Neurochemical interactions in the parabrachial nucleus mediating visceral inputs to visceral thalamic neurons.
Neurochemical interactions in the parabrachial nucleus mediating visceral inputs to visceral thalamic neurons.
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臂旁核中的神经化学相互作用介导内脏丘脑神经元的内脏输入。
DOI：
10.1152/ajpregu.1995.268.3.r786
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发表时间：
1995
期刊：
影响因子：
--
通讯作者：
David F. Cechetto
中科院分区：
文献类型：
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作者：
Tarek M. Saleh;David F. Cechetto
以前，我们证明，多巴胺能和去甲肾上腺素能受体介导的中继内脏信息通过臂旁核（PBN）和降钙素基因相关肽（CGRP），P物质（SP），生长抑素（SOM），神经降压素（NT），和胆囊收缩素（CCK）可以调节这些反应。在用水合氯醛麻醉并通气的雄性Wistar大鼠（17）中检查了这些神经递质和神经肽的相互作用，并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，引起内脏丘脑神经元（VTN）单单位和多单位活动的变化。VTN活动的周刺激时间和连续时间直方图之前和之后，200-nl注射肽，神经递质激动剂或拮抗剂，或人工脑脊液到PBN。PBN内联合注射CGRP和SP可协同抑制自发性VTN活动和迷走神经诱发的VTN反应。联合注射NT和苯肾上腺素（PE）到PBN只产生了一个附加的增加自发活动的VTN。在PBN中预先施用SOM阻断了α-肾上腺素能激动剂（苯肾上腺素）注射对VTN自发活动的兴奋作用，而CGRP、SP或CCK对α-激动剂诱导的反应没有影响。预先注射α-肾上腺素能拮抗剂（酚妥拉明）阻止NT在PBN中的兴奋作用。将CGRP、SP、NT或CCK注入PBN并不改变VTN对谷氨酸的反应。这些结果表明，在PBN的主要神经递质的肽相互作用的机制，并表明神经肽的主要神经递质突触前或突触后的行为。
Previously we demonstrated that glutamatergic and noradrenergic receptors mediate the relay of visceral information through the parabrachial nucleus (PBN) and that calcitonin gene-related peptide (CGRP), substance P (SP), somatostatin (SOM), neurotensin (NT), and cholecystokinin (CCK) may modulate these responses. The interactions of these neurotransmitters and neuropeptides were examined in male Wistar rats (17) that were anesthetized with chloral hydrate and ventilated and in which 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 of visceral thalamic neurons (VTNs). Peristimulus-time and continuous-time histograms of VTN activity were made before and after 200-nl injections of peptides, neurotransmitter agonists or antagonists, or artificial cerebrospinal fluid into the PBN. Combined injection of CGRP and SP into the PBN produced a synergistic inhibition of spontaneous VTN activity and the vagally evoked VTN response. Combined injection of NT and phenylephrine (PE) into the PBN produced only an additive increase in the spontaneous activity of VTNs. Prior administration of SOM in the PBN blocked the excitatory action of an alpha-adrenergic agonist (phenylephrine) injection on the spontaneous activity of VTNs, whereas CGRP, SP, or CCK had no effect on the alpha-agonist-induced response. Prior injection of an alpha-adrenergic antagonist (phentolamine) prevented the excitatory effect of NT in the PBN. Injection of CGRP, SP, NT, or CCK into the PBN did not change the response of VTNs to application of glutamate. These results suggest mechanisms for peptide interaction with primary neurotransmitters in the PBN and indicate whether the neuropeptides are acting before the primary neurotransmitter synapse or postsynaptically.