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脑啡肽能系统参与黑质对下丘脑诱导的捕食攻击行为的调节。

Enkephalinergic involvement in substantia nigra in the modulation of hypothalamically-induced predatory attack behavior.

作者信息

Saha S N, Bhatia S C, Nayar U

机构信息

Department of Physiology, All India Institute of Medical Sciences, New Delhi 110 029.

出版信息

Indian J Physiol Pharmacol. 2003 Jul;47(3):311-7.

Abstract

The present study was carried out in five cats which did not attack the rats spontaneously. Predatory attack on an anaesthetized rat was elicited by electrical stimulation of lateral hypothalamus at a mean current strength of 650 microA. The attack was accompanied by minimal affective display and culminated in neck biting. Microinfusions of DAME (delta-alanine methionine enkephaline) in 500 ng dose in substantia nigra facilitated the predatory attack and there was a significant reduction in the threshold current strength for affective display as well as somatomotor components. Microinfusions of naloxone, an opioid antagonist in 1.0 microg dose when DAME effect was at its peak reversed the facilitatory effects and the threshold returned to the control levels within 10 minutes of naloxone infusion at the same locus. Microinfusions of naloxone alone in similar dosage completely blocked the predatory attack response as indicated by an increase in the threshold current strength for somatomotor as well as affective display components. The somatomotor were completely inhibited and could not be elicited even when the current strength was increased to 1000 microA. Control injections of saline in similar volumes (0.5 microl) failed to produce any response Microinfusions of naloxone in lower dose (250 ng) failed to produce any blocking effect. These findings indicate that hypothalamically elicited predatory attack is facilitated by enkephalinergic mechanisms operating at the midbrain level.

摘要

本研究在五只不会自发攻击大鼠的猫身上进行。通过以平均650微安的电流强度电刺激下丘脑外侧来引发对麻醉大鼠的捕食性攻击。这种攻击伴随着最小程度的情感表现,最终以咬颈部告终。在黑质中微量注射500纳克剂量的DAME(δ-丙氨酸甲硫氨酸脑啡肽)促进了捕食性攻击,并且情感表现以及躯体运动成分的阈值电流强度显著降低。当DAME的作用达到峰值时,以1.0微克剂量微量注射阿片类拮抗剂纳洛酮,可逆转促进作用,并且在同一部位注射纳洛酮后10分钟内阈值恢复到对照水平。单独以类似剂量微量注射纳洛酮完全阻断了捕食性攻击反应,这表现为躯体运动以及情感表现成分的阈值电流强度增加。躯体运动完全被抑制,即使电流强度增加到1000微安也无法引发。以类似体积(0.5微升)注射生理盐水作为对照未能产生任何反应。以较低剂量(250纳克)微量注射纳洛酮未能产生任何阻断作用。这些发现表明,下丘脑引发的捕食性攻击受到中脑水平的脑啡肽能机制的促进。

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