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毒蕈碱受体在前庭脊髓反射增益的小脑控制中的作用:细胞机制

Role of muscarinic receptors in the cerebellar control of the vestibulospinal reflex gain: cellular mechanisms.

作者信息

Andre P, Pompeiano O, White S R

机构信息

Department of Physiology and Biochemistry, University of Pisa, Italy.

出版信息

Acta Otolaryngol Suppl. 1995;520 Pt 1:87-91. doi: 10.3109/00016489509125197.

DOI:10.3109/00016489509125197
PMID:8749088
Abstract

Most of the inhibitory Purkinje (P-) cells of the cerebellar anterior vermis fire out-of-phase with respect to the excitatory vestibulospinal neurons during roll tilt of the animal, thus exerting a positive influence on the gain of the vestibulospinal reflex (VSR). The responses of these P-cells depend on activation of glutamatergic excitatory mossy fibers-granule cells, but they are likely to be shaped by GABAergic inhibitory interneurons. The cerebellar cortex contains cholinergic fibers and both muscarinic and nicotinic receptors. In decerebrate cats intravermal injection of the muscarinic agonist bethanechol increased the VSR gain. The cellular mechanisms underlying these gain changes were studied in anesthetized Sprague-Dawley rats by microiontophoresis. Application of bethanechol (10-60 nA, 300 s) increased the response of vermal P-cells to pulses of glutamate (22/33 cells) or GABA (23/25 cells). These effects, which were blocked by the muscarinic antagonist scopolamine, lasted up to 15-40 min and occurred regardless of whether bethanecol altered the basal firing rate of the cells. We propose that the increase of P-cell responses to both excitatory and inhibitory neurotransmitters following activation of muscarinic receptors enhances the amplitude of modulation of these neurons to animal tilt, thus increasing the gain of the VSR.

摘要

在动物发生侧倾时,小脑前叶蚓部的大多数抑制性浦肯野(P-)细胞与兴奋性前庭脊髓神经元呈反相放电,从而对前庭脊髓反射(VSR)的增益产生积极影响。这些P细胞的反应依赖于谷氨酸能兴奋性苔藓纤维-颗粒细胞的激活,但它们很可能受到GABA能抑制性中间神经元的塑造。小脑皮质含有胆碱能纤维以及毒蕈碱型和烟碱型受体。在去大脑的猫中,向蚓部内注射毒蕈碱激动剂氨甲酰甲胆碱可增加VSR增益。通过微离子电泳法在麻醉的Sprague-Dawley大鼠中研究了这些增益变化的细胞机制。应用氨甲酰甲胆碱(10 - 60 nA,300 s)可增加蚓部P细胞对谷氨酸脉冲(22/33个细胞)或GABA脉冲(23/25个细胞)的反应。这些效应被毒蕈碱拮抗剂东莨菪碱阻断,持续长达15 - 40分钟,且无论氨甲酰甲胆碱是否改变细胞的基础放电率都会发生。我们提出,毒蕈碱受体激活后P细胞对兴奋性和抑制性神经递质反应的增强,提高了这些神经元对动物倾斜的调制幅度,从而增加了VSR的增益。

相似文献

1
Role of muscarinic receptors in the cerebellar control of the vestibulospinal reflex gain: cellular mechanisms.毒蕈碱受体在前庭脊髓反射增益的小脑控制中的作用:细胞机制
Acta Otolaryngol Suppl. 1995;520 Pt 1:87-91. doi: 10.3109/00016489509125197.
2
Muscarinic receptors in the cerebellar vermis modulate the gain of the vestibulospinal reflexes in decerebrate cats.小脑蚓部的毒蕈碱受体调节去大脑猫的前庭脊髓反射增益。
Arch Ital Biol. 1992 Jul;130(3):213-45.
3
Role of the spinocerebellum in adaptive gain control of cat's vestibulospinal reflex.脊髓小脑在猫前庭脊髓反射适应性增益控制中的作用。
Acta Otolaryngol Suppl. 1995;520 Pt 1:82-6. doi: 10.3109/00016489509125196.
4
Noradrenergic and cholinergic modulations of corticocerebellar activity modify the gain of vestibulospinal reflexes.去甲肾上腺素能和胆碱能对皮质小脑活动的调节会改变前庭脊髓反射的增益。
Ann N Y Acad Sci. 1992 May 22;656:519-36. doi: 10.1111/j.1749-6632.1992.tb25233.x.
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Noradrenergic influences on the cerebellar cortex: effects on vestibular reflexes under basic and adaptive conditions.去甲肾上腺素能对小脑皮质的影响:基础和适应条件下对前庭反射的作用。
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6
Depression of the vestibulospinal reflex adaptation by intravermal microinjection of GABA-A and GABA-B agonists in the cat.猫小脑蚓部微量注射GABA-A和GABA-B激动剂对前庭脊髓反射适应性的抑制作用
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7
The muscarinic agonist, bethanechol, enhances GABA-induced inhibition of Purkinje cells in the cerebellar cortex.毒蕈碱激动剂,氨甲酰甲胆碱,增强了γ-氨基丁酸(GABA)对小脑皮质浦肯野细胞的抑制作用。
Brain Res. 1994 Feb 21;637(1-2):1-9. doi: 10.1016/0006-8993(94)91210-6.
8
Activation of muscarinic receptors induces a long-lasting enhancement of Purkinje cell responses to glutamate.毒蕈碱受体的激活会诱导浦肯野细胞对谷氨酸的反应产生持久增强。
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9
Injections of beta-noradrenergic substances in the cerebellar anterior vermis of cats affect adaptation of the vestibulospinal reflex gain.向猫的小脑前叶蚓部注射β-去甲肾上腺素能物质会影响前庭脊髓反射增益的适应性。
Arch Ital Biol. 1994 Jul;132(3):117-45.
10
Nicotinic receptors in the cerebellar vermis modulate the gain of the vestibulospinal reflexes in decerebrate cats.小脑蚓部的烟碱受体调节去大脑猫的前庭脊髓反射增益。
Arch Ital Biol. 1993 Jan;131(1):1-24.