TY - JOUR
T1 - State-dependent calcium signaling in dendritic spines of striatal medium spiny neurons
AU - Carter, Adam G.
AU - Sabatini, Bernardo L.
N1 - Funding Information:
We thank members of the Sabatini lab, N. Blair, and M. Xu-Freidman for comments on the manuscript. This work was supported by NIH T32 NS07484 (to A.G.C.) and Burroughs Wellcome Fund Career Award, McKnight Technological Innovations Grant, and NINDS (RO1 NS046579-01A) (to B.L.S.). The authors declare that they have no financial conflicts of interests.
PY - 2004/10/28
Y1 - 2004/10/28
N2 - Striatal medium spiny neurons (MSNs) in vivo undergo large membrane depolarizations known as state transitions. Calcium (Ca) entry into MSNs triggers diverse downstream cellular processes. However, little is known about Ca signals in MSN dendrites and spines and how state transitions influence these signals. Here, we develop a novel approach, combining 2-photon Ca imaging and 2-photon glutamate uncaging, to examine how voltage-sensitive Ca channels (VSCCs) and ionotropic glutamate receptors contribute to Ca signals in MSNs. We find that upstate transitions switch the VSCCs available in dendrites and spines, decreasing T-type while enhancing L-type channels. Moreover, these transitions change the dominant synaptic Ca source from Ca-permeable AMPA receptors to NMDA receptors. Finally, pairing bAPs with synaptic inputs generates additional synaptic Ca signals due to enhanced Ca influx through NMDA receptors. By altering the sources, amplitude, and kinetics of spine Ca signals, state transitions may gate synaptic plasticity and gene expression in MSNs.
AB - Striatal medium spiny neurons (MSNs) in vivo undergo large membrane depolarizations known as state transitions. Calcium (Ca) entry into MSNs triggers diverse downstream cellular processes. However, little is known about Ca signals in MSN dendrites and spines and how state transitions influence these signals. Here, we develop a novel approach, combining 2-photon Ca imaging and 2-photon glutamate uncaging, to examine how voltage-sensitive Ca channels (VSCCs) and ionotropic glutamate receptors contribute to Ca signals in MSNs. We find that upstate transitions switch the VSCCs available in dendrites and spines, decreasing T-type while enhancing L-type channels. Moreover, these transitions change the dominant synaptic Ca source from Ca-permeable AMPA receptors to NMDA receptors. Finally, pairing bAPs with synaptic inputs generates additional synaptic Ca signals due to enhanced Ca influx through NMDA receptors. By altering the sources, amplitude, and kinetics of spine Ca signals, state transitions may gate synaptic plasticity and gene expression in MSNs.
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U2 - 10.1016/j.neuron.2004.10.013
DO - 10.1016/j.neuron.2004.10.013
M3 - Article
C2 - 15504328
AN - SCOPUS:7044220658
SN - 0896-6273
VL - 44
SP - 483
EP - 493
JO - Neuron
JF - Neuron
IS - 3
ER -