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Nucleus of the solitary tract catecholaminergic neurons modulate the cardiovascular response to psychological stress in rats

机译:孤儿儿茶酚胺能神经元核调节大鼠对心理压力的心血管反应

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Catecholaminergic neurons within the central nervous system are an integral part of stress-related neurocircuitry, and the nucleus of the solitary tract (NTS) plays a critical role in cardiovascular regulation. We tested the hypothesis that NTS catecholaminergic neurons attenuate psychological stress-induced increases in blood pressure and promote neuroendocrine activation in response to psychological stress. Anti-dopamine-β-hydroxylase antibody conjugated to the neurotoxin saporin (DSAP) or saline vehicle was microinjected into the NTS to lesion catecholaminergic neurons in male Sprague-Dawley rats, and 17 days later the rats were subjected to 60 min of restraint stress for five consecutive days. DSAP treatment significantly enhanced the integrated increase in mean arterial pressure during restraint on the first (800 ± 128 and 1115 ± 116 mmHg (min) for saline- and DSAP-treated rats) and fifth days (655 ± 116 and 1035 ± 113 mmHg (min) for saline- and DSAP-treated rats; P 0.01 for overall effect of DSAP treatment) of restraint. In contrast, after 60 min of restraint plasma corticosterone concentration was significantly lower in DSAP-treated compared with saline-treated rats (25.9 ± 7 compared with 46.8 ± 7 μg dl -1 for DSAP- and saline-treated rats; P 0.05). DSAP treatment also significantly reduced baseline plasma adrenaline concentration (403 ± 69 compared with 73 ± 29 pg ml -1 for saline- and DSAP-treated rats), but did not alter the magnitude of the adrenaline response to restraint. The data suggest that NTS catecholaminergic neurons normally inhibit the arterial pressure response, but help maintain the corticosterone response to restraint stress.
机译:中枢神经系统中的儿茶酚胺能神经元是与压力相关的神经回路的组成部分,孤立道(NTS)的核在心血管调节中起关键作用。我们测试了NTS儿茶酚胺能神经元减弱心理压力引起的血压升高并促进神经内分泌激活以响应心理压力的假设。将与神经毒素皂素(DSAP)或生理盐水载体偶联的抗多巴胺-β-羟化酶抗体微注射到NTS中,对雄性Sprague-Dawley大鼠的儿茶酚胺能神经元进行损伤,并在17天后对大鼠施加60分钟的束缚压力连续五天。 DSAP治疗显着增强了在第一天(对于接受盐水和DSAP处理的大鼠的第一时间(800±128和1115±116 mmHg(分钟))和第五天(655±116和1035±113 mmHg(对于盐水和DSAP处理过的大鼠,最低);对于DSAP处理的总体效果,P <0.01)。相反,束缚60分钟后,DSAP治疗组血浆皮质酮浓度明显低于生理盐水处理组大鼠(25.9±7,而DSAP和生理盐水处理组大鼠则为46.8±7μgdl -1; P <0.05) 。 DSAP处理还显着降低了基线血浆肾上腺素浓度(对于盐水和DSAP处理的大鼠,肾上腺素浓度为403±69,而73±29 pg ml -1),但并未改变肾上腺素对约束的反应幅度。数据表明,NTS儿茶酚胺能神经元通常会抑制动脉压反应,但有助于维持皮质酮对约束性压力的反应。

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