1. Parvalbumin Interneurons of Central Amygdala Regulate the Negative Affective States and the Expression of Corticotrophin-Releasing Hormone During Morphine Withdrawal
- Author
-
Feifei Wang, Minjie Shen, Li Wang, Lan Ma, and Changyou Jiang
- Subjects
0301 basic medicine ,Corticotropin-Releasing Hormone ,PV ,Anxiety ,0302 clinical medicine ,Saccharin ,Pharmacology (medical) ,Opioidergic ,biology ,Behavior, Animal ,Morphine ,Central nucleus of the amygdala ,musculoskeletal, neural, and ocular physiology ,Miniature Postsynaptic Potentials ,Substance Withdrawal Syndrome ,Up-Regulation ,Psychiatry and Mental health ,medicine.anatomical_structure ,Parvalbumins ,Phenotype ,CRH ,Psychology ,medicine.drug ,Signal Transduction ,Elevated plus maze ,morphine withdrawal ,Genotype ,Mice, Transgenic ,Optogenetics ,Neurotransmission ,Amygdala ,03 medical and health sciences ,Interneurons ,medicine ,Animals ,RNA, Messenger ,Regular Research Article ,Maze Learning ,Pharmacology ,Central Amygdaloid Nucleus ,Excitatory Postsynaptic Potentials ,Feeding Behavior ,digestive system diseases ,negative affective states ,Mice, Inbred C57BL ,Affect ,Disease Models, Animal ,030104 developmental biology ,nervous system ,central amygdala ,biology.protein ,Neuroscience ,030217 neurology & neurosurgery ,Parvalbumin - Abstract
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.
- Published
- 2016