Memory hippocampus anatomy
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The hippocampus is formed by 2 sheets of cells folded into interlocking Cs. Anatomy: The rat hippocampus is shown in a cut-away view.
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Longer-term LTP maintenance requires protein synthesis, but more specific mechanisms required for such prolonged synaptic change are not fully known. Metabolic poisons or molecular genetic manipulations that interfere with these different enzymes either reduce the duration of LTP or block LTP induction altogether. Calcium influx through the NMDA receptor initiates an enzyme phosphorylation cascade that includes the activation of Ca-calmodulin–dependent kinase II (CaMKII), protein kinases, and CREB (cyclic adenosine monophosphate–responsive element binding protein). This dual gating of the NMDA receptor provides a mechanistic explanation for many of the induction properties of long-term potentiation (LTP), including associativity and synaptic specificity.
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Simultaneous GLU binding to NMDA receptors and postsynaptic depolarization leads to calcium (Ca) influx. N-methyl D-aspartate (NMDA) receptors are colocalized in synapses that also contain non-NMDA (eg, AMPA ) glutamate (GLU) receptors. Axons from CA3 pyramidal neurons form glutamatergic synapses on CA1 neurons. At the top right, a single cornu ammonis 1 (CA1) pyramidal neuron and the hippocampal synapse are shown. The hippocampal slice, circled in the lower left figure, is expanded to show the trisynaptic circuit. A, The anatomy of the hippocampus, at increasing magnifications from left to right (adapted from Amaral and Witter 6).