Peptides in the parabrachial nucleus modulate visceral input to the thalamus.

Peptides in the parabrachial nucleus modulate visceral input to the thalamus.
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臂旁核中的肽调节丘脑的内脏输入。

DOI:
10.1152/ajpregu.1993.264.4.r668
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发表时间:
1993
期刊:
The American journal of physiology
影响因子:
--
通讯作者:
D. Cechetto
D. Cechetto
中科院分区:
--
文献类型:
--
作者:
T. Saleh;D. Cechetto

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通过记录迷走神经刺激前后臂旁核丘脑神经元活动反应的变化,探讨神经肽在内脏上行通路中的作用。25只雄性Wistar大鼠用水合氯醛麻醉并通气,连续监测血压和心率。以亚最大电流强度刺激左颈迷走神经,引起基底丘脑腹侧内脏旁细胞传递核单和多单位活动的变化。在注射200-nl多肽或人工脑脊液(CSF)对照前后,绘制刺激前后丘脑活动直方图。在5 mM处注射降钙素基因相关肽(CGRP)或在2 mM处注射P物质(SP)可显著降低丘脑神经元活动的诱发反应,分别为87-100%和85-100%。注射生长抑素(SOM, 1 mM)没有显著改变迷走神经刺激引起的反应,但显著抑制丘脑单位的自发放电,导致反应-背景比增加10倍。这表明PB中的SOM抑制平行通路中的细胞,该通路终止于丘脑内脏神经元,但不是上升内脏感觉通路的一部分。1 mM神经紧张素(NT)可显著增强丘脑神经元自发活动和迷走神经诱发反应(278 ~ 508%)。低剂量(0.0002-0.2 mM)胆囊收缩素(CCK)减弱,而最高剂量(2 mM)短暂激发丘脑单位的自发活性,然后抑制其活性。(摘要删节250字)
The role of neuropeptides in ascending visceral pathways was investigated by recording the changes in the response of thalamic neuronal activity evoked by vagal stimulation before and after peptide injection in the parabrachial nucleus (PB). Male Wistar rats (n = 25) were anesthetized with chloral hydrate and ventilated, and blood pressure and heart rate were continuously monitored. The left cervical vagus nerve was stimulated at submaximal current intensities to elicit changes in single and multiunit activity in the parvocellular visceral relay nuclei in the ventral basal thalamus. Peristimulustime histograms of thalamic activity were made before and after 200-nl injections of peptides or artificial cerebrospinal fluid (CSF) controls in the PB. Injection of calcitonin gene-related peptide (CGRP) at 5 mM or substance P (SP) at 2 mM into the PB significantly attenuated the evoked response of thalamic neuronal activity by 87-100% and 85-100%, respectively. Injections of somatostatin (SOM; 1 mM) did not significantly alter the response evoked by vagal stimulation but significantly inhibited the spontaneous firing of thalamic units, resulting in a 10-fold increase in the response-to-background ratio. This suggests that SOM in the PB inhibits cells in a parallel pathway that terminates on thalamic visceral neurons but that are not part of the ascending visceral sensory pathway. Spontaneous thalamic neuronal activity and vagally evoked responses were significantly enhanced (278-508%) by injection of 1 mM neurotensin (NT) in the PB. Cholecystokinin (CCK) at low doses (0.0002-0.2 mM) attenuated while the highest dose, 2 mM, briefly excited the spontaneous activity of thalamic units before inhibiting their activity.(ABSTRACT TRUNCATED AT 250 WORDS)