Neuroscience Textbook Ch3 PDF

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txtbook summary ch 3 -- professor: Gerald Voebel ...

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Neuroscience Textbook Ch. 3 EPSP: Na/Ca influx IPSP: local hyperpolarization Cl influx/K efflux EPSP and IPSP can sum Presynaptic facilitation:  DEPOLARIZAES second neuron  Ca influx into second neuron  Action potential duration increases Presynaptic inhibition: think of a beach to block out painful thoughts of cold  HYPERPOLARIZES second neuron  Action potential duration decreases  Ca influx reduced Neuromodulators- released into ECF Neurotransmitters – released into synaptic cleft  Iontropic  Metabotropic (2nd messenger g-proteim) Slow acting neurotransmitters regulate fast transmission by controlling the amount of neuro released Ach = PNS Glutamate: neuronal cell death Glycine: inhibits postsynapse in spinal/brainstem GABA: inhibits CNS at interneurons in spinal Glycine + GABA: prevent neuronal overactivity (prevent seizures and dystonia) Dopamine – produced in the substanita nigra  Motor activity, cognition, addiction/reward motivation  Coke and amphetamine – prevent dopamine reuptake to prolong dopamine activity in the synapse Norepi  Increases attention to sensory  PNS- adrenal gland  CNS- brain stem, hypothalamus and thalamus  Overactivity/high NE levels = fear and PTSD hallucinations Serotonin  Affects mood, pain perception, arousal

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High = alert Low = depression Prozac (flouoxetine) blocks serotonin reuptake

Histamine  Hypothalamus  Hormonal function and increased arousal Substance P peptide  Stimulated nerve endings at injury site  CNS – carries info from spinal to brain Galaline  Inhibits insulin  Controls food intake Opioids  Inhibit CNS neurons responsible for pain  Spinal cord, hypothalamus, gray matter Calcitonin gene-related peptide  Phosphorylates Ach to decrease the likelihood Ach will bind to receptor Nitric Oxide  Regulates vascular system  Diffused through cell membrane to reach receptor  LTP 1st messenger: neurotransmitter 2nd messenger: G-protein 3rd messenger: Ca G-Protein- amplifys signals with cascade  Activate genes that make various transmitters  Open ion channels  Modualate Ca o Internal stores of Ca open G-Protein Second Messenger – Metatropic 1. Receptor changes shape when transmitter binds 2. Activtes G-protein 3. Gprotein subunits (a,b,y) break free and bind to membrane ion channels 4. Ionchannel changes shape and opens 5. Subunits deactivate RTK

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Adds phosphates to tyrosine then phosphorylates molecules to initate signal cascade Dysfunction: MS and schizo

Ach Receptors  Nicotinic o Ionotropic  Na/Ca in to depolarize o Alzheimers – Nicotinic receptors lost  Fix: increase Ach  Muscarinic o G-protein receptors o Smooth muscle Glutamate Receptors  AMPA o Fast depolarization of postsynaptic  NMDA – voltage and ligand gated o Glutamate must be bound to receptor AND membrane depolarize SIMULTANEOUSLY o Produce LTP o High glutamate = neuronal death o Overactivity of NMDA receptors = epilepsy GABA Receptors  GABAa o Opens Cl channels to hyperpolarize o Decreases anxiety  GABAb o Slow acting- G protein receptor Dopamine Receptor – Metatropic  Stops activity of Ca channel  L-DOPA precursor to dopamine  Alters movement, motivation and thinking Norepi Receptor  Alpha in gut – relaxation  Beta in the heart- contraction Serotonin  Low levels- depression  Fluoxetine blocks serotonin reuptake so serotonin stays in receptors for longer  Ligand Na/K channels Agonist- binds to receptor and mimics transmitter effects Antagonist- binds to receptor to prevent release of transmitter

Myasthenia Gravis  Autoimmune attacks nicotinic receptors on muscle cells  Normal Ach amounts but no receptors to receive them  Muscle use leads to weakness  Eyelids droop]  Fix: decrease Ach...