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Publication : Parvalbumin Interneurons of Central Amygdala Regulate the Negative Affective States and the Expression of Corticotrophin-Releasing Hormone During Morphine Withdrawal.

First Author  Wang L Year  2016
Journal  Int J Neuropsychopharmacol Volume  19
Issue  11 PubMed ID  27385383
Mgi Jnum  J:314824 Mgi Id  MGI:6754459
Doi  10.1093/ijnp/pyw060 Citation  Wang L, et al. (2016) Parvalbumin Interneurons of Central Amygdala Regulate the Negative Affective States and the Expression of Corticotrophin-Releasing Hormone During Morphine Withdrawal. Int J Neuropsychopharmacol 19(11)
abstractText  BACKGROUND: The central nucleus of the amygdala (CeA) is a crucial component of the neuronal circuitry mediating aversive emotion. Its role in the negative affective states during drug withdrawal includes changes in opioidergic, GABAergic, and corticotropin-releasing factor neurotransmission. However, the modulation of the neurobiological interconnectivity in the CeA and its effects in the negative reinforcement of drug dependents are poorly understood. METHOD: We performed electrophysiological recordings to assess the membrane excitability of parvalbumin (PV)(+) interneurons in the CeA during chronic morphine withdrawal. We tested the morphine withdrawal-induced negative affective states, such as the aversive (assessed by conditioned place aversion), anxiety (assessed by elevated plus maze), and anhedonic-like (assessed by saccharin preference test) behaviors, as well as the mRNA level of corticotropin-releasing hormone (CRH) via optogenetic inhibition or activation of PV(+) interneurons in the CeA. RESULT: Chronic morphine withdrawal increased the firing rate of CeA PV(+) interneurons. Optogenetic inhibition of the activity of CeA PV(+) interneurons attenuated the morphine withdrawal-induced negative affective states, such as the aversive, anxiety, and anhedonic-like behaviors, while direct activation of CeA PV(+) interneurons could trigger those negative affective-like behaviors. Optogenetic inhibition of the CeA PV(+) interneurons during the morphine withdrawal significantly attenuated the elevated CRH mRNA level in the CeA. CONCLUSION: The activity of PV(+) interneurons in the CeA was up-regulated during chronic morphine withdrawal. The activation of PV(+) interneurons during morphine withdrawal was crucial for the induction of the negative emotion and the up-regulation of CRH mRNA levels in the CeA.
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