The role of intracellular calcium stores in synaptic plasticity and memory consolidation

•Intracellular calcium stores regulate synaptic plasticity and signalling cascades underlying memory.•Ryanodine receptors promote the consolidation of labile memory into long-term memory.•IP3 receptors are required during long-term memory formation.•Altered calcium release from intracellular stores may produce memory deficits.

Memory processing requires tightly controlled signalling cascades, many of which are dependent upon intracellular calcium (Ca2+). Despite this, most work investigating calcium signalling in memory formation has focused on plasma membrane channels and extracellular sources of Ca2+. The intracellular Ca2+ release channels, ryanodine receptors (RyRs) and inositol (1,4,5)-trisphosphate receptors (IP3Rs) have a significant capacity to regulate intracellular Ca2+ signalling. Evidence at both cellular and behavioural levels implicates both RyRs and IP3Rs in synaptic plasticity and memory formation. Pharmacobehavioural 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 Ca2+ 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 Ca2+ release from intracellular stores also has significant implications for neurodegenerative conditions.