Chitravanshi Vineet C, Kawabe Kazumi, Sapru Hreday N
Department of Neurological Surgery, Rutgers New Jersey Medical School, Newark, New Jersey.
Department of Neurological Surgery, Rutgers New Jersey Medical School, Newark, New Jersey
Am J Physiol Heart Circ Physiol. 2015 Jul 1;309(1):H174-84. doi: 10.1152/ajpheart.00801.2014. Epub 2015 May 8.
We have previously reported that stimulation of the hypothalamic arcuate nucleus (ARCN) by microinjections of N-methyl-d-aspartic acid (NMDA) elicits tachycardia, which is partially mediated via inhibition of vagal inputs to the heart. The neuronal pools and neurotransmitters in them mediating tachycardia elicited from the ARCN have not been identified. We tested the hypothesis that the tachycardia elicited from the ARCN may be mediated by inhibitory neurotransmitters in the nucleus ambiguus (nAmb). Experiments were done in urethane-anesthetized, artificially ventilated, male Wistar rats. In separate groups of rats, unilateral and bilateral microinjections of muscimol (1 mM), gabazine (0.01 mM), and strychnine (0.5 mM) into the nAmb significantly attenuated tachycardia elicited by unilateral microinjections of NMDA (10 mM) into the ARCN. Histological examination of the brains showed that the microinjections sites were within the targeted nuclei. Retrograde anatomic tracing from the nAmb revealed direct bilateral projections from the ARCN and hypothalamic paraventricular nucleus to the nAmb. The results of the present study suggest that tachycardia elicited by stimulation of the ARCN by microinjections of NMDA is mediated via GABAA and glycine receptors located in the nAmb.
我们之前曾报道，通过微量注射N-甲基-D-天冬氨酸（NMDA）刺激下丘脑弓状核（ARCN）会引发心动过速，这部分是通过抑制心脏的迷走神经输入介导的。介导ARCN引发心动过速的神经元池及其内的神经递质尚未明确。我们检验了这样一个假说，即ARCN引发的心动过速可能由疑核（nAmb）中的抑制性神经递质介导。实验在氨基甲酸乙酯麻醉、人工通气的雄性Wistar大鼠中进行。在不同组的大鼠中，向nAmb单侧和双侧微量注射蝇蕈醇（1 mM）、gabazine（0.01 mM）和士的宁（0.5 mM）可显著减弱由向ARCN单侧微量注射NMDA（10 mM）所引发的心动过速。对大脑的组织学检查显示微量注射部位在目标核内。从nAmb进行逆行解剖追踪揭示了从ARCN和下丘脑室旁核到nAmb的直接双侧投射。本研究结果表明，通过微量注射NMDA刺激ARCN所引发的心动过速是通过位于nAmb中的GABAA和甘氨酸受体介导的。
