POTENTIAL CANDIDATES FOR TREATING DEFICITS ASSOCIATED WITH DEVELOPMENTAL ETHANOL EXPOSURE IN A RODENT MODEL: SOLIDAGO NEMORALIS & DIMETHOXYBENZYLIDENE-ANABASINE

Prenatal alcohol exposure (Fetal Alcohol Syndrome [FAS] and Fetal Alcohol Spectrum Disorders [FASD’s]) represents the leading preventable cause of intellectual disabilities in the western world, with FASDs estimated to affect approximately 2-5% of live births in the United States at an approximate annual cost of $3.6 billion (CDC, 2015; May et al., 2009). Ethanol (ETOH) exposure during development can lead to a variety of long-term behavioral impairments including problems with executive functioning, motor coordination, spatial learning, attention, and hyperactivity (Jones, 2011; Mattson & Riley, 1998). Much research has been conducted to develop pharmacological and/or environmental interventions to reduce these deficits, however, there are currently no clinically approved medications to treat the deficits related to fetal ETOH exposure. The current study used a developmental “3rd trimester” ETOH exposure model in neonatal rats to test the hypothesis that compounds targeting the nicotinic system will reduce deficits associated with ETOH exposure. Both compounds demonstrated promise in reducing some of the effects of developmental ethanol exposure, with DMXB-A treatment after ethanol exposure reducing balance deficits in females and spatial memory deficits in males. Solidago nemoralis treatment after ETOH exposure reduced learning and memory deficits in males and balance and executive functioning deficits in both sexes. With these results and previous work in this lab and others there appears to be ample evidence for their usefulness in reducing various forms of neurotoxicity. The long-term goal of this research is to evaluate the usefulness of both DMXB-A & Solidago nemoralis (SN) in treating deficits related to developmental ETOH exposure in humans and hopefully develop a treatment for these disorders