Prenatal Ethanol Exposure Alters Ethanol‐Induced Dopamine Release in Nucleus Accumbens and Striatum in Male and Female Rats

Abstract

Using in vivo microdialysis, ethanol-induced dopamine release in nucleus accumbens and striatum was examined in adult male and female Long-Evans rats exposed prenatally to ethanol and in controls. Following dialysis, ethanol intake was measured in an operant paradigm. Control rats showed increased dopamine release in nucleus accumbens and striatum in response to 0.5 g/kg ethanol, but not to 1.0 g/kg. Fetal ethanol-exposed rats showed no dopamine response at 0.5 g/kg. At 1.0 g/kg, fetal ethanol-exposed males showed increased dopamine release in both structures. Prenatally exposed females showed no change in accumbens, and decreased release in striatum. Fetal ethanol exposure did not significantly influence ethanol intake. The findings suggest that prenatal ethanol exposure influences subsequent neurochemical responses to ethanol; however, how these neurochemical measures are related to ethanol intake could not be determined in the present study. Data are discussed in terms of sex-specific shifts in the dose-response function for ethanol-induced dopamine release resulting from prenatal ethanol exposure.

Sex, strain, and estrous cycle influences on alcohol drinking in rats

“…Additionally, Morales et al (2011) reported that male and female Sprague-Dawley rats exhibited similar levels of acute and chronic tolerance to the social suppressing effects of alcohol, thus supporting the hypothesis that sex differences in alcohol drinking observed in the present study were unrelated to tolerance to alcohol. For operant alcohol self-administration, we did not observe sex differences, consistent with some previous studies (van Haaren and Anderson, 1994; Moore and Lynch, 2015), although Blanchard et al (1993) reported that females self-administered more alcohol (10%, w/v) in a fixed ratio 3 schedule of reinforcement compared with males. Importantly, the lack of sex differences in operant self-administration that was observed herein persisted after chronic intermittent alcohol vapor exposure, a model that produces reliable signs of alcohol dependence (Vendruscolo and Roberts, 2014).…”

Neurofunctional Effects of Developmental Alcohol Exposure in Alcohol-Preferring and Alcohol-Nonpreferring Rats

“…In fact, it has been shown that a binge-like alcohol exposure throughout gestation reduced the content of DA in the entire fetal brain (Maier et al 1996). Moreover, adult rats prenatally exposed to alcohol showed no changes in baseline DA levels and an increased DA release (NAC and striatum) in response to a challenge dose of alcohol (Blanchard et al 1993). In addition, prenatal alcohol treatment significantly reduced the number of spontaneously active DA neurons in the substantia nigra and ventral tegmental area in 3-and 5-month-old male offspring (Shen et al 1999).…”

Effects of ethanol exposure and withdrawal on dendritic morphology and spine density in the nucleus accumbens core and shell

“…Prenatal ethanol exposure induces long-term modifications in the nervous system associated with increased voluntary ethanol consumption in adulthood (Barbier et al, 2009; Barbier et al, 2008) which may be partially attributed to reductions in dendritic morphology of MSNs (Rice et al, 2012) and/or elevated dopamine in the NAc (Blanchard et al, 1993). Acute analysis following prenatal and perinatal ethanol exposure, however, failed to detect effects on MSN morphology (Lawrence, Otero, & Kelly, 2012), suggesting that morphological changes in the NAc may be time dependent.…”