Prenatal ethanol exposure decreases hippocampal 3H-vinylidene kainic acid binding in 45-day-old rats.

Abstract:

:The effect of prenatal ethanol exposure on the kainate-sensitive subtype of glutamate receptor binding sites was studied using in vitro 3H-vinylidene kainic acid (VKA) autoradiography. Pregnant Sprague-Dawley rats were fed a liquid diet containing either 3.35% or 6.7% ethanol throughout gestation. Pair-fed dams received isocalorically matched liquid diets and a lab chow ad lib group served as control for paired feeding. At 45 days of age, the offspring were sacrificed and their brains analyzed for specific 3H-VKA binding. Compared to pair-fed controls, specific 3H-VKA binding was reduced by 13% to 32% in dorsal and ventral hippocampal CA3 stratum lucidum, entorhinal cortex and cerebellum of 45-day-old rats whose mothers consumed either 3.35% or 6.7% ethanol diets. The binding site reductions were statistically significant only in the ventral hippocampal formation and entorhinal cortex of the 3.35% ethanol diet group rats. Saturation of binding studies in the ventral hippocampal formation of 3.35% ethanol rats indicated that the decrease in specific 3H-VKA binding was due to a decrease in the total number of binding sites. Given the excitatory effect of kainic acid on the spontaneous firing rate of hippocampal CA3 pyramidal neurons, the reduction of kainate-sensitive glutamate binding in this region is consistent with the electrophysiological observation of decreased spontaneous activity of CA3 pyramidal neurons in fetal alcohol rats.

journal_name

Neurotoxicol Teratol

authors

Farr KL,Montano CY,Paxton LL,Savage DD

doi

10.1016/0892-0362(88)90093-1

subject

Has Abstract

pub_date

1988-11-01 00:00:00

pages

563-8

issue

6

eissn

0892-0362

issn

1872-9738

pii

0892-0362(88)90093-1

journal_volume

10

pub_type

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