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血管加压素对大鼠舌下运动神经元的作用:突触前和突触后效应。

Action of vasopressin on hypoglossal motoneurones of the rat: presynaptic and postsynaptic effects.

作者信息

Palouzier-Paulignan B, Dubois-Dauphin M, Tribollet E, Dreifuss J J, Raggenbass M

机构信息

Department of Physiology, University Medical Center, Geneva, Switzerland.

出版信息

Brain Res. 1994 Jul 4;650(1):117-26. doi: 10.1016/0006-8993(94)90213-5.

Abstract

The distribution of vasopressin binding sites in the hypoglossal nucleus of newborn rats was determined using autoradiography on film and a radioiodinated vasopressor antagonist. These sites predominated in the ventromedial and dorsal divisions of the nucleus. The effect of vasopressin on hypoglossal neurones was studied in brainstem slices of newborn animals, using the single-electrode voltage-clamp technique. Vasopressin, at 0.1-0.5 microM, generated a sustained inward current in a majority of neurones, an action which was mediated by V1-type receptors. Antidromic activation or morphological characterization of biocytin-labelled neurones indicate that part of the vasopressin-sensitive cells were motoneurones. When synaptic transmission was blocked by perfusing the preparation with a low-calcium/high-magnesium solution, the average vasopressin current decreased by 65%; and following TTX treatment, the peptide current decreased by 55%. In contrast, in a low-calcium solution, i.e., under conditions of reduced synaptic transmission but of increased neuronal excitability, the vasopressin current was not significantly altered. These results may be interpreted by assuming that the action of vasopressin is in part postsynaptic and in part presynaptic, the latter effect probably depending upon action potential propagation. Current-voltage relations suggest that the postsynaptic effect of vasopressin was due to the induction of a non-inactivating inward current, reversing in polarity at around -15 mV. The data raise the possibility that, in young animals, endogenous vasopressin may modulate the activity of hypoglossal motoneurones.

摘要

利用胶片放射自显影技术和放射性碘化血管加压素拮抗剂,测定了新生大鼠舌下神经核中血管加压素结合位点的分布。这些位点在该神经核的腹内侧和背侧区域占主导地位。采用单电极电压钳技术,在新生动物的脑干切片中研究了血管加压素对舌下神经元的作用。0.1 - 0.5微摩尔的血管加压素在大多数神经元中产生持续的内向电流,这一作用由V1型受体介导。生物胞素标记神经元的逆向激活或形态学特征表明,部分对血管加压素敏感的细胞是运动神经元。当用低钙/高镁溶液灌注标本阻断突触传递时,血管加压素平均电流降低了65%;用河豚毒素处理后,肽电流降低了55%。相反,在低钙溶液中,即在突触传递减少但神经元兴奋性增加的条件下,血管加压素电流没有明显改变。这些结果可以解释为,血管加压素的作用部分是突触后作用,部分是突触前作用,后者的作用可能取决于动作电位的传播。电流-电压关系表明,血管加压素的突触后作用是由于诱导了一种非失活的内向电流,其极性在约-15 mV处反转。这些数据增加了一种可能性,即在幼小动物中,内源性血管加压素可能调节舌下运动神经元的活动。

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