Elsevier, Neuroscience & Biobehavioral Reviews, 7(37), p. 1211-1239, 2013
DOI: 10.1016/j.neubiorev.2013.04.011
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Memory processing requires tightly controlled signalling cascades, many of which are dependent upon intracellular calcium. Despite this, most work investigating calcium (Ca(2+)) signalling in memory formation has focused on plasma membrane channels and extracellular sources of Ca(2+). The intracellular Ca(2+) release channels, ryanodine receptors (RyRs) and inositol (1,4,5)-trisphosphate receptors (IP3Rs) have a significant capacity to regulate intracellular Ca(2+) signalling. Evidence at both cellular and behavioral levels implicates both RyRs and IP3Rs in synaptic plasticity and memory formation. Pharmacobehavioral experiments using young chicks trained on a single-trial discrimination avoidance task have been particularly useful by demonstrating that RyRs and IP3Rs have distinct roles in memory formation. RyR-dependent Ca(2+) release appears to aid the consolidation of labile memory into a persistent long-term memory trace. In contrast, IP3Rs are required during long-term memory. This review discusses various functions for RyRs and IP3Rs in memory processing, including neuro- and glio-transmitter release, dendritic spine remodelling, facilitating vasodilation, and the regulation of gene transcription and dendritic excitability. Altered Ca(2+) release from intracellular stores also has significant implications for neurodegenerative conditions.