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A model for the induction of long-term potentiation at Schaffer collateral synapses A. During normal, low-frequency synaptic transmission glutamate
released from the terminals of CA3 Schaffer collateral axons acts on both NMDA and AMPA receptors in the postsynaptic membrane of dendritic spines
(the site of excitatory input) of CA1 neurons. Sodium and K+ flow through the AMPA receptors but not through the NMDA receptors because their pore is
blocked by Mg2+ at negative membrane potentials.
B. During a high-frequency tetanus the large depolarization of the postsynaptic membrane (caused by strong activation of the AMPA receptors) relieves
2+, Na+, and K+ to flow through these channels. The resulting increase of Ca2+ in the dendritic spine
the Mg2+ blockade
of Prefrontal
the NMDACortex,
receptors,
allowing Caand
Source:
Hippocampus,
the Biology of Explicit Memory Storage, Principles of Neural Science, Fifth Editon
triggers calcium-dependent kinases—calcium/calmodulin–dependent kinase (CaMKII) and protein kinase C (PKC)—as well as the tyrosine kinase Fyn,
Citation: Kandel ER, Schwartz JH, Jessell TM, Siegelbaum SA, Hudspeth AJ, Mack S. Principles of Neural Science, Fifth Editon; 2012 Available
leading to induction of LTP.
at: http://mhmedical.com/ Accessed: May 11, 2017
C. Second-messenger
activated during
induction
of LTP
have two main effects on synaptic transmission. Phosphorylation through activation of
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protein kinases, including PKC, enhances current through the AMPA receptors, in part by causing insertion of new receptors into the spine synapses. In