Suppression of evoked IPSPs by arachidonic acid and prostaglandin F2α

James Owens; Philip A Schwartzkroin

doi:10.1016/0006-8993(95)00405-F

Suppression of evoked IPSPs by arachidonic acid and prostaglandin F_2α

James Owens, Philip A Schwartzkroin

Research output: Contribution to journal › Article › peer-review

1 Scopus citations

Abstract

Arachidonic acid (AA) and certain prostagladins appear to antagonize GABA_A receptors in synaptoneurosomes [18]. We report here that perfusing hippocampal slices with AA or prstaglandin F_2α diminishes evoked IPSP conductance and increases CA1 pyramidal cell input resistance. The effects of the two compounds were similar, though not identical, in time course, magnitude, and response to washout. These findings suggest that high levels of AA and its metabolites may bias neurons towards excitation.

Original language	English (US)
Pages (from-to)	223-228
Number of pages	6
Journal	Brain Research
Volume	691
Issue number	1-2
DOIs	https://doi.org/10.1016/0006-8993(95)00405-F
State	Published - Sep 11 1995
Externally published	Yes

Keywords

CA1
Eicosanoid
Epilepsy
Excitotoxicity
Hippocampus
Input resistance

ASJC Scopus subject areas

Developmental Biology
Molecular Biology
Clinical Neurology
Neuroscience(all)

Access to Document

10.1016/0006-8993(95)00405-F

Cite this

@article{887086a5651144efaa1c3c5fe3f73c4d,

title = "Suppression of evoked IPSPs by arachidonic acid and prostaglandin F2α",

abstract = "Arachidonic acid (AA) and certain prostagladins appear to antagonize GABAA receptors in synaptoneurosomes [18]. We report here that perfusing hippocampal slices with AA or prstaglandin F2α diminishes evoked IPSP conductance and increases CA1 pyramidal cell input resistance. The effects of the two compounds were similar, though not identical, in time course, magnitude, and response to washout. These findings suggest that high levels of AA and its metabolites may bias neurons towards excitation.",

keywords = "CA1, Eicosanoid, Epilepsy, Excitotoxicity, Hippocampus, Input resistance",

author = "James Owens and Schwartzkroin, {Philip A}",

year = "1995",

month = sep,

day = "11",

doi = "10.1016/0006-8993(95)00405-F",

language = "English (US)",

volume = "691",

pages = "223--228",

journal = "Brain Research",

issn = "0006-8993",

publisher = "Elsevier",

number = "1-2",

}

TY - JOUR

T1 - Suppression of evoked IPSPs by arachidonic acid and prostaglandin F2α

AU - Owens, James

AU - Schwartzkroin, Philip A

PY - 1995/9/11

Y1 - 1995/9/11

N2 - Arachidonic acid (AA) and certain prostagladins appear to antagonize GABAA receptors in synaptoneurosomes [18]. We report here that perfusing hippocampal slices with AA or prstaglandin F2α diminishes evoked IPSP conductance and increases CA1 pyramidal cell input resistance. The effects of the two compounds were similar, though not identical, in time course, magnitude, and response to washout. These findings suggest that high levels of AA and its metabolites may bias neurons towards excitation.

AB - Arachidonic acid (AA) and certain prostagladins appear to antagonize GABAA receptors in synaptoneurosomes [18]. We report here that perfusing hippocampal slices with AA or prstaglandin F2α diminishes evoked IPSP conductance and increases CA1 pyramidal cell input resistance. The effects of the two compounds were similar, though not identical, in time course, magnitude, and response to washout. These findings suggest that high levels of AA and its metabolites may bias neurons towards excitation.

KW - CA1

KW - Eicosanoid

KW - Epilepsy

KW - Excitotoxicity

KW - Hippocampus

KW - Input resistance

UR - http://www.scopus.com/inward/record.url?scp=0029163148&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0029163148&partnerID=8YFLogxK

U2 - 10.1016/0006-8993(95)00405-F

DO - 10.1016/0006-8993(95)00405-F

M3 - Article

C2 - 8590057

AN - SCOPUS:0029163148

VL - 691

SP - 223

EP - 228

JO - Brain Research

JF - Brain Research

SN - 0006-8993

IS - 1-2

ER -