Prenatal exposure to ethanol decreases physiological plasticity in the hippocampus of the adult rat.
Prenatal exposure to ethanol has been associated with birth defects ranging in severity from physical dysmorphias and profound mental retardation to more subtle compromises of cognitive and behavioral function. Recent evidence has shown the hippocampus to be damaged both morphologically and neurochemically after such exposure in experimental animals. The functional implications of these changes have just recently begun to be addressed. We now report that long-term potentiation and potassium-induced excitability are decreased in hippocampal slices from adult animals exposed to ethanol in-utero. These deficits reflect a decrease in the plasticity of the hippocampal formation. This alteration may be one factor contributing to the memory and learning deficits associated with in-utero exposure to ethanol.
Swartzwelder
H S
HS
Department of Medicine, Duke University Medical Center, Durham, NC.
Farr
K L
KL
Wilson
W A
WA
Savage
D D
DD
D000818:Animals; D004305:Dose-Response Relationship, Drug; D000431:Ethanol / Q000008:administration & dosage / Q000097:blood / Q000494:pharmacology*; D005071:Evoked Potentials / Q000187:drug effects*; D005260:Female; D006624:Hippocampus / Q000187:drug effects* / Q000503:physiopathology; D009473:Neuronal Plasticity / Q000187:drug effects*; D011188:Potassium / Q000134:cerebrospinal fluid; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects; D051381:Rats; D011919:Rats, Inbred Strains
D000431:Ethanol; D011188:Potassium