Effects of alcohol exposure during development on play behavior and c-Fos expression in response to play behavior

Abstract

Developmental exposure to alcohol can produce characteristic physiological and cognitive deficits, often termed Fetal Alcohol Spectrum Disorder (FASD). More recently, social deficits have been shown to occur both in FASD and animal models of FASD; the behavioral and neural bases of these deficits remain to be determined. It was hypothesized that changes in sensory processing may in part underlie the social deficits seen in FASD. This study used a rat model of FASD and social play, a behavior critical to adult social functioning, to begin to examine this hypothesis. Somatosensory cues from dorsal contact to the nape of the neck, critical to the initiation of pinning, were systematically degraded by administration of different doses of xylocaine, a topical anesthetic. Neuronal activity after 1h of play was assessed by measurement of c-Fos immunoreactivity (IR) in different brain regions. Ethanol-exposed rats showed an increased frequency of pinning during social play and were more sensitive to the degradation of somatosensory cues compared to the control groups, suggesting difficulties in processing somatosensory cues. Neuronal activity in the somatosensory cortex induced by play was significantly decreased in the ethanol-exposed group compared to the non-treated group. The c-Fos IR in the nucleus accumbens was altered in a sexually dimorphic manner in the ethanol-exposed group. Thus, the behavioral and brain measures are consistent with the hypothesis that ethanol exposure during development induces alterations in social play via deficits in processing somatosensory cues that are important to social play.

Acute alcohol exposure during neurulation: Behavioral and brain structural consequences in adolescent C57BL/6J mice

“…Brunssen et al, 2013, Ey et al, 2011) in which sensory processing and social motivations have been impaired. The neural circuitry associated with altered social behavior in prenatal alcohol-exposed rodents is thought to include the somatosensory cortex, frontal cortex, amygdala, and nucleus accumbens (Lawrence et al, 2008, Hamilton et al, 2010a, Hamilton et al, 2010b). Although specific volume defects were not observed following GD8 alcohol exposure, shape defects of the corpus callosum suggest some abnormal wiring may have occurred that would impact function.…”

The impact of prenatal alcohol exposure on social, cognitive and affective behavioral domains: Insights from rodent models

“…3). The majority of rodent studies show that aggressive play is decreased in adolescent and adult males across PAE exposures (Charles Lawrence, Cale Bonner, Newson, & Kelly, 2008; Kelly & Dillingham, 1994; Lugo, Marino, Cronise, & Kelly, 2003; Meyer & Riley, 1986; Wellmann et al, 2015). However, some studies have shown increases in wrestling behaviors in males (Hamilton et al, 2010, 2014; Royalty, 1990).…”

“…Studies showing decreases in aggressive play behaviors utilized either high-dose gavage or moderate liquid-diet paradigms, which may result in short withdrawal periods and more stable BACs, respectively. However, in the two studies showing increased aggressive play behaviors, one utilized a 4-h voluntary drinking-in-the-dark paradigm and the other a lower dose gavage (2 g/kg/day compared to 3–5 g/kg/day) (Charles Lawrence et al, 2008; Royalty, 1990). In these paradigms, the withdrawal periods are most likely much longer.…”

Unilateral whisker clipping exacerbates ethanol-induced social and somatosensory behavioral deficits in a sex- and age-dependent manner

“…In addition to altered social behavior, sensory detection and processing of somatosensory stimuli are also impaired following prenatal ethanol exposure [2, 6]. This may be due, in part, to the ethanol-induced alteration in the structure of somatosensory cortex [5, 26-30].…”