Sexually Dimorphic Effects of Alcohol Exposure during Development on the Processing of Social Cues

Abstract

The results suggest that ethanol exposure during development caused a deficit in memory duration but not encoding in males and a deficit in encoding but not memory duration in females. The deficit in ethanol-exposed females may be related to changes in oxytocin receptors in the amygdala.

Activity and social behavior in a complex environment in rats neonatally exposed to alcohol

“…These results are supported by previous rodent and human studies. Work with prenatal alcohol exposure models has reported similar decreases in play fighting behaviors and social recognition in male rats (Kelly & Dillingham, 1994; Kelly, Leggett, & Cronise, 2009; Middleton, Varlinskaya, & Mooney, 2012; Mooney & Varlinskaya, 2011). Additionally, children with FASD exhibit impaired social functioning independent of IQ (Thomas, Kelly, Mattson, & Riley, 1998).…”

An examination of sex differences in the effects of early-life opiate and alcohol exposure

“…Males exposed to fetal alcohol also exhibit decreases in social investigation, contact behaviour and play fighting, indicating that alcohol has striking effects on typical social behaviour in males [101]. While males have greater levels of oxytocin receptor binding than females in the amygdala overall and this is thought to play a role in social behaviour, fetal alcohol exposure decreased oxytocin receptor binding similarly in both males and females [100], which suggests that similar neural consequences of fetal alcohol exposure in males and females may not produce similar effects on behaviour. Fetal alcohol exposure, particularly during the third trimester equivalent, results in deficits in the ability of hippocampal synapses to express long-term potentiation in adolescent and adult males; however, the same cannot be said for females [102].…”

Alcohol and Developing Neuronal Circuits

“…Inhibition of glycogen synthase kinase 3 (lithium); inhibition of cannabinoid receptor-1 (SR141716A) (Sadrian et al, 2012) (Subbanna et al, 2013) Impaired hippocampal cholinergic transmission Choline supplementation (Monk et al, 2012) Excitotoxic damage during alcohol withdrawal Inhibition of NMDA receptors (eliprodil; CP-101,606; memantine) (Lewis et al, 2012) (Idrus et al, 2011) ↓Parallel fiber-Purkinje cell synapses in the cerebellum Motor training (Klintsova et al, 2002) ↑Oxidative stress in several brain regions Voluntary exercise; omega-3 fatty acid supplementation (Brocardo et al, 2012) (Patten et al, 2013) ↓Purkinje neuron and microglia numbers Peroxisome proliferator-activated receptor-γ agonists (15-deoxy-Δ12,15 prostaglandin J2 and pioglitazone) (Kane et al, 2011) that several laboratories have undertaken studies on regions that have received relatively little attention, such as the amygdala, striatum, visual and barrel cortex, agranular insular cortex, and prelimbic cortex (Cullen, Burne, Lavidis, & Moritz, 2013;Hamilton et al, 2010;Kelly, Leggett, & Cronise, 2009;Medina & Krahe, 2008;Middleton, Varlinskaya, & Mooney, 2012;Zhou, Wang, & Zhu, 2010;Zhou, Wang, & Zhu, 2012). Functional neuroimaging studies have begun to shed light on the deficits in network connectivity that are present in the brains of patients with FASDs (Diwadkar et al, 2013;Meintjes et al, 2010;Wozniak et al, 2013).…”