Neurosteroid modulation of glutamate release in hippocampal neurons: Lack of an effect of a chronic prenatal ethanol exposure paradigm
Alcoholism: Clinical & Experimental Research. 2003-07-01; 27(7): 1194-1198
DOI: 10.1097/01.ALC.0000075828.50697.70
Lire sur PubMed
1. Alcohol Clin Exp Res. 2003 Jul;27(7):1194-8.
Neurosteroid modulation of glutamate release in hippocampal neurons: lack of an
effect of a chronic prenatal ethanol exposure paradigm.
Carta M(1), Partridge LD, Savage DD, Valenzuela CF.
Author information:
(1)Department of Neurosciences, University of New Mexico Health Sciences Center,
Albuquerque, USA.
BACKGROUND: Pregnenolone sulfate (PREGS) is a promnesic neurosteroid that is
abundantly expressed in the hippocampus of rodents. Studies have shown that the
modulation of postsynaptic ligand-gated ion channels by this neurosteroid is
impaired in preparations from the brains of fetal ethanol-exposed animals. In
this study, we examined whether the presynaptic actions of PREGS also are
affected by exposure to ethanol in utero.
METHODS: Rat dams were exposed to one of the following diets during pregnancy:
(1) 5% ethanol liquid diet, (2) 0% ethanol liquid diet with pair-feeding, and (3)
ad libitum controls. We then studied the presynaptic actions of PREGS on (1)
alpha-amino-3-hydroxy-5-methylisoxazole-4-propionate (AMPA) receptor-mediated
miniature excitatory postsynaptic currents (mEPSCs) recorded from cultured
hippocampal neurons in the whole-cell patch-clamp configuration and (2)
paired-pulse facilitation of NMDA receptor-dependent excitatory postsynaptic
potentials that were intracellularly recorded from CA1 pyramidal neurons in
hippocampal slices from adult rats.
RESULTS: Chronic prenatal ethanol exposure affected neither basal mEPSC frequency
nor its potentiation by PREGS. Basal paired-pulse facilitation (i.e., in the
absence of PREGS) was unaffected by fetal ethanol exposure. Chronic prenatal
ethanol exposure did not affect the PREGS-induced potentiation of paired-pulse
facilitation.
CONCLUSIONS: Chronic prenatal ethanol exposure does not affect the basal
probability of glutamate release in immature or mature hippocampal neurons.
Moreover, the presynaptic actions of the neurosteroid PREGS also are unaffected
by this exposure. Given that modulation of glutamate release could have a role in
the mechanism of the promnesic actions of this neurosteroid, future studies are
warranted to determine whether PREGS can ameliorate learning and memory deficits
in fetal ethanol-exposed animals.
DOI: 10.1097/01.ALC.0000075828.50697.70
PMID: 12878928 [Indexed for MEDLINE]