Journal article
Presynaptic factors in the regulation of DSI expression in hippocampus
Neuropharmacology, Vol.43(4), pp.550-562
2002
DOI: 10.1016/S0028-3908(02)00168-5
PMID: 12367601
Abstract
We studied the mechanisms by which GABA release is reduced in the retrograde signaling process called depolarization-induced suppression of inhibition (DSI). DSI is mediated by endocannabinoids in acute and cultured organotypic hippocampal slices. We examined a variety of K
+ channel antagonists to determine the nature of the K
+ channel that, when blocked, reduces DSI. Among 4-AP, TEA, dendrotoxin, Cs, margatoxin, and charybdotoxin, only 4-AP was highly effective in blocking DSI, suggesting that a K
+ channel composed in part of K
V1.4, K
V1.5 or K
V1.7 subunits can readily regulate DSI. The inhibition of DSI by 4-AP is largely overcome by reducing [Ca
2+]
o, however, suggesting that DSI expression can be prevented by saturation of the release process when a K
V1.X channel is inhibited. DSI of agatoxin- and TTX-insensitive mIPSCs was unaffected by 4-AP, but was largely occluded by ω-conotoxin GVIA, indicating that block of presynaptic N-type Ca
2+ channels is probably a major mechanism of DSI expression. Significant DSI of mIPSCs remained in ω-conotoxin, hence we infer that block of N-channels does not fully explain hippocampal DSI expression.
Details
- Title: Subtitle
- Presynaptic factors in the regulation of DSI expression in hippocampus
- Creators
- Namita Varma - University of Maryland School of Medicine, Department of Physiology, 655 W. Baltimore St., 21201 Baltimore, MD, USADarrin H Brager - University of Maryland School of Medicine, Department of Physiology, 655 W. Baltimore St., 21201 Baltimore, MD, USAWade Morishita - University of Maryland School of Medicine, Department of Physiology, 655 W. Baltimore St., 21201 Baltimore, MD, USARobert A Lenz - University of Maryland School of Medicine, Department of Physiology, 655 W. Baltimore St., 21201 Baltimore, MD, USABarry London - University of Pittsburgh Medical Center, Department of Cardiology, 15213 Pittsburgh, PA, USABradley Alger - University of Maryland School of Medicine, Department of Physiology, 655 W. Baltimore St., 21201 Baltimore, MD, USA
- Resource Type
- Journal article
- Publication Details
- Neuropharmacology, Vol.43(4), pp.550-562
- Publisher
- Elsevier Ltd
- DOI
- 10.1016/S0028-3908(02)00168-5
- PMID
- 12367601
- ISSN
- 0028-3908
- eISSN
- 1873-7064
- Language
- English
- Date published
- 2002
- Academic Unit
- Molecular Physiology and Biophysics; Cardiovascular Medicine; Internal Medicine
- Record Identifier
- 9984025318502771
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