Acute restraint stress augments the rewarding memory of cocaine through activation of α1 adrenoceptors in the medial prefrontal cortex of mice
| Autor: | Hironori Kamii, Junko Yanagida, Masaki Domoto, Masabumi Minami, Satoshi Deyama, Akihiro Yamanaka, Eiichi Hinoi, Xueting Li, Hitoki Sasase, Tong Zhang, Shintaro Wada, Katsuyuki Kaneda, Kazuki Nagayasu, Naoya Nishitani, Shuji Kaneko |
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| Rok vydání: | 2020 |
| Předmět: |
0301 basic medicine
medicine.medical_specialty Stimulation Inhibitory postsynaptic potential behavioral disciplines and activities 03 medical and health sciences Cellular and Molecular Neuroscience 0302 clinical medicine Postsynaptic potential Internal medicine medicine Prefrontal cortex Pharmacology Chemistry musculoskeletal neural and ocular physiology Conditioned place preference Yohimbine 030104 developmental biology medicine.anatomical_structure Endocrinology nervous system Excitatory postsynaptic potential Pyramidal cell psychological phenomena and processes 030217 neurology & neurosurgery medicine.drug |
| Zdroj: | Neuropharmacology. 166:107968 |
| ISSN: | 0028-3908 |
| Popis: | Stress augments the rewarding memory of cocaine, which plays a critical role in inducing cocaine craving. However, the neurobiological mechanisms underlying the enhancing effect of stress remain unclear. Here, we show that noradrenaline (NA) transmission in the medial prefrontal cortex (mPFC) mediates stress-induced enhancement of cocaine craving. When mice were exposed to acute restraint stress immediately before the posttest session of the cocaine-induced conditioned place preference (CPP) paradigm, the CPP score was significantly higher than that in non-stressed mice. Because extracellular NA levels have been reported to be increased in the mPFC during stress exposure, we assessed the effects of NA on mPFC layer 5 pyramidal cell activity. Whole-cell recordings revealed that NA application induces depolarization and a concomitant increase in spontaneous excitatory postsynaptic currents (sEPSCs). The NA effects were inhibited by terazosin, but not by yohimbine or timolol, and the sEPSC increase was not observed in the presence of tetrodotoxin, suggesting the involvement of postsynaptic α1, but not α2 or β, adrenoceptors in the NA effects. Additionally, intra-mPFC injection of terazosin before stress exposure attenuated the stress-induced increase in cocaine CPP. Intra-mPFC injection of phenylephrine, an α1 adrenoceptor agonist, before the posttest session without stress exposure significantly enhanced cocaine CPP. Furthermore, chemogenetic suppression of mPFC pyramidal cells with inhibitory DREADD (designer receptors exclusively activated by designer drugs) also suppressed the stress-induced CPP enhancement. These findings suggest that the stress-induced increase in NA transmission activates mPFC pyramidal cells via α1 adrenoceptor stimulation, leading to enhancement of cocaine craving-related behavior. |
| Databáze: | OpenAIRE |
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