Neurotransmitter modulation of VIP release from cat cerebral cortex.
Neurotransmitter modulation of VIP release from cat cerebral cortex.
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猫大脑皮层 VIP 释放的神经递质调节。
DOI：
10.1152/ajpregu.1986.250.1.r104
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发表时间：
1986
期刊：
影响因子：
--
通讯作者：
Go,VL
中科院分区：
文献类型：
--
作者：
Wang,JY;Yaksh,TL;Harty,GJ;Go,VL
通过灌流猫大脑皮层软脑膜表面，观察了在体脑皮层血管活性肠多肽样免疫反应性（VIP LI）的释放。几种神经递质[γ-氨基丁酸（GABA），阿片类，去甲肾上腺素，乙酰胆碱，和谷氨酸盐]通过给予其受体的相应激动剂和拮抗剂来研究。虽然GABA和阿片激动剂不影响VIP-LI的静息释放，但GABA拮抗剂（印防己毒素和荷包牡丹碱）和阿片拮抗剂（纳洛酮和纳洛酮）显著增加VIP-LI的静息释放。诱发释放从皮质的VIP-LI（通过电刺激皮质或中脑网状结构）抑制GABA和μ-，但不是δ-，κ-或σ-阿片受体激动剂。谷氨酸和红藻氨酸增加大脑皮质VIP-LI的静息释放。去甲肾上腺素能神经元（α 2而非α 1）对皮层VIP-LI释放的诱发释放显示抑制作用。静息时VIP-LI释放被胆碱能药物（卡巴胆碱）增强。刺激中脑网状结构对VIP-LI释放的易化作用由阿托品证实。这些观察结果表明，特征的相互作用，反映了电路调制皮层VIP释放神经元的活动。
The cortical release of vasoactive intestinal polypeptide-like immunoreactivity (VIP-LI) in vivo was examined by superfusion of the pial surface of the cerebral cortex of the cat. The modulation of cortical VIP release by several neurotransmitters [gamma-aminobutyric acid (GABA), opioids, norepinephrine, acetylcholine, and glutamate] normally present in the cerebral cortex was studied by administering respective agonists and antagonists for their receptors. Although GABA and opiate agonists did not influence the resting release of VIP-LI, GABA antagonists (picrotoxin and bicuculline) and opiate antagonists (naloxone and naltrexone) significantly elevated the resting release. The evoked release from cortex of VIP-LI (by electrical stimulation of the cortex or mesencephalic reticular formation) was suppressed by GABA and mu- but not delta-, kappa-, or sigma-opioid receptor agonists. Glutamate and kainic acid increased the resting release of VIP-LI from the cerebral cortex. Noradrenergic (alpha 2 but not alpha 1) displayed an inhibitory effect on the evoked release of cortical VIP-LI release. Resting VIP-LI release was enhanced by cholinergic agents (carbachol). The facilitatory effects of mesencephalic reticular formation stimulation on VIP-LI release were demonstrated by atropine. These observations suggest characteristic interactions reflecting the circuitry modulating the activity of cortical VIP-releasing neurons.