9 - BIO 317: Lecture 9 Prof. William Collins Ofce: 534 Life...

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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
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Synaptic Plasticity
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Possible Mechanisms Facilitation Depression
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The rodent hippocampus
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Long-term potentiation of Schaffer collateral-CA1 synapses
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LTP of Schaffer collateral-CA1 synapses
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LTP of Schaffer collateral-CA1 synapses
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LTP of Schaffer collateral-CA1 synapses
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LTP at a CA1 pyramidal neuron receiving inputs from two independent pathways
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Pairing presynaptic and postsynaptic activity causes LTP
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LTP Requires Depolarization of Postsynaptic Neuron Synaptic strengthening occurs when neurotransmitter binds to depolarized post synaptic membrane.
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The NMDA receptor channel can open only during depolarization
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Signaling mechanisms underlying LTP
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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 10/05/2011 for the course BIO 317 taught by Professor Simonhalegoua during the Spring '08 term at SUNY Stony Brook.

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9 - BIO 317: Lecture 9 Prof. William Collins Ofce: 534 Life...

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