Ca2+ signaling in dendritic spines

Recent studies have revealed that Ca2+ signals evoked by action potentials or by synaptic activity within individual dendritic spines are regulated at multiple levels. Ca2+ influx through glutamate receptors and voltage-sensitive Ca2+ channels located on spines depends on the channel subunit composition, the activity of kinases and phosphatases, the local membrane potential and past patterns of activity. Furthermore, sources of spine Ca2+ interact nonlinearly such that activation of one Ca2+ channel can enhance or depress the activity of others. These studies have revealed that each spine is a complex and partitioned Ca2+ signaling domain capable of autonomously regulating the electrical and biochemical consequences of synaptic activity.