إدمان المخدرات: الفرق بين النسختين

 ΔFosB، عامل <nowiki/>[[نسخ (وراثة)|النسخ الجيني]]، من المعروف الآن أنه عنصر حاسم وعامل مشترك في تكوين تقريبا جميع أشكال الإدمان السلوكية والإدمان على المواد،<ref name="Nestler">{{Citeاستشهاد journalبدورية محكمة|عنوان=Transcriptional and epigenetic mechanisms of addiction|تاريخ=November 2011|صحيفة=Nat. Rev. Neurosci.|العدد=11|DOI=10.1038/nrn3111|المجلد=12|صفحات=623–637|PMID=21989194|اقتباس=ΔFosB has been linked directly to several addiction-related behaviors&nbsp;... Importantly, genetic or viral overexpression of ΔJunD, a dominant negative mutant of JunD which antagonizes ΔFosB- and other AP-1-mediated transcriptional activity, in the NAc or OFC blocks these key effects of drug exposure14,22–24. This indicates that ΔFosB is both necessary and sufficient for many of the changes wrought in the brain by chronic drug exposure. ΔFosB is also induced in D1-type NAc MSNs by chronic consumption of several natural rewards, including sucrose, high fat food, sex, wheel running, where it promotes that consumption14,26–30. This implicates ΔFosB in the regulation of natural rewards under normal conditions and perhaps during pathological addictive-like states.}}</ref><ref name="ΔFosB reward">{{Citeاستشهاد journalبدورية محكمة|عنوان=Sex, drugs, and rock 'n' roll: hypothesizing common mesolimbic activation as a function of reward gene polymorphisms|صحيفة=J. Psychoactive Drugs|العدد=1|DOI=10.1080/02791072.2012.662112|سنة=2012|المجلد=44|صفحات=38–55|PMID=22641964|اقتباس=It has been found that deltaFosB gene in the NAc is critical for reinforcing effects of sexual reward. Pitchers and colleagues (2010) reported that sexual experience was shown to cause DeltaFosB accumulation in several limbic brain regions including the NAc, medial pre-frontal cortex, VTA, caudate, and putamen, but not the medial preoptic nucleus. Next, the induction of c-Fos, a downstream (repressed) target of DeltaFosB, was measured in sexually experienced and naive animals. The number of mating-induced c-Fos-IR cells was significantly decreased in sexually experienced animals compared to sexually naive controls. Finally, DeltaFosB levels and its activity in the NAc were manipulated using viral-mediated gene transfer to study its potential role in mediating sexual experience and experience-induced facilitation of sexual performance. Animals with DeltaFosB overexpression displayed enhanced facilitation of sexual performance with sexual experience relative to controls. In contrast, the expression of DeltaJunD, a dominant-negative binding partner of DeltaFosB, attenuated sexual experience-induced facilitation of sexual performance, and stunted long-term maintenance of facilitation compared to DeltaFosB overexpressing group. Together, these findings support a critical role for DeltaFosB expression in the NAc in the reinforcing effects of sexual behavior and sexual experience-induced facilitation of sexual performance.&nbsp;... both drug addiction and sexual addiction represent pathological forms of neuroplasticity along with the emergence of aberrant behaviors involving a cascade of neurochemical changes mainly in the brain's rewarding circuitry.}}</ref><ref name="Natural and drug addictions">{{Citeاستشهاد بدورية journalمحكمة|عنوان=Natural rewards, neuroplasticity, and non-drug addictions|تاريخ=December 2011|صحيفة=Neuropharmacology|العدد=7|DOI=10.1016/j.neuropharm.2011.03.010|المجلد=61|صفحات=1109–22|PMID=21459101|الأخير=Olsen CM}}</ref> ولكن ليس الاعتماد.

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