17β-Estradiol Potentiates the Reinstatement of Cocaine Seeking in Female Rats: Role of the Prelimbic Prefrontal Cortex and Cannabinoid Type-1 Receptors

被引:29
作者
Doncheck, Elizabeth M. [1 ]
Urbanik, Luke A. [1 ]
DeBaker, Margot C. [1 ]
Barron, Laura M. [1 ]
Liddiard, Gage T. [1 ]
Tuscher, Jennifer J. [2 ]
Frick, Karyn M. [2 ]
Hillard, Cecilia J. [3 ,4 ]
Mantsch, John R. [1 ]
机构
[1] Marquette Univ, Dept Biomed Sci, 561 N 15th St,Schroeder Complex 446, Milwaukee, WI 53233 USA
[2] Univ Wisconsin, Dept Psychol, Milwaukee, WI 53201 USA
[3] Med Coll Wisconsin, Dept Pharmacol & Toxicol, Milwaukee, WI 53226 USA
[4] Med Coll Wisconsin, Neurosci Res Ctr, Milwaukee, WI 53226 USA
关键词
MENSTRUAL-CYCLE PHASE; NUCLEUS-ACCUMBENS; OVARIAN HORMONES; SEX-DIFFERENCES; ESTROUS-CYCLE; DRUG-SEEKING; EXOGENOUS PROGESTERONE; STRESS-RESPONSE; SMOKED COCAINE; ESTRADIOL;
D O I
10.1038/npp.2017.170
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Clinical observations imply that female cocaine addicts experience enhanced relapse vulnerability compared with males, an effect tied to elevated estrogen phases of the ovarian hormone cycle. Although estrogens can enhance drug-seeking behavior, they do not directly induce reinstatement on their own. To model this phenomenon, we tested whether an estrogen could augment drug-seeking behavior in response to an ordinarily subthreshold reinstatement trigger. Following cocaine self-administration and extinction, female rats were ovariectomized to isolate estrogen effects on reinstatement. Although neither peak proestrus levels of the primary estrogen 17 beta-estradiol (E2; 10 mu g/kg, i.p., 1-h pretreatment) nor a subthreshold cocaine dose (1.25 mg/kg, i.p.) alone were sufficient to reinstate drug-seeking behavior, pretreatment with E2 potentiated reinstatement to the ordinarily subthreshold cocaine dose. Furthermore, E2 microinfusions revealed that E2 (5 mu g/0.3 mu l, 15-min pretreatment) acts directly within the prelimbic prefrontal cortex (PrL-PFC) to potentiate reinstatement. As E2 has been implicated in endocannabinoid mobilization, which can disinhibit PrL-PFC projection neurons, we investigated whether cannabinoid type-1 receptor (CB1R) activation is necessary for E2 to potentiate reinstatement. The CB1R antagonist AM251 (1 or 3 mg/kg, i.p., 30-min pretreatment) administered prior to E2 and cocaine suppressed reinstatement in a dose-dependent manner. Finally, PrL-PFC AM251 microinfusions (300 ng/side, 15-min pretreatment) also suppressed E2-potentiated reinstatement. Together, these results suggest that E2 can augment reactivity to an ordinarily subthreshold relapse trigger in a PrL-PFC CB1R activation-dependent manner.
引用
收藏
页码:781 / 790
页数:10
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