TY - JOUR
T1 - Modulation of presynaptic calcium transients by metabotropic glutamate receptor activation
T2 - A differential role in acute depression of synaptic transmission and long-term depression
AU - Faas, Guido C.
AU - Adwanikar, Hita
AU - Gereau IV, Robert W.
AU - Saggau, Peter
PY - 2002/8/15
Y1 - 2002/8/15
N2 - Activation of group I metabotropic glutamate receptors (mGluRs) can induce acute depression of excitatory synaptic transmission and long-term depression (LTD) in area CA1 of the rat hippocampus. The underlying mechanisms for both forms of depression are unknown. By measuring presynaptic calcium transients, we show that a reduction in the stimulation-induced presynaptic calcium rise that triggers vesicular release causes the acute depression of transmission by group I mGluRs. In contrast, the mechanism underlying mGluR-induced LTD does not involve a persistent change in stimulation-induced calcium influx. However, analysis of paired-pulse facilitation experiments suggests a presynaptic location for expression of this form of LTD. Furthermore, we show that mGluR-induced LTD can be completely blocked by a specific mGluR5 antagonist, whereas mGluR1 antagonists strongly attenuate the acute depression of transmission. These results support the hypothesis that the acute depression of transmission caused by activation of group I mGluRs involves regulation of stimulation-induced presynaptic calcium transients, whereas mGluR-induced LTD involves a distinct presynaptic modulation downstream of calcium influx.
AB - Activation of group I metabotropic glutamate receptors (mGluRs) can induce acute depression of excitatory synaptic transmission and long-term depression (LTD) in area CA1 of the rat hippocampus. The underlying mechanisms for both forms of depression are unknown. By measuring presynaptic calcium transients, we show that a reduction in the stimulation-induced presynaptic calcium rise that triggers vesicular release causes the acute depression of transmission by group I mGluRs. In contrast, the mechanism underlying mGluR-induced LTD does not involve a persistent change in stimulation-induced calcium influx. However, analysis of paired-pulse facilitation experiments suggests a presynaptic location for expression of this form of LTD. Furthermore, we show that mGluR-induced LTD can be completely blocked by a specific mGluR5 antagonist, whereas mGluR1 antagonists strongly attenuate the acute depression of transmission. These results support the hypothesis that the acute depression of transmission caused by activation of group I mGluRs involves regulation of stimulation-induced presynaptic calcium transients, whereas mGluR-induced LTD involves a distinct presynaptic modulation downstream of calcium influx.
KW - Calcium
KW - DHPG
KW - Hippocampus
KW - LTD
KW - Presynaptic
KW - mGluR
UR - http://www.scopus.com/inward/record.url?scp=0037104730&partnerID=8YFLogxK
U2 - 10.1523/jneurosci.22-16-06885.2002
DO - 10.1523/jneurosci.22-16-06885.2002
M3 - Article
C2 - 12177186
AN - SCOPUS:0037104730
SN - 0270-6474
VL - 22
SP - 6885
EP - 6890
JO - Journal of Neuroscience
JF - Journal of Neuroscience
IS - 16
ER -