da Silva Luis Felipe Souza, Menescal-de-Oliveira Leda
Department of Physiology, Faculty of Medicine of Ribeirão Preto, University of São Paulo, 14049-900 Ribeirão Preto, SP, Brazil.
Brain Res Bull. 2007 Apr 2;72(1):25-31. doi: 10.1016/j.brainresbull.2006.12.005. Epub 2007 Jan 12.
Tonic immobility (TI) is an inborn defensive behavior characterized by a temporary state of profound and reversible motor inhibition elicited by some forms of physical restraint. Previous results from our laboratory have demonstrated that nucleus raphe magnus (NRM) is also a structure involved in the modulation of TI behavior, as chemical stimulation through carbachol decreases the duration of TI in guinea pigs. In view of the fact that GABAergic and opioidergic circuits participate in the regulation of neuronal activity in the NRM and since these neurotransmitters are also involved in the modulation of TI, the objective of the present study was to evaluate the role of these circuits of the NRM in the modulation of the behavioral TI response. Microinjection of morphine (4.4 nmol/0.2 microl) or bicuculline (0.4 nmol/0.2 microl) into the NRM increased the duration of TI episodes while muscimol (0.5 nmol/0.2 microl) decreased it. The effect of morphine injection into the NRM was blocked by previous microinjection of naloxone (2.7 nmol/0.2 microl). Muscimol at 0.25 nmol did not produce any change in TI duration; however, it blocked the increased response induced by morphine. Our results indicate a facilitatory role of opioidergic neurotransmission in the modulation of the TI response within the NRM, whereas GABAergic activity plays an inhibitory role. In addition, in the present study the modulation of TI in the NRM possibly occurred via an interaction between opioidergic and GABAergic systems, where the opioidergic effect might be due to inhibition of tonically active GABAergic interneurons.
紧张性不动(TI)是一种先天性防御行为,其特征是由某些形式的身体约束引发的深度且可逆的运动抑制的暂时状态。我们实验室之前的结果表明,中缝大核(NRM)也是参与调节TI行为的一个结构,因为通过卡巴胆碱进行化学刺激可缩短豚鼠的TI持续时间。鉴于GABA能和阿片样物质能回路参与NRM中神经元活动的调节,并且由于这些神经递质也参与TI的调节,本研究的目的是评估NRM的这些回路在调节行为TI反应中的作用。向NRM微量注射吗啡(4.4 nmol/0.2微升)或荷包牡丹碱(0.4 nmol/0.2微升)会增加TI发作的持续时间,而注射蝇蕈醇(0.5 nmol/0.2微升)则会缩短其持续时间。预先向NRM微量注射纳洛酮(2.7 nmol/0.2微升)可阻断向NRM注射吗啡的作用。0.25 nmol的蝇蕈醇不会使TI持续时间产生任何变化;然而,它可阻断吗啡诱导的反应增强。我们的结果表明,阿片样物质能神经传递在调节NRM内的TI反应中起促进作用,而GABA能活动起抑制作用。此外,在本研究中,NRM中TI的调节可能是通过阿片样物质能和GABA能系统之间的相互作用发生的,其中阿片样物质能效应可能是由于抑制了持续活动的GABA能中间神经元。