Alcohol interactions with channel activation and desensitization at 5-HT[sub 3] and GABA[sub A] receptors
- Vanderbuilt Medical School, Nashville, TN (United States)
Ethanol (EtOH) and trichloroethanol (TCEt) potentiate 5-HT[sub 3] receptor-mediated ion current in NCB-20 neuroblastoma cells and nodose ganglion neurons. TCEt potentiates GABA[sub A] receptor-mediated current in dorsal root ganglion neurons. Whole-cell patch-clamp recording was used to examine the interactions of alcohols with current activation and receptor desensitization. Alcohols increased the potency of 5-HT, consistent with an increase in channel activation rate. Current decay rate increased in the presence of alcohols such that potentiation decreased with time following in onset of agonist + alcohol treatment. Potentiation of 5-HT-activated current by EtOH was 61 [plus minus] 17% above control at the start of application but was absent 10 sec after current onset. Agonist pretreatment decreased potentiation by subsequent agonist + alcohol application. Potentiation by TCEt of 5-HT-activated current decreased from 96% above control with simultaneous application of 5-HT + TCEt to 44% after a 30 sec 5-HT treatment. This agonist- and time-dependent loss of potentiation was observed prior to the onset of current decay when low agonist concentrations were used. Agonist pretreatment appears to drive the channel into an alcohol-insensitive. Current activated by GABA + TCEt recovers from desensitization produced by GABA alone more slowly than recovery tested in the absence of TCEt.
- OSTI ID:
- 7159847
- Report Number(s):
- CONF-9202109-; CODEN: FAJOEC
- Journal Information:
- FASEB Journal (Federation of American Societies for Experimental Biology); (United States), Vol. 6:1; Conference: American Society for Biochemistry and Molecular Biology and Biophysical Society joint meeting, Houston, TX (United States), 9-13 Feb 1992; ISSN 0892-6638
- Country of Publication:
- United States
- Language:
- English
Similar Records
Low doses of alcohol potentiate GABA sub B inhibition of spontaneous activity of hippocampal CA1 neurons in vivo
el-aminobutyric acid (GABA) mediated transmembrane chloride flux with membrane vesicles from rat brain measured by quench flow technique: kinetic homogeneity of ion flux and receptor desensitization
Related Subjects
AMINOBUTYRIC ACID
RECEPTORS
ETHANOL
BIOLOGICAL EFFECTS
SEROTONIN
BIOCHEMICAL REACTION KINETICS
NERVE CELLS
TIME DEPENDENCE
TUMOR CELLS
ALCOHOLS
AMINES
AMINO ACIDS
ANIMAL CELLS
AROMATICS
AUTONOMIC NERVOUS SYSTEM AGENTS
AZAARENES
AZOLES
CARBOXYLIC ACIDS
DRUGS
HETEROCYCLIC COMPOUNDS
HYDROXY COMPOUNDS
INDOLES
KINETICS
MEMBRANE PROTEINS
NEUROREGULATORS
ORGANIC ACIDS
ORGANIC COMPOUNDS
ORGANIC NITROGEN COMPOUNDS
PROTEINS
PYRROLES
RADIOPROTECTIVE SUBSTANCES
REACTION KINETICS
SOMATIC CELLS
SYMPATHOMIMETICS
TRYPTAMINES
560300* - Chemicals Metabolism & Toxicology