TY - JOUR
T1 - Modulation of transmitter release by presynaptic resting potential and background calcium levels
AU - Awatramani, Gautam B.
AU - Price, Gareth D.
AU - Trussell, Laurence O.
N1 - Funding Information:
We thank Drs. K. Delaney, C. Jahr, and V. Shahrezaei for comments on the manuscript. This work was supported by NIH grant DC04450.
PY - 2005/10/6
Y1 - 2005/10/6
N2 - Activation of presynaptic ion channels alters the membrane potential of nerve terminals, leading to changes in transmitter release. To study the relationship between resting potential and exocytosis, we combined pre- and postsynaptic electrophysiological recordings with presynaptic Ca2+ measurements at the calyx of Held. Depolarization of the membrane potential to between -60 mV and -65 mV elicited P/Q-type Ca2+ currents of < 1 pA and increased intraterminal Ca2+ by < 100 nM. These small Ca2+ elevations were sufficient to enhance the probability of transmitter release up to 2-fold, with no effect on the readily releasable pool of vesicles. Moreover, the effects of mild depolarization on release had slow kinetics and were abolished by 1 mM intraterminal EGTA, suggesting that Ca 2+ acted through a high-affinity binding site. Together, these studies suggest that control of resting potential is a powerful means for regulating synaptic function at mammalian synapses.
AB - Activation of presynaptic ion channels alters the membrane potential of nerve terminals, leading to changes in transmitter release. To study the relationship between resting potential and exocytosis, we combined pre- and postsynaptic electrophysiological recordings with presynaptic Ca2+ measurements at the calyx of Held. Depolarization of the membrane potential to between -60 mV and -65 mV elicited P/Q-type Ca2+ currents of < 1 pA and increased intraterminal Ca2+ by < 100 nM. These small Ca2+ elevations were sufficient to enhance the probability of transmitter release up to 2-fold, with no effect on the readily releasable pool of vesicles. Moreover, the effects of mild depolarization on release had slow kinetics and were abolished by 1 mM intraterminal EGTA, suggesting that Ca 2+ acted through a high-affinity binding site. Together, these studies suggest that control of resting potential is a powerful means for regulating synaptic function at mammalian synapses.
UR - http://www.scopus.com/inward/record.url?scp=25644432154&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=25644432154&partnerID=8YFLogxK
U2 - 10.1016/j.neuron.2005.08.038
DO - 10.1016/j.neuron.2005.08.038
M3 - Article
C2 - 16202712
AN - SCOPUS:25644432154
SN - 0896-6273
VL - 48
SP - 109
EP - 121
JO - Neuron
JF - Neuron
IS - 1
ER -