5 -羟色胺水平之间的相关性和单细胞解雇鼠中缝核的马格努斯。

文章的细节

引用

Hentall ID, Kurle PJ,白色TR

5 -羟色胺水平之间的相关性和单细胞解雇鼠中缝核的马格努斯。

神经科学。2000;95 (4):1081 - 8。

PubMed ID
10682715 (在PubMed
]
文摘

血清素释放和电活动之间的关系是研究原子核中缝马格努斯的老鼠与戊巴比妥麻醉。5 -羟色胺水平监测通过碳纤维微电极的快速循环伏安法(通常在1赫兹)。单细胞射击通过相同的微电极记录,除了在伏安法波形和相关电气工件(总计约30 ms)。多管微量吸液管的电极伏安法被用于电离子透入疗法结合药物。细胞被抑制,兴奋或不受有害影响机械的皮肤刺激。这些分别指定为(M)的细胞,在细胞(M)和中性细胞(M), M表示机械。在捏3分钟,5 -羟色胺缓慢上涨近七14 (M)细胞和26 46 (M)细胞;它下降了接近两个(M)细胞;不变,那是在所有其他细胞,包括六个中性细胞(M)。更好的时空范围内,接近四个七(M)细胞,10,14 (M)细胞和0 4中性细胞(M),平均5 -羟色胺水平下降明显在+ / - 100 ms的自发的峰值。 Lower serotonin may have caused the higher spike probability; the converse is theoretically unlikely, since delays between release and detection are estimated to exceed 100 ms. Increased serotonin and decreased firing were always seen following iontophoresis or intravenous injection (1 mg/kg) of the serotonin re-uptake inhibitor clomipramine (n = 7). Iontophoresis of +/- propranolol, whose serotonergic actions include antagonism and partial agonism at 5-HT1 receptors, also increased serotonin and decreased firing (n=4). Methiothepin (intravenous, 1 mg/kg), whose serotonergic actions include 5-HT1 and 5-HT2 antagonism, typically raised serotonin levels (four of five cells) and always blocked inhibition by clomipramine (n = 3). Iontophoresis of glutamate always lowered serotonin and increased firing (n = 4). Since serotonin levels and firing were usually inversely correlated, except near on(M) cells during pinch, we propose that serotonin is released from terminals of incoming nociceptive afferents. Prior neuroanatomical knowledge favors a midbrain origin for these afferents, while some of the drug findings suggest that their terminals possess inhibitory serotonergic autoreceptors, possibly of 5-HT1b subtype. The released serotonin could contribute to the inhibition of off(M) cells and excitation of on(M) cells by noxious stimulation, since inhibitory 5-HT1a receptors and excitatory 5-HT2 receptors, respectively, have previously been shown to dominate their serotonergic responses.

DrugBank数据引用了这篇文章

药物靶点
药物 目标 生物 药理作用 行动
氯丙咪嗪 5 -羟色胺受体2 蛋白质 人类
是的
拮抗剂
细节