Premium
Requirement of rapid Ca 2+ entry and synaptic activation of metabotropic glutamate receptors for the induction of long‐term depression in adult rat hippocampus
Author(s) -
Otani Satoru,
Connor John A.
Publication year - 1998
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1111/j.1469-7793.1998.761bg.x
Subject(s) - metabotropic glutamate receptor , long term depression , postsynaptic potential , neuroscience , chemistry , schaffer collateral , metabotropic receptor , nmda receptor , excitatory postsynaptic potential , synaptic plasticity , glutamate receptor , stimulation , inhibitory postsynaptic potential , medicine , endocrinology , biology , receptor , biochemistry , ampa receptor
1 During block of γ‐aminobutyric acid‐A‐mediated inhibition, low‐frequency stimulation (2 Hz, 900 pulses) to Schaffer collateral‐CA1 neuron synapses of adult rat hippocampus induced an N ‐methyl‐D‐aspartate receptor‐independent, postsynaptic Ca 2+ ‐dependent depression of synaptic strength (long‐term depression; LTD). 2 Ratio imaging with fura‐2 revealed moderate dendritic [Ca 2+ ] increases (≈500 nM) during only the initial ≈30 s of the 7.5 min stimulation period. Conditioning for 30 s was, however, insufficient to induce LTD. 3 The [Ca 2+ ] changes were insensitive to the metabotropic glutamate receptor (mGluR) antagonist (+)‐α‐methyl‐4‐carboxyphenylglycine (MCPG). MCPG, however, completely blocked LTD when present during conditioning. 4 The [Ca 2+ ] changes were abolished by postsynaptic hyperpolarization (‐110 mV at the soma). Hyperpolarizing neurons to ‐110 mV during conditioning significantly attenuated LTD induction. 5 LTD induction was also blocked by the postsynaptic presence of the protein kinase C inhibitor peptide PKC(19‐36). 6 These results suggest that LTD induction in adult hippocampus by prolonged low‐frequency stimulation depends on both a rapid Ca 2+ influx through voltage‐sensitive channels and synaptic stimulation of mGluRs which may be coupled to phospholipase C.