Epidemiologic trends in drug abuse : proceedings /

Latest issue consulted: Jan. 2005Some v. distributed to depository libraries in microficheIssues for published in 2 vols: V.1, Highlights and executive summary; and V.2, Proceedings (titles vary)Mode of access: Internet.Issued by: National Institute on Drug Abuse, Division of Epidemiology and Prevention Research, 1989-19 ; by: National Institute on Drug Abuse, Division of Epidemiology, Services and Prevention Research, Issues also available in American Statistics Index (ASI) Microfiche Collectio

Ethanol exposure during the third trimester equivalent results in long-lasting decreased synaptic efficacy but not plasticity in the CA1 region of the rat hippocampus

Fetal alcohol syndrome is a major cause of mental retardation. We investigated possible long-lasting effects of alcohol on the hippocampus using a model for human third trimester brain development. Treatment of neonatal rats with an ethanol vapor atmosphere of 39.4 +/- 2.6 mg ethanol/liter of air for 3 h a day from postnatal day 4 through 9 produced daily blood ethanol levels of 351 +/- 14 mg/dL. Separation control animals were removed from their mothers in parallel with the ethanol vapor treatment, while suckle controls were left to develop normally. We prepared hippocampal slices from these animals between postnatal days 45 and 60 and recorded extracellular responses to Schaffer collateral stimulation. The maximum population spike in the CA1 pyramidal region and population excitatory postsynaptic potentials in the stratum radiatum did not differ significantly between groups. However, slices prepared from ethanol-treated rats as opposed to separation and suckle controls required larger stimulus currents to produce normal postsynaptic responses. In addition, the ratio of the population excitatory postsynaptic potential (pEPSP) slope to the presynaptic volley was significantly reduced in ethanol-treated rats. Ethanol vapor-treated rats and separation control rats did not exhibit any significant changes in long-term potentiation or paired-pulse potentiation compared with normal suckle controls. These results suggest that early postnatal ethanol treatment produces a long-lasting reduction in synaptic efficacy but not plasticity. Synapse 31:51-58, 1999. (C) 1999 Wiley-Liss, Inc