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弱电鱼裸背电鳗社会交流中起搏器调制的控制

The control of pacemaker modulations for social communication in the weakly electric fish Sternopygus.

作者信息

Keller C H, Kawasaki M, Heiligenberg W

机构信息

Institute of Neuroscience, University of Oregon, Eugene 97403.

出版信息

J Comp Physiol A. 1991 Oct;169(4):441-50. doi: 10.1007/BF00197656.

Abstract

Nearly sinusoidal electric organ discharges (EODs) of the weakly electric fish Sternopygus, occur at a regular rate within a range from 50 to 200 Hz and are commanded by a medullary pacemaker nucleus (Pn). During courtship and aggression, the rate of EODs is modulated as smooth EOD-frequency rises or brief EOD-interruptions (Hopkins 1974b). The present study examines the control of such modulations. Rises were elicited by L-glutamate stimulation of the diencephalic prepacemaker nucleus, the only previously known source of input to the Pn. We demonstrate an additional input to the Pn, the sublemniscal prepacemaker nucleus (SPPn). L-glutamate stimulation of this area caused EOD-interruptions. The Pn contains electrotonically coupled 'pacemaker cells' which generate the rhythm of the EODs, as well as 'relay cells' which transmit the command pulse to the spinal motor neurons that innervate the electric organ. Pacemaker cells recorded intracellularly during EOD-interruptions continued firing at their regular frequency but with slightly increased jitter. Relay cells, on the other hand, were strongly depolarized and fired spikelets at a greatly increased frequency during EOD-interruptions. Thus EOD-interruptions were caused by SPPn input to relay cells that caused their massive depolarization, blocking the normal input from pacemaker cells without greatly affecting pacemaker cell firing characteristics. Application to the Pn of an antagonist to NMDA-type glutamate receptors blocked EOD-frequency rises and EOD-interruptions. Antagonists to quisqualate/kainate receptor-types were ineffective.

摘要

弱电鱼线翎电鳗的电器官放电(EOD)几乎呈正弦波,在50至200赫兹的范围内以固定频率发生,并由延髓起搏器核(Pn)控制。在求偶和攻击过程中,EOD的频率会随着EOD频率的平稳上升或短暂的EOD中断而受到调制(霍普金斯,1974b)。本研究探讨了这种调制的控制机制。通过对间脑前起搏器核进行L-谷氨酸刺激引发频率上升,间脑前起搏器核是之前已知的唯一向Pn输入信号的来源。我们发现了Pn的另一个输入源,即亚丘脑前起搏器核(SPPn)。对该区域进行L-谷氨酸刺激会导致EOD中断。Pn包含电突触耦合的“起搏器细胞”,它们产生EOD的节律,以及“中继细胞”,这些中继细胞将指令脉冲传递给支配电器官的脊髓运动神经元。在EOD中断期间进行细胞内记录时,起搏器细胞继续以其正常频率放电,但抖动略有增加。另一方面,中继细胞在EOD中断期间强烈去极化,并以大幅增加的频率发放小尖峰。因此,EOD中断是由SPPn对中继细胞的输入引起的,这导致中继细胞大量去极化,阻断了起搏器细胞的正常输入,而对起搏器细胞的放电特性影响不大。将NMDA型谷氨酸受体拮抗剂应用于Pn可阻断EOD频率上升和EOD中断。quisqualate/kainate受体类型的拮抗剂则无效。

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