Lecture 9 (317.11)

Lecture 9 (317.11) - BIO 317 Lecture 9 Prof William Collins...

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1 Prof. William Collins OfFce: 534 Life Sciences Building OfFce Hours: Mondays, 4:00-5:00 PM or by appointment Recommended Reading: Matthews – Chapter 9 Handout#2 - Autoantibodies to Ion Channels BIO 317: Lecture 9 Synaptic Plasticity
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2 Possible Mechanisms Facilitation Depression The rodent hippocampus
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3 Long-term potentiation of Schaffer collateral-CA1 synapses LTP of Schaffer collateral-CA1 synapses
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4 LTP of Schaffer collateral-CA1 synapses LTP of Schaffer collateral-CA1 synapses
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5 LTP at a CA1 pyramidal neuron receiving inputs from two independent pathways Pairing presynaptic and postsynaptic activity causes LTP
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6 LTP Requires Depolarization of Postsynaptic Neuron Synaptic strengthening occurs when neurotransmitter binds to depolarized post synaptic membrane. The NMDA receptor channel can open only during depolarization
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7 Signaling mechanisms underlying LTP Autoimmune Diseases of the Neuromuscular Junction Myasthenia Gravis – Activity-dependent skeletal muscle weakness – Caused by antibodies directed against nAChR Arthrogryposis Multiplex Congenita – Fetal muscle paralysis deformities – Caused by maternal antibodies that block nAChR function Lambert-Eaton Myasthenic Syndrome – Skeletal muscle weakness – Caused by antibodies directed against presynaptic voltage-dependent Ca ++ channels
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This note was uploaded on 12/06/2011 for the course BIO 317 taught by Professor Simonhalegoua during the Fall '08 term at SUNY Stony Brook.

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Lecture 9 (317.11) - BIO 317 Lecture 9 Prof William Collins...

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