Feng A S, Bullock T H
J Neurobiol. 1978 Jul;9(4):255-66. doi: 10.1002/neu.480090403.
Intracellular recordings were made from pacemaker-command cells of the electric organ discharge (EOD) of the weakly electric fish Eigenmannia virescens. The fish was immobilized with gallamine triethiodide (Flaxedil) which silenced the EOD. A simulated EOD of this fish (ca. 300 Hz) and a sine wave simulating a neighbor, a few Hz higher (+deltaF) or lower (-deltaF) were introduced into the bath to elicit the "jamming avoidance response" (JAR), monitored through the pacemaker potential. We observed that accompanying the JAR there is a minute hyperpolarizing postsynaptic potential (hpsp) superimposed on the pacemaker potential. A shift in the phase of the hpsp occurs with a change in the sign of deltaF, and therefore of the JAR. Assuming that the behaviorally correlated hpsp is inhibitory, it suggests that mutual inhibition may play a role in regulating the synchronous firing frequency of command neurons, which are electrically coupled with one-another. Scheich and Bullock (1974) proposed a neuronal scheme for the JAR in which they suggest that two systems (P and T) operate together in the nervous system. The T system affects the pacemaker cells at a precise, variable phase of the pacemaker cycle. Although the present results indeed reveal a shift in the hpsp with a change in the sign of deltaF, the actual significance of this shift remains to be evaluated. The unexpected direction of the shift suggests either that the hpsp is excitatory at the phases when it occurs, or that effectiveness of inhibition decreases at later phases in this case instead of increasing as in other cases, or that the hpsp opposes the JAR. The parallel P system is probably more important in explaining the JAR, acting by a DC level control rather than a phase control.
对弱电鱼艾氏电鳗(Eigenmannia virescens)电器官放电(EOD)的起搏器指令细胞进行了细胞内记录。用三碘季铵酚(加拉明,Flaxedil)使鱼固定,该药物可使EOD沉默。将这种鱼的模拟EOD(约300Hz)以及模拟频率比其高几赫兹(+δF)或低几赫兹(-δF)的邻居的正弦波引入浴槽中,以引发“干扰回避反应”(JAR),通过起搏器电位进行监测。我们观察到,伴随JAR出现的是叠加在起搏器电位上的微小超极化突触后电位(hpsp)。hpsp的相位会随着δF符号的变化而变化,进而JAR也会改变。假设与行为相关的hpsp具有抑制作用,这表明相互抑制可能在调节彼此电耦合的指令神经元的同步放电频率中发挥作用。谢希和布洛克(Scheich和Bullock,1974)提出了一种用于JAR的神经元模式,他们认为在神经系统中有两个系统(P和T)共同运作。T系统在起搏器周期的精确、可变相位影响起搏器细胞。尽管目前的结果确实揭示了hpsp会随着δF符号的变化而发生相位变化,但这种变化的实际意义仍有待评估。这种变化的意外方向表明,要么hpsp在其出现的相位是兴奋性的,要么在这种情况下抑制作用的有效性在后期阶段会降低而不是像其他情况那样增加,要么hpsp与JAR相反。并行的P系统可能在解释JAR方面更为重要,它通过直流电平控制而非相位控制起作用。