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 investiga ted possible long-lasting effects of alcohol on the hippocampus using a mod el 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 fo r 3 h a day from postnatal day 4 through 9 produced daily blood ethanol lev els of 351 +/- 14 mg/dL. Separation control animals were removed from their mothers in parallel with the ethanol vapor treatment, while suckle control s were left to develop normally. We prepared hippocampal slices from these animals between postnatal days 45 and 60 and recorded extracellular respons es to Schaffer collateral stimulation. The maximum population spike in the CA1 pyramidal region and population excitatory postsynaptic potentials in t he stratum radiatum did not differ significantly between groups. However, s lices prepared from ethanol-treated rats as opposed to separation and suckl e controls required larger stimulus currents to produce normal postsynaptic responses. In addition, the ratio of the population excitatory postsynapti c potential (pEPSP) slope to the presynaptic volley was significantly reduc ed in ethanol-treated rats. Ethanol vapor-treated rats and separation contr ol rats did not exhibit any significant changes in long-term potentiation o r paired-pulse potentiation compared with normal suckle controls. These res ults 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.