Fetal alcohol spectrum disorder (FASD) includes a constellation of symptoms and deficits in social behavior has become acknowledged as possibly one of the most debilitating symptoms. However, the behavioral and neural mechanism giving rise to the social deficits seen in FASD and the degree to which the environment plays a role in these social deficits remains unknown. Thus, the environment of alcohol-exposed pups will be modified such that they are exposed to intensive norma social interactions during development, isolation during the juvenile period, and abnormal mothering behavior in order to examine mitigating or exacerbating factors in the social deficits. Interactions of environment will be examined across different doses of alcohol, with the prediction that effects of low doses of alcohol will be more sensitive to environmental manipulations. Based on evidence from this laboratory and others, it is hypothesized that the ethanol-induced social deficits might arise from changes in mu opioid system. This hypothesis is examined using autoradiography and microinjectior techniques. Behavioral analyses of the social deficits observed in animals exposed to alcohol during development has demonstrated that the deficits are not likely due to changes in social motivationanc some evidence suggests that there are deficits in the ability to process social cues. The social response of animals to different gradations of sensory cues and the ability to detect social cues inthe olfactory, auditory and somatosensory domains will be examined. Using the additive factors method, the contribution of deficits in social cue processing to social deficits in general in ethanol-exposed animals will be determined. c-Fos immunoreactivity will be used to examine the neural structures contributing to the sensory processing deficit. The rat model of FASD used in this proposal entails exposure during both the prenatal and postnatal period, mimicking the effect of alcohol exposure during all three trimesters in the humans. FASD continues to be a public health problem occurring large expenses both to society and the individual. The proposed studies will use a rat model of FASD to delineate the behavioral and neurobiological mechanism underlying the social deficits in this disorder and the contribution of social environments to the impact of ethanol during development. These findings can then be translated into both biological and behavioral treatments for FASD. PERFORMANCE S TE(S)(organization, city, state) Department of Psychology University of South Carolina Columbia, SC PHS 398 (Rev. 09/04) Page 2 Form Page 2 Principal Investigator/Program Director (Last, first, middle): KELLY, Sandra, Jean KEY PERSONNEL. See instructions. Use continuation pages as needed to provide the required information in the format shown below. Start with Principal Investigator. List all other key personnel in alphabetical order, last name first. Name eRA Commons User Name Organization Role on Project KELLY, Sandra,J. SJKELLY University of South Carolina PrincipalInvestigator OTHER SIGNIFICANT CONTRIBUTORS Name Organization Role on Project Sweitzer, Sarah, M. University of South Carolina Consultant School of Medicine Human Embryonic Stem Cells Bl No D Yes If the proposed project involves human embryonic stem cells, list below the registration number of the specific cell line(s) from the following lis http://stemcells.nih.gov/reqistrv/index.asp. Usecontinuation pages as needed. If a specific line cannot be referenced at this time, include a statement that one from the Registry will be used. Cell Line Disclosure Permission Sfate/nenf.Applicable to SBIR/STTR Onlv.See Instructions. fZlYes DlMo PHS 398 (Rev. 09/04) Page2-continued Form Page 2-continued Number the following pages consecutively throughout the application. Do not use suffixes such as 4a, 4b. Principal Investigator/Program Director (Last, first, middle): KELLY, Sandra, Jean The name of the principal investigator/program director must be provided at the top of each printed page and each continuation page. RESEARCH GRANT TABLE OFCONTENTS P""""""""e Numbers Face Page 1 Description,

National Institute of Health (NIH)
National Institute on Alcohol Abuse and Alcoholism (NIAAA)
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Study Section
Special Emphasis Panel (ZRG1-IFCN-A (05))
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Matochik, John A
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University of South Carolina at Columbia
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Macht, Victoria A; Kelly, Sandra J; Gass, Justin T (2017) Sex-specific effects of developmental alcohol exposure on cocaine-induced place preference in adulthood. Behav Brain Res 332:259-268
Perkins, Amy E; Fadel, Jim R; Kelly, Sandra J (2015) The effects of postnatal alcohol exposure and galantamine on the context pre-exposure facilitation effect and acetylcholine efflux using in vivo microdialysis. Alcohol 49:193-205
Perkins, Amy; Lehmann, Claudia; Lawrence, R Charles et al. (2013) Alcohol exposure during development: Impact on the epigenome. Int J Dev Neurosci 31:391-7
Otero, Nicha K H; Thomas, Jennifer D; Saski, Christopher A et al. (2012) Choline supplementation and DNA methylation in the hippocampus and prefrontal cortex of rats exposed to alcohol during development. Alcohol Clin Exp Res 36:1701-9
Lawrence, R Charles; Otero, Nicha K H; Kelly, Sandra J (2012) Selective effects of perinatal ethanol exposure in medial prefrontal cortex and nucleus accumbens. Neurotoxicol Teratol 34:128-35
Kelly, Sandra J; Goodlett, Charles R; Hannigan, John H (2009) Animal models of fetal alcohol spectrum disorders: impact of the social environment. Dev Disabil Res Rev 15:200-8
Newsom, R J; Kelly, S J (2008) Perinatal delta-9-tetrahydrocannabinol exposure disrupts social and open field behavior in adult male rats. Neurotoxicol Teratol 30:213-9
Charles Lawrence, R; Cale Bonner, H; Newsom, Ryan J et al. (2008) Effects of alcohol exposure during development on play behavior and c-Fos expression in response to play behavior. Behav Brain Res 188:209-18
Lugo Jr, Joaquin N; Marino, Melissa D; Gass, Justin T et al. (2006) Ethanol exposure during development reduces resident aggression and testosterone in rats. Physiol Behav 87:330-7
Lugo Jr, Joaquin N; Wilson, Marlene A; Kelly, Sandra J (2006) Perinatal ethanol exposure alters met-enkephalin levels of male and female rats. Neurotoxicol Teratol 28:238-44

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