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.