Long-term potentiation - Homo sapiens (human)

Hippocampal long-term potentiation (LTP), a long-lasting increase in synaptic efficacy, is the molecular basis for learning and memory. Tetanic stimulation of afferents in the CA1 region of the hippocampus induces glutamate release and activation of glutamate receptors in dendritic spines. A large increase in [Ca2+]i resulting from influx through NMDA receptors leads to constitutive activation of CaM kinase II (CaM KII) . Constitutively active CaM kinase II phosphorylates AMPA receptors, resulting in potentiation of the ionic conductance of AMPA receptors. Early-phase LTP (E-LTP) expression is due, in part, to this phosphorylation of the AMPA receptor. It is hypothesized that postsynaptic Ca2+ increases generated through NMDA receptors activate several signal transduction pathways including the Erk/MAP kinase and cAMP regulatory pathways. The convergence of these pathways at the level of the CREB/CRE transcriptional pathway may increase expression of a family of genes required for late-phase LTP (L-LTP).

Organismal Systems; Nervous system
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nt06460  Alzheimer disease
nt06461  Huntington disease
nt06462  Spinocerebellar ataxia
nt06464  Amyotrophic lateral sclerosis
nt06465  Prion disease
nt06466  Pathways of neurodegeneration
nt06528  Calcium signaling

Homo sapiens (human) [GN:hsa]

PMID:15652868

PMID:10652548

PMID:11378299

PMID:15803158

PMID:14715912

PMID:15857686

PMID:9697848