Journal
NEUROSCIENCE
Volume 136, Issue 1, Pages 269-279Publisher
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.neuroscience.2005.07.015
Keywords
ethanol; ifenprodil; synapses; memory; plasticity; neurodevelopment
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Funding
- NIAAA NIH HHS [AA12951] Funding Source: Medline
- NIA NIH HHS [AG18434] Funding Source: Medline
- NIMH NIH HHS [MH45493] Funding Source: Medline
- NATIONAL INSTITUTE OF MENTAL HEALTH [R29MH045493, R01MH045493] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE ON AGING [R01AG018434] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE ON ALCOHOL ABUSE AND ALCOHOLISM [R01AA012951] Funding Source: NIH RePORTER
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To determine factors that contribute to the learning deficits observed in individuals with fetal alcohol syndrome, we examined the effects of early postnatal ethanol exposure on forms of synaptic plasticity thought to underlie memory. Treatment of rat pups with ethanol on postnatal day 7 impaired the induction of N-methyl-D-aspartate receptor-dependent long-term potentiation and abolished homosynaptic long-term depression in the CA1 region of hippocampal slices prepared at postnatal day 30. An N-methyl-(D)-aspartate receptor-independent form of long-term potentiation induced by very high frequency stimulation could be induced in slices from ethanol-treated rats. Defects in long-term depression correlated with a diminished contribution of ifenprodil-sensitive N-methyl-D-aspartate receptors to synaptic transmission and defects in a spontaneous alternation behavioral task. Rats exposed to ethanol on postnatal day 7 also exhibited diminished sensitivity of synaptic N-methyl-D-aspartate receptors to block by ethanol at postnatal day 30 and decreased behavioral sedation to systemic ethanol injections. These results indicate that changes in synaptic plasticity and N-methyl-D-aspartate receptor function are likely to provide a neural substrate for the cognitive and behavioral changes that follow developmental ethanol exposure. (c) 2005 Published by Elsevier Ltd on behalf of IBRO.
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