Abstract
Depolarization-induced suppression of inhibition (DSI) is a transient reduction of GABA(A) receptor-mediated IPSCs that is mediated by a retrograde signal from principal cells to interneurons. Using whole-cell recordings, we tested the hypothesis that mGluRs are involved in the DSI process in hippocampal CA1, as has been proposed for cerebellar DSI. Group II mGluR agonists failed to affect either evoked monosynaptic IPSCs or DSI, and forskolin, which blocks cerebellar DSI, did not affect CA1 DSI. Group I and group III mGluR agonists reduced IPSCs, but only group I agonists occluded DSI. (S)-MCPG blocked (1S,3R)-ACPD-induced IPSC suppression and markedly reduced DSI, whereas group III antagonists had no effect on DSI. Many other similarities between DSI and the (1S,3R)-ACPD-induced suppression of IPSCs also were found. Our data suggest that a glutamate-like substance released from pyramidal cells could mediate CA1 DSI by reducing GABA release from interneurons via the activation of group I mGluRs.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 4870-4882 |
| Number of pages | 13 |
| Journal | Journal of Neuroscience |
| Volume | 18 |
| Issue number | 13 |
| State | Published - Jul 1 1998 |
| Externally published | Yes |
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Keywords
- GABA
- IPSP
- MGluR
- Retrograde signal
- Synaptic inhibition
- Voltage clamp
ASJC Scopus subject areas
- Neuroscience(all)
Cite this
Evidence for metabotropic glutamate receptor activation in the induction of depolarization-induced suppression of inhibition in hippocampal CA1. / Morishita, Wade; Kirov, Sergei A; Alger, Bradley E.
In: Journal of Neuroscience, Vol. 18, No. 13, 01.07.1998, p. 4870-4882.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Evidence for metabotropic glutamate receptor activation in the induction of depolarization-induced suppression of inhibition in hippocampal CA1
AU - Morishita, Wade
AU - Kirov, Sergei A
AU - Alger, Bradley E.
PY - 1998/7/1
Y1 - 1998/7/1
N2 - Depolarization-induced suppression of inhibition (DSI) is a transient reduction of GABA(A) receptor-mediated IPSCs that is mediated by a retrograde signal from principal cells to interneurons. Using whole-cell recordings, we tested the hypothesis that mGluRs are involved in the DSI process in hippocampal CA1, as has been proposed for cerebellar DSI. Group II mGluR agonists failed to affect either evoked monosynaptic IPSCs or DSI, and forskolin, which blocks cerebellar DSI, did not affect CA1 DSI. Group I and group III mGluR agonists reduced IPSCs, but only group I agonists occluded DSI. (S)-MCPG blocked (1S,3R)-ACPD-induced IPSC suppression and markedly reduced DSI, whereas group III antagonists had no effect on DSI. Many other similarities between DSI and the (1S,3R)-ACPD-induced suppression of IPSCs also were found. Our data suggest that a glutamate-like substance released from pyramidal cells could mediate CA1 DSI by reducing GABA release from interneurons via the activation of group I mGluRs.
AB - Depolarization-induced suppression of inhibition (DSI) is a transient reduction of GABA(A) receptor-mediated IPSCs that is mediated by a retrograde signal from principal cells to interneurons. Using whole-cell recordings, we tested the hypothesis that mGluRs are involved in the DSI process in hippocampal CA1, as has been proposed for cerebellar DSI. Group II mGluR agonists failed to affect either evoked monosynaptic IPSCs or DSI, and forskolin, which blocks cerebellar DSI, did not affect CA1 DSI. Group I and group III mGluR agonists reduced IPSCs, but only group I agonists occluded DSI. (S)-MCPG blocked (1S,3R)-ACPD-induced IPSC suppression and markedly reduced DSI, whereas group III antagonists had no effect on DSI. Many other similarities between DSI and the (1S,3R)-ACPD-induced suppression of IPSCs also were found. Our data suggest that a glutamate-like substance released from pyramidal cells could mediate CA1 DSI by reducing GABA release from interneurons via the activation of group I mGluRs.
KW - GABA
KW - IPSP
KW - MGluR
KW - Retrograde signal
KW - Synaptic inhibition
KW - Voltage clamp
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UR - http://www.scopus.com/inward/citedby.url?scp=0032125264&partnerID=8YFLogxK
M3 - Article
C2 - 9634553
AN - SCOPUS:0032125264
VL - 18
SP - 4870
EP - 4882
JO - Journal of Neuroscience
JF - Journal of Neuroscience
SN - 0270-6474
IS - 13
ER -