Ca(2+) signaling in dendritic spines.
Recent studies have revealed that Ca(2+) signals evoked by action potentials or by synaptic activity within individual dendritic spines are regulated at multiple levels. Ca(2+) influx through glutamate receptors and voltage-sensitive Ca(2+) 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 Ca(2+) interact nonlinearly such that activation of one Ca(2+) channel can enhance or depress the activity of others. These studies have revealed that each spine is a complex and partitioned Ca(2+) signaling domain capable of autonomously regulating the electrical and biochemical consequences of synaptic activity.
Bloodgood
Brenda L
BL
Department of Neurobiology, Harvard Medical School, 220 Longwood Avenue, Boston, MA 02115, USA.
Sabatini
Bernardo L
BL
D000818:Animals; D002118:Calcium / Q000378:metabolism; D015220:Calcium Channels / Q000502:physiology; D020013:Calcium Signaling / Q000502:physiology*; D049229:Dendritic Spines / Q000502:physiology*; D008954:Models, Biological; D009474:Neurons / Q000166:cytology; D017470:Receptors, Glutamate / Q000378:metabolism
D015220:Calcium Channels; D017470:Receptors, Glutamate; D002118:Calcium