Early Life Stress as a Risk Factor for Substance use Disorders: Clinical and Neurobiological Substrates.

Autor: Varghese SP; Department of Mental Health, Captain James A. Lovell Federal Health Care Center, North Chicago, IL 60064, USA ; Departments of Psychiatry and Behavioral Sciences, Rosalind Franklin University of Medicine and Science, North Chicago, IL 60064, USA., Montalvo-Ortiz JL; Departments of Psychiatry and Behavioral Sciences, Northwestern University, Feinberg School of Medicine, Chicago, IL 60611, USA., Csernansky JG; Departments of Psychiatry and Behavioral Sciences, Northwestern University, Feinberg School of Medicine, Chicago, IL 60611, USA., Eiger RI; Departments of Psychiatry and Behavioral Sciences, Jesse Brown Veterans Affairs Medical Center, University of Illinois at Chicago, College of Medicine, Chicago, IL 60612, USA., Herrold AA; Departments of Psychiatry and Behavioral Sciences, Northwestern University, Feinberg School of Medicine, Chicago, IL 60611, USA ; Department of Psychiatry and Behavioral Sciences, Center of Innovation for Complex Chronic Healthcare, Edward Hines Jr., Veteran Affairs Hospital, Hines, IL 60141, USA., Koola MM; Department of Psychiatry, Clinical Research Program, Sheppard Pratt Health System, University of Maryland School of Medicine, Baltimore, MD 21204, USA., Dong H; Departments of Psychiatry and Behavioral Sciences, Northwestern University, Feinberg School of Medicine, Chicago, IL 60611, USA.
Jazyk: angličtina
Zdroj: Indian journal of psychological medicine [Indian J Psychol Med] 2015 Jan-Mar; Vol. 37 (1), pp. 36-41.
DOI: 10.4103/0253-7176.150816
Abstrakt: Background: Early Life Stress (ELS) can profoundly influence an individual's genotype and phenotype. Effects of ELS can manifest in the short-term, late life and even in subsequent generations. ELS activate corticotrophin releasing factor (CRF); CRF influences drug seeking and addiction. The aim of this study was to examine the effects of endogenous elevated levels of CRF on addiction.
Materials and Methods: Inducible forebrain over-expression of CRF mice (tetop-CRH x CaMKII-tTA) was used for this study. Morphine (10 mg/kg) was administered every other day for 10 days or with increasing doses of morphine: 20, 40, 60, 80, 100, and 100 mg/kg. The behavioral trials including morphine sensitization, Somatic Opiate Withdrawal Symptoms (SOWS) were conducted in a single, open field, activity. After behavioral trial, animals were perfused for immunohistochemistry analysis.
Results: CRF-over expressed (CRF-OE) mice showed increase in morphine sensitization and withdrawal symptoms after morphine administration compared to wild type (WT) mice. The two-way ANOVA in the morphine sensitization study showed a significant effect of treatment (P<0.05) and genotype for distance traveled (P<0.01). In the SOWS study, opiate withdrawal symptoms such as rearings, circling behavior, grooming, and jump in CRF-OE were amplified in parallel to WT mice. In the immunohistochemistry study, pro-dynorphine (PDYN) expression was increased after morphine administration in both amygdala and nucleus accumbens (NAcc).
Conclusions: CRF-OE in the forebrain increases the sensitization and withdrawal symptoms in morphine treated mice. On exposure to morphine, in CRF-OE mice the PDYN protein expression was increased as compared to WT mice in the amygdala and NAcc.
Databáze: MEDLINE
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