Effects of neonatal alcohol exposure on vasoactive intestinal polypeptide neurons in the rat suprachiasmatic nucleus

Aug 13, 2009Alcohol (Fayetteville, N.Y.)

Effects of early alcohol exposure on brain cells controlling daily rhythms in rats

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Abstract

Neonatal alcohol exposure decreased the total number and density of vasoactive intestinal polypeptide (VIP) neurons in the suprachiasmatic nucleus (SCN) by about 35% in adult rats exposed to 6.0 g/kg/day.

Long-term changes in the SCN may disrupt light-dark regulation of circadian behavior in adult rats following neonatal alcohol exposure.
The pattern of photoentrainment, rate of re-entrainment to shifted light-dark cycles, and phase-shifting responses to light are all potentially affected.
VIP mRNA expression remained unchanged despite significant alterations in the immunostaining of VIP neurons in the SCN.
The anatomical distribution of VIP mRNA-expressing neurons was similar in control and alcohol-exposed groups.
VIP neuronal populations in the SCN appear to be vulnerable to the effects of alcohol during critical periods of brain development.

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Neonatal alcohol exposure produces long-term changes in the suprachiasmatic nucleus (SCN) that are presumably responsible for disturbances in the light-dark regulation of circadian behavior in adult rats, including the pattern of photoentrainment, rate of re-entrainment to shifted light-dark cycles, and phase-shifting responses to light. Because SCN neurons containing vasoactive intestinal polypeptide (VIP) receive direct photic input via the retinohypothalamic tract and thus play an important role in the circadian regulation of the SCN clock mechanism by light, the present study examined the long-term effects of neonatal alcohol exposure on VIP neuronal populations within the SCN of adult rats. Male Sprague-Dawley rat pups were exposed to alcohol (EtOH; 3.0, 4.5, or 6.0 g/kg/day) or isocaloric milk formula (gastrostomy control; GC) on postnatal days 4-9 using artificial-rearing methods. At 2-3 months of age, animals from the suckle control (SC), GC, and EtOH groups were exposed to constant darkness (DD) and SCN tissue was harvested for subsequent analysis of either VIP mRNA expression by quantitative polymerase chain reaction (PCR) and in situ hybridization or of VIP-immunoreactive (ir) neurons using stereological methods. Neonatal alcohol exposure had no impact on VIP mRNA expression but dramatically altered immunostaining of neurons containing this peptide within the SCN of adult rats. The relative abundance of VIP mRNA and anatomical distribution of neurons expressing this transcript were similar among all control- and EtOH-treated groups. However, the total number and density of VIP-ir neurons within the SCN were significantly decreased by about 35% in rats exposed to alcohol at a dose of 6.0 g/kg/day relative to that observed in both control groups. These results demonstrate that VIP neuronal populations in the SCN are vulnerable to EtOH-induced insult during brain development. The observed alterations in SCN neurons containing VIP may have an impact upon clock responses to light input and thus contribute to the long-term effects of neonatal alcohol exposure on the photic regulation of circadian behavior.

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Effects of neonatal alcohol exposure on vasoactive intestinal polypeptide neurons in the rat suprachiasmatic nucleus

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