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

Abstract

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.

Effects of Ethanol Exposure during Distinct Periods of Brain Development on Hippocampal Synaptic Plasticity

“…These results, in combination with the results from the present study, indicate that alcohol exposure during the second trimester does not reduce LTP in either the DG or CA1 sub-regions of the hippocampus. These results are also in line with previous studies that have shown that ethanol exposure during the 3rd trimester equivalent does not affect synaptic plasticity in the CA1 [42,43] and that ethanol exposure only during the 1st, 2nd, or 3rd trimester equivalent does not result in deficits in spatial navigation [42,44]. Overall, these results indicate that ethanol exposure during a limited period of brain development is not enough to robustly alter hippocampal synaptic plasticity (and possibly hippocampal-sensitive behaviours; [42,44]) when animals reach early adulthood.…”

Long‐lasting synaptic modification in the rat hippocampus resulting from NMDA receptor blockade during development

“…The results of this study are similar to those in our previously published study on the effects of neonatal ethanol administration (Bellinger et al, 1999). Ethanol, which is an NMDA receptor antagonist (Lovinger et al, 1989;Lovinger et al, 1990), also produced a lasting reduction in synaptic efficacy without altering LTP or paired-pulse facilitation when administered to neonatal animals.…”

Perinatal exposure to alcohol disturbs spatial learning and glutamate transmission-related gene expression in the adult hippocampus

“…Most importantly, we detected a hippocampus‐dependent impairment of spatial learning. This effect is in accordance with deficits of ethanol‐exposed children and other valid animal models using similar doses and time windows (Bellinger et al. , 1999; Mameli et al.…”