CaM-kinases: Modulators of synaptic plasticity

Thomas R. Soderling

Research output: Contribution to journalReview articlepeer-review

204 Scopus citations


Calcium signaling is crucial for several aspects of plasticity at glutamatergic synapses, and studies over the past two to three years have identified key functions for Ca2+/calmodulin-dependent protein kinases II and IV (CaM-KII and CaM-KIV). Sustained activation of CaM-KII localized at the postsynaptic density results in phosphorylation of numerous synaptic substrates including ion channels, other signaling molecules and scaffolding proteins, to modulate synaptic transmission within minutes. More prolonged responses may be effected through enhanced dendritic protein synthesis of CaM-KII and regulation of nuclear gene transcription by CaM-KIV.

Original languageEnglish (US)
Pages (from-to)375-380
Number of pages6
JournalCurrent Opinion in Neurobiology
Issue number3
StatePublished - Jun 1 2000
Externally publishedYes

ASJC Scopus subject areas

  • Neuroscience(all)


Dive into the research topics of 'CaM-kinases: Modulators of synaptic plasticity'. Together they form a unique fingerprint.

Cite this