Teixeira Duarte Terence, Hoffmann Anette, de Souza Fim Pereira Aparecida, Aparecida Lopes Corrêa Sônia
Department of Physiology, School of Medicine, University of São Paulo, Av. Bandeirantes 3900, 14049-900, Ribeirão Preto, SP, Brazil.
Brain Res. 2006 May 30;1092(1):117-28. doi: 10.1016/j.brainres.2006.03.082. Epub 2006 May 11.
The purpose of this study is to examine the pathways involved in the electromotor (electric organ discharge interruptions) and skeletomotor responses (defense-like) observed by blockade of GABAergic control of the torus semicircularis dorsalis (TSd) of the awake weakly electric fish Gymnotus carapo, described in a former study. Microinjection of NMDA (5 mM) into the pacemaker nucleus (PM) through a guide cannula previously implanted caused a prolonged interruption of the electric organ discharge (EOD) intermingled with reduction in frequency, similar to that described for TSd GABA(A) blockade, but without noticeable skeletomotor effects. The EOD alterations elicited by bicuculline microinjections (0.245 mM) into the TSd could be blocked or attenuated by a previous microinjection of AP-5 (0.5 mM), an NMDA antagonist, into the PM. Labeled terminals are found in the nucleus electrosensorius (nE) after injection of the biotinylated dextran amine (BDA) tracer into the TSd and into the sublemniscal prepacemaker nucleus (SPPn) subsequent to the tracer injection into the nE. Defense-like responses but not EOD interruptions are observed after microinjections of NMDA (5 mM) into the rhombencephalic reticular formation (RF), where labeled terminals are seen after BDA injection into the TSd and somata are filled after injection of the tracer into the spinal cord. In this last structure, marked fibers are seen subsequent to injection of BDA into the RF. These results suggest that two distinct pathways originate from the torus: one for EOD control, reaching PM through nE and SPPn, and the other one for skeletomotor control reaching premotor reticular neurons. Both paths could be activated by toral GABA(A) blockade.
本研究的目的是探究在前一项研究中所描述的，通过阻断清醒弱电鱼裸背电鳗背侧半规管（TSd）的GABA能控制所观察到的电动（电器官放电中断）和骨骼运动反应（防御样）所涉及的途径。通过先前植入的引导套管将NMDA（5 mM）微量注射到起搏器核（PM）中，导致电器官放电（EOD）长时间中断，并伴有频率降低，这与TSd GABA(A)阻断所描述的情况相似，但没有明显的骨骼运动效应。向TSd微量注射荷包牡丹碱（0.245 mM）所引发的EOD改变，可以通过先前向PM微量注射NMDA拮抗剂AP-5（0.5 mM）来阻断或减弱。在将生物素化葡聚糖胺（BDA）示踪剂注射到TSd中，以及在将示踪剂注射到电感觉核（nE）后再注射到次丘脑前起搏器核（SPPn）中之后，在电感觉核中发现了标记的终末。向菱脑网状结构（RF）微量注射NMDA（5 mM）后，观察到防御样反应，但未观察到EOD中断，在将BDA注射到TSd后，在RF中可见标记的终末，在将示踪剂注射到脊髓后，可见神经元胞体被填充。在最后一个结构中，向RF注射BDA后可见明显的纤维。这些结果表明，有两条不同的途径起源于半规管：一条用于EOD控制，通过nE和SPPn到达PM，另一条用于骨骼运动控制，到达运动前网状神经元。两条途径都可被半规管GABA(A)阻断激活。
