen in dementia (Alz)—decrease memory function  Synthesized one-set from two precursors (Choline and acetyl CoA) –action terminated by Ache  Drugs that inhibit ACHE (irreversible (never gas) and reversible (cognitive enhancers)  Process: Action potential arrives at terminalclosed Ca channels open and Ca rushes intriggers vesicles to fuse with membrane and release Ach molecules Attach to receptors on postsynaptictrigger opening on Na channelsAch is immediately broken down at receptor by Ache into choline and acetatereuptaken  Distributed widely in brain: cell bodies are in septal nuclie and nucei basalis (which project to 1) forebrain—hippocampus, cerebral cortex) and mid brain region projects to thalamus, basal ganglia medulla, pons, cerebellum) Catecholamine: DA and NE  Refers to compounds that contain a catechol nucleus and an amine group (DA,NE, and EN in the PNS)  Biosynthesis starts with amino acid tyrosine; following synthesis transmitter stored in vesicles and release controlled by presynaptic receptors (auto receptors) that act as negative feedback when large amount of NE are present in cleft, excess NT act on auto receptors to reduce further production and release (if auto receptor is blocked by antagonist—more NE is available in cleft) After release, NE and DA attach to post synaptic receptor, within the terminal, cat
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