The Biochemical Core of the proposed TSRI Alcohol Research Center is comprised of two components designed to provide sample analyses and chemical compounds (pharmacological and otherwise) to the Center at large. The biochemical analysis component of the Core will provide analyses of endocannabinoids (Roberto/Siggins and Parsons components, Taffe pilot project), amino acids (Roberto/Siggins and Parsons components), monoamines (Rivier component and Taffe pilot), CRF (Roberto/Siggins component), NPY (Zorrilla/Weiss and Roberto/Siggins components) and neuroactive steroids (animal models core). These analyses will be performed on in vivo brain microdialysis samples, post-mortem brain tissue, and plasma from rats as well as in primate CSF using highly sensitive and selective methods including LC-MS, CE-LIF, HPLC-ED and RIA techniques. The Core will also provide consultation regarding optimum sample collection, handling and storage, and will guide experimental design involving in vivo microdialysis techniques. The chemical compound repository component of the Core will provide the necessary standards for the assays described above as well as for any required internal standards. This component will also coordinate the standardization of sensitivity and reproducibility of standard curves used in these assays. The required CRF, neuropeptide Y, endocannabinoid, amino acid, monoamine, and neurosteroid ligands will also be analyzed for purity as they become available. Ligands which cannot be obtained commercially will be synthesized as necessary.

National Institute of Health (NIH)
National Institute on Alcohol Abuse and Alcoholism (NIAAA)
Comprehensive Center (P60)
Project #
Application #
Study Section
Special Emphasis Panel (ZAA1)
Project Start
Project End
Budget Start
Budget End
Support Year
Fiscal Year
Total Cost
Indirect Cost
Scripps Research Institute
La Jolla
United States
Zip Code
Logrip, Marian L; Oleata, Christopher; Roberto, Marisa (2017) Sex differences in responses of the basolateral-central amygdala circuit to alcohol, corticosterone and their interaction. Neuropharmacology 114:123-134
Natividad, Luis A; Buczynski, Matthew W; Herman, Melissa A et al. (2017) Constitutive Increases in Amygdalar Corticotropin-Releasing Factor and Fatty Acid Amide Hydrolase Drive an Anxious Phenotype. Biol Psychiatry 82:500-510
Kimbrough, Adam; de Guglielmo, Giordano; Kononoff, Jenni et al. (2017) CRF1 Receptor-Dependent Increases in Irritability-Like Behavior During Abstinence from Chronic Intermittent Ethanol Vapor Exposure. Alcohol Clin Exp Res 41:1886-1895
Mason, Barbara J (2017) Emerging pharmacotherapies for alcohol use disorder. Neuropharmacology 122:244-253
Luczak, Susan E; Liang, Tiebing; Wall, Tamara L (2017) Age of Drinking Initiation as a Risk Factor for Alcohol Use Disorder Symptoms is Moderated by ALDH2*2 and Ethnicity. Alcohol Clin Exp Res 41:1738-1744
Irimia, Cristina; Buczynski, Matthew W; Natividad, Luis A et al. (2017) Dysregulated Glycine Signaling Contributes to Increased Impulsivity during Protracted Alcohol Abstinence. J Neurosci 37:1853-1861
Melroy-Greif, Whitney E; Wilhelmsen, Kirk C; Yehuda, Rachel et al. (2017) Genome-Wide Association Study of Post-Traumatic Stress Disorder in Two High-Risk Populations. Twin Res Hum Genet 20:197-207
Varodayan, Florence P; Bajo, Michal; Soni, Neeraj et al. (2017) Chronic alcohol exposure disrupts CB1 regulation of GABAergic transmission in the rat basolateral amygdala. Addict Biol 22:766-778
Roberto, Marisa; Varodayan, Florence P (2017) Synaptic targets: Chronic alcohol actions. Neuropharmacology 122:85-99
Varodayan, Florence P; de Guglielmo, Giordano; Logrip, Marian L et al. (2017) Alcohol Dependence Disrupts Amygdalar L-Type Voltage-Gated Calcium Channel Mechanisms. J Neurosci 37:4593-4603

Showing the most recent 10 out of 184 publications