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向室旁核结节漏斗神经元的儿茶酚胺能投射:II. 刺激腹侧去甲肾上腺素能上行束的效应:共传递的证据

Catecholaminergic projections to tuberoinfundibular neurones of the paraventricular nucleus: II. Effects of stimulation of the ventral noradrenergic ascending bundle: evidence for cotransmission.

作者信息

Saphier D, Feldman S

机构信息

Department of Neurology, Hadassah University Hospital, Jerusalem, Israel.

出版信息

Brain Res Bull. 1989 Dec;23(6):397-404. doi: 10.1016/0361-9230(89)90180-9.

Abstract

In order to further elucidate the neural mechanisms underlying the control of adrenocortical secretion, responses of paraventricular nucleus (PVN) tuberoinfundibular neurones were examined following stimulation of the ventral noradrenergic ascending bundle (VNAB). Stimulation at low frequencies (0.5/5 Hz) excited the majority (52/64, 81%) of cells but only 15 showed a clear-cut, stimulus-locked, activation with onset latency of 44.5 +/- 10.0 msec and offset at 71.9 +/- 11.3 msec: the remaining 37 excited cells showed overall increases in firing after delivery of 5-10 stimuli. High frequency (50 Hz) trains of stimuli reversed the direction of response to inhibition for 14/52 of the excited cells. Inhibition of (nor)adrenaline synthesis by alpha-methylparatyrosine was without effect upon the firing of cells examined or the distribution and latencies of their responses following low frequency stimulation; high frequency trains reversed the response direction of only 4/35 cells, (p less than 0.05 vs. control rats; chi 2-test). Intracerebroventricular administration of 6-hydroxydopamine, a catecholaminergic neurotoxin, reduced the proportion of cells excited by the stimulation (10/47; p less than 0.005; chi 2-test). Unit responses to painful somatosensory stimuli were recorded from the majority of the cells tested (74%), except following 6-hydroxydopamine treatment, when only 38% were excited (p less than 0.005; chi 2-test). The results demonstrate that the VNAB provides an excitatory input to the PVN and that noradrenaline is probably responsible for this effect but a cotransmitter (neuropeptide Y?) may also be responsible for the observed excitatory responses. Inhibitory responses following high frequency stimulation were probably also mediated by (nor)adrenaline.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

为了进一步阐明肾上腺皮质分泌控制的神经机制,在刺激腹侧去甲肾上腺素能上行束(VNAB)后,检测了室旁核(PVN)结节漏斗神经元的反应。低频(0.5/5Hz)刺激使大多数(52/64,81%)细胞兴奋,但只有15个细胞表现出明确的、刺激锁定的激活,起始潜伏期为44.5±10.0毫秒,结束潜伏期为71.9±11.3毫秒:其余37个兴奋细胞在给予5 - 10次刺激后放电总体增加。高频(50Hz)刺激串使14/52的兴奋细胞的反应方向转为抑制。α-甲基对酪氨酸抑制(去)肾上腺素合成对所检测细胞的放电或低频刺激后其反应的分布及潜伏期没有影响;高频刺激串仅使4/35的细胞反应方向逆转(与对照大鼠相比,p<0.05;卡方检验)。脑室内注射儿茶酚胺能神经毒素6 - 羟基多巴胺降低了受刺激兴奋的细胞比例(10/47;p<0.005;卡方检验)。除6 - 羟基多巴胺处理后,大多数受试细胞(74%)记录到对疼痛性躯体感觉刺激的单位反应,此时只有38%的细胞兴奋(p<0.005;卡方检验)。结果表明,VNAB为PVN提供兴奋性输入,去甲肾上腺素可能是造成这种效应的原因,但一种共递质(神经肽Y?)也可能是观察到的兴奋性反应的原因。高频刺激后的抑制反应可能也由(去)肾上腺素介导。(摘要截短于250字)

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