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

Abstract

Prenatal exposure to ethanol results in sensory deficits and altered social interactions in animal and clinical populations. Sensory stimuli serve as important cues and shape sensory development; developmental exposure to ethanol or sensory impoverishment can impair somatosensory development, but their combined effects on behavioral outcomes are unknown. We hypothesized that 1) chronic prenatal ethanol exposure would disrupt social interaction and somatosensory performance during adolescence, 2) that a mild sensory impoverishment (neonatal unilateral whisker clipping; WC) would have a mildly impairing to sub-threshold effect on these behavioral outcomes, and 3) that the effect of ethanol would be exacerbated by WC. Long-Evans dams were fed a liquid diet containing ethanol or pair-fed with non-ethanol diet on gestational day (G) 6-G21. Chow-fed control animals were also included. One male and female pup per litter underwent WC on postnatal day (P)1, P3, and P5. Controls were unclipped. Offspring underwent social interaction on P28 or P42, and gap-crossing (GC) on P31 or P42. Ethanol-exposed pups played less and crossed shorter gaps than control pups regardless of age or sex. WC further exacerbated ethanol-induced play fighting and GC deficits in all males but only in 28-day-old females. WC alone reduced sniffing in all males and in younger females. Thus, prenatal ethanol exposure induced deficits in social interaction and somatosensory performance during adolescence. Sensory impoverishment exacerbates ethanol's effect in 28-day-old male and female animals and in 42-day-old males, suggesting sex-and age-dependent changes in outcomes in ethanol-exposed offspring.

Prenatal Ethanol Exposure and Whisker Clipping Disrupt Ultrasonic Vocalizations and Play Behavior in Adolescent Rats

“…This dysregulation was also noted by Spear’s group in adolescent rats following acute exposure to ethanol just prior to social interactions [23]. We also reported that neonatal unilateral whisker clipping (WC) further decreased the number of play fighting interactions by a pair that contained an ethanol-exposed animal [22]. Ethanol-exposed rats appear to be particularly vulnerable to deprivation of sensory input regarding playful social interactions; it is possible that the disrupted relationship between USV social cues and play reflects the inability of these animals to interpret cues from a conspecific and integrate rapidly changing sensory input.…”

“…Subjects used in this study are the same as previously described [22]. Dams were timed-pregnant Long Evans rats (Harlan, Frederick, MD, USA), that arrived on gestational day (G)3 (G1 was the day on which a sperm-positive plug was first identified).…”

“…We previously reported that prenatal ethanol exposure decreased play fighting behavior in two separate cohorts of animals [17,22]. In one cohort, adolescent males exposed to ethanol prenatally showed increased latency to emit 50 kHz USVs with no change in the number of USV calls [17].…”

Ethanol and Caffeine Effects on Social Interaction and Recognition in Mice: Involvement of Adenosine A2A and A1 Receptors

“…Alternatively, it is possible that MSX3 blocks ethanol’s amnestic effects because it robustly increases active sniffing of the conspecific. It has been demonstrated that sensory impoverishment in rats (by whisker clipping) exacerbates ethanol-induced deficits in social interaction (Wellmann and Mooney, 2015). Thus, under different experimental conditions that promote sensory exploration (such as sniffing behavior), it could be possible that ethanol’s amnestic effects would be diminished.…”

Early ontogeny as a unique developmental epoch for learning, memory and consequences of alcohol exposure: A Festschrift to honor the work of Dr. Norman E. Spear

“…Furthermore, Comeau et al (this issue) [18] examined how PAE (liquid ethanol diet from G1–G21) impacted sensitivity of adolescents to chronic mild stress (imposed from P31–41), and showed that PAE enhanced the sensitivity of adolescents to stress-related deficits in cognitive function in female rats. Furthermore, Wellmann and Mooney (this issue) [19] showed that prenatal alcohol exposure (liquid ethanol diet from G6–G21) produced profound social deficits that persisted into late adolescence for both male and female offspring. Interestingly, when PAE was combined with a mild sensory challenge (unilateral whisker clipping during the first post-natal week), the effects of PAE on social deficits were potentiated through adolescence, with effects of the combined PAE/whisker clipping challenge persisting longer in males (still present at P42) relative to females (no combined effect by P42).…”