title: Unilateral lesion of the nigrostriatal pathway decreases the response of interneurons in medial prefrontal cortex to 5-HT 2A/2C receptor stimulation in the rat.
abstract: The aim of the present study was to investigate changes in the firing rate and pattern of interneurons in the medial prefrontal cortex (mPFC), and effects of 5-HT(2A/2C) receptor agonist DOI and antagonist ritanserin, and the selective 5-HT(2C) receptor antagonist SB 242084 on the neuronal firing in rats with 6-hydroxydopamine (6-OHDA) lesions of the substantia nigra pars compacta (SNc) by extracellular recording in vivo. The lesion of the SNc decreased the firing rate of the interneurons compared to sham-lesioned rats, and firing pattern of these interneurons changed toward a more burst-firing. Administration of DOI (20-320 microg/kg, i.v.) dose-dependently increased the firing rate of all interneurons examined in sham-lesioned and the 6-OHDA-lesioned rats. The excitation was significant at doses higher than 40 microg/kg and 320 microg/kg in sham-lesioned and the 6-OHDA-lesioned rats, respectively. This dose, which produced marked effect in the 6-OHDA-lesioned rats, was much higher than that of sham-lesioned rats. The local application of DOI (5 microg) in mPFC increased the firing rate of the interneurons in sham-lesioned rats, while having no effect on the firing rate in the 6-OHDA-lesioned rats. The excitatory effect of DOI in sham-lesioned and the 6-OHDA-lesioned rats was completely or partially reversed by ritanserin or SB 242084. The results of our study show that lesion of the SNc leads to a decrease in the firing rate of interneurons in mPFC and fire with a more burst pattern, and decreased response of the interneurons to DOI in rat.
authors: Department of Neurology, Second Affiliated Hospital, Medical School of Xi'an Jiaotong University, Xi'an 710004, China. zhangqj@mail.xjtu.edu.cn
authors: Qiao Jun
authors: QJ
authors: Zhang
authors: Shuang
authors: S
authors: Wang
authors: Jian
authors: J
authors: Liu
authors: Umar
authors: U
authors: Ali
authors: Zhen Hua
authors: ZH
authors: Gui
authors: Zhong Heng
authors: ZH
authors: Wu
authors: Yan Ping
authors: YP
authors: Hui
authors: Yong
authors: Y
authors: Wang
authors: Li
authors: L
authors: Chen
mesh_terms: D000200:Action Potentials / Q000187:drug effects / Q000502:physiology; D018663:Adrenergic Agents / Q000633:toxicity; D000631:Aminopyridines / Q000494:pharmacology; D000662:Amphetamines / Q000494:pharmacology; D000704:Analysis of Variance; D000818:Animals; D001058:Apomorphine / Q000494:pharmacology; D003342:Corpus Striatum / Q000187:drug effects / Q000293:injuries / Q000502:physiology*; D018491:Dopamine Agonists / Q000494:pharmacology; D004305:Dose-Response Relationship, Drug; D007211:Indoles / Q000494:pharmacology; D007395:Interneurons / Q000187:drug effects / Q000502:physiology*; D008297:Male; D009434:Neural Pathways / Q000293:injuries / Q000502:physiology; D016627:Oxidopamine / Q000633:toxicity; D017397:Prefrontal Cortex / Q000166:cytology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D044402:Receptor, Serotonin, 5-HT2A / Q000378:metabolism*; D058826:Serotonin 5-HT2 Receptor Agonists; D058830:Serotonin 5-HT2 Receptor Antagonists; D018490:Serotonin Agents / Q000494:pharmacology; D013378:Substantia Nigra / Q000187:drug effects / Q000293:injuries / Q000502:physiology*; D014446:Tyrosine 3-Monooxygenase / Q000378:metabolism
chemical_list: C107820:6-chloro-5-methyl-1-((2-(2-methylpyrid-3-yloxy)pyrid-5-yl)carbamoyl)indoline; D018663:Adrenergic Agents; D000631:Aminopyridines; D000662:Amphetamines; D018491:Dopamine Agonists; D007211:Indoles; D044402:Receptor, Serotonin, 5-HT2A; D058826:Serotonin 5-HT2 Receptor Agonists; D058830:Serotonin 5-HT2 Receptor Antagonists; D018490:Serotonin Agents; D016627:Oxidopamine; D014446:Tyrosine 3-Monooxygenase; D001058:Apomorphine; C015952:4-iodo-2,5-dimethoxyphenylisopropylamine