TheBulla ocular circadian pacemaker
- 1 January 1987
- journal article
- research article
- Published by Springer Nature in Journal of Comparative Physiology A
- Vol. 161 (3) , 347-354
- https://doi.org/10.1007/bf00603960
Abstract
We have used intracellular recording to directly measure the effects of three experimental agents, light, elevated potassium seawater, and lowered sodium seawater on the membrane potential of the putative circadian pacemaker neurons of theBulla eye. These agents were subsequently tested for effects on the free running period of the circadian pacemaker. We report that: When applied to the eye, light and elevated potassium seawater depolarized the putative pacemaker neurons, while lowered sodium seawater hyperpolarized them. The membrane potential changes induced by these agents are sustained for at least one hour, suggesting that they produce persistent changes in the average membrane potential of the putative pacemaker neurons. The amplitude of the membrane potential response to the depolarizing agents varies with the phase of the circadian cycle. Depolarizations induced by light and elevated potassium seawater are twice as large during the subjective night than they are during the subjective day. No significant difference was found in the response to lowered sodium seawater at different phases. Continuous application of each of these agents caused a lengthening of the free running period of theBulla eye. Constant light increased the period by 0.9 h, while the other depolarizing treatment (elevated potassium seawater) increased the free running period by 0.6 h. Both treatments increased the mean peak impulse frequency of treated eyes. The hyperpolarizing treatment also increased the period of the ocular pacemaker (+0.8 h), but had little effect on peak impulse frequency. Simultaneous chronic application of a depolarizing period lengthening treatment (constant light) and a hyperpolarizing period lengthening treatment (lowered sodium seawater) resulted in cancellation of their effects on freerunning period. In conclusion, we find that continuous application of agents which change the membrane potential of the putative circadian pacemaker neurons lengthens the free running period of theBulla ocular circadian pacemaker. We have previously reported that transient changes in membrane potential shift the phase of theBulla ocular rhythm. Thus membrane potential can influence two fundamental properties of theBulla circadian oscillator suggesting that it is an important element of the circadian oscillator mechanism.This publication has 25 references indexed in Scilit:
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