Notes for Vertebrate Physiology Test 2

Notes for - Notes for Vertebrate Physiology Test 2 Postsynaptic potential depolarizing potential on the postsynaptic membrane Excitatory

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Notes for Vertebrate Physiology Test 2 Postsynaptic potential – depolarizing potential on the postsynaptic membrane Excitatory Postsynaptic Potential (EPSP) – Causes a postsynaptic potential to occur through depolarization or increase in Na channel conductance Temporal Summation – Addition or Subtraction of potentials during a short time period Spatial Summation – Addition or Subtraction of potentials from different areas Inhibitory Postsynaptic Potential (IPSP) – Causes a postsynaptic potential not to occur due to hyperpolarization or increase in K or Cl channel conductance. Integration – process by which IPSPs and EPSPs are combined to determine the potential Neuromuscular Junction (NMJ) – The area where motor neurons synapse with muscles to control movement - Katz Acetylcholine – Chemical Synaptic NT at the NMJ End-Plate Potential (EPP) – Depolarizing action potential found in the muscle Acetylcholinesterase – enzyme in the NMJ that breaks down ACH to acetate and choline Vagusstoff – Ach found in the heart that stimulates the Vagus nerve to slow down heart rate Criterion for identification of a substance as NT o Nerve stimulation must cause release of substance and release must come from nerve o Effects of nerve stimulation can be mimicked by manually adding NT (iontophoresis) o Responses to drugs must occur that can also bind to the receptor Ach Receptors o Nicotinic – Ionotropic
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Found in the NMJ in skeletal cells and in ganglionic cells Agonist – Nicotine Antagonist – Curare o Muscarinic (slows heart rate) Metabotropic Found in smooth muscle and cardiac muscle Agonist – Muscarine Antagonist – Atropine o Eserine is also an antagonist that is an antiacetylcholinesterase Pain is regulated by Substance P Parkinson’s is due to problems with Dopamine Huntington’s is due to problems with GABA Current flow (I during a post-synaptic potential) – I na = ΔG Na (V m -E Na ) Reversal Potential – Point at which K and Na conductance are equivalent o Ach release is attempting to get the muscle to this point o Occurs at -15 mV which is halfway between the Na conductance x Driving force (+50) and the K conductance x Driving force (-85) To determine which ions were involved in generation of EPPs, varying Na, K, and Cl were used. Cl amounts were the only one that didn’t change the reversal potential Ach works by simultaneously increasing the conductance of the postsynaptic membrane to Na and K Receptors are controlled by whether the Ach channels are bound or not, not due to voltage changes An ionic mechanism of inhibition occurs where conductance changes to K and Cl occurs, but not to Na Ach inhibition of the beat rate in the heart is due to K conductance changes
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Presynaptic inhibition can occur where less Calcium enters the presynaptic cell The location of the synapse on the nerve cell also has an effect
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This note was uploaded on 11/11/2010 for the course BIO 365R taught by Professor Draper during the Fall '08 term at University of Texas at Austin.

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Notes for - Notes for Vertebrate Physiology Test 2 Postsynaptic potential depolarizing potential on the postsynaptic membrane Excitatory

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