Ethanol Attenuates Spatial Memory Deficits and Increases mGlu1a Receptor Expression in the Hippocampus of Rats Exposed to Prenatal Stress
Alcoholism: Clinical and Experimental Research. 2009-08-01; 33(8): 1346-1354
DOI: 10.1111/j.1530-0277.2009.00964.x
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BACKGROUND: Although it is generally believed that chronic ethanol consumption
impairs learning and memory, results obtained in experimental animals are not
univocal, and there are conditions in which ethanol paradoxically improves
cognitive functions. In the present work, we investigated the effects of prenatal
stress and of chronic ethanol exposure during adulthood on spatial memory in
rats.
METHODS: Rats were subjected to a prenatal stress delivered as 3 daily 45-minute
sections of restraint stress to the mothers during the last 10 days of pregnancy
(PRS rats). After 7 months of ethanol exposure (ethanol 10%, oral intake), memory
performances were evaluated in a spatial discrimination test in control and PRS
male rats. Then, the oxidative damages and the expression of metabotropic
glutamate (mGlu) receptors were assessed in their hippocampus.
RESULTS: Chronic ethanol exposure resulted in a reduced performance in a spatial
recognition task in control animals. Unexpectedly, however, the same treatment
attenuated spatial memory deficits in rats that had been subjected to prenatal
stress. This paradigm of ethanol administration did not produce detectable signs
of oxidative damage in the hippocampus in either unstressed or PRS rats.
Interestingly, ethanol intake resulted in differential effects in the expression
of mGlu receptor subtypes implicated in mechanisms of learning and memory. In
control rats, ethanol intake reduced mGlu2/3 and mGlu5 receptor levels in the
hippocampus; in PRS rats, which exhibited a constitutive reduction in the levels
of these mGlu receptor subtypes, ethanol increased the expression of mGlu1a
receptors but did not change the expression of mGlu2/3 or mGlu5 receptors.
CONCLUSION: Our findings support the idea that stress-related events occurring
before birth have long-lasting effects on brain function and behavior, and
suggest that the impact of ethanol on cognition is not only dose- and
duration-dependent, but also critically influenced by early life experiences.