The regulation of chloride homeostasis in the small nonspiking visual interneurons of the fly compound eye.

1. We have used intracellular recordings and ionophoretic injections in vivo to investigate the ion exchange mechanisms responsible for the maintenance of the ion gradients in the large monopolar cells (LMCs) of the first optic ganglion of the blowfly, Calliphora vicinia. 2. Ionophoretic chloride injections caused a rapid approximately 20-mV depolarization of the resting potential (Erp) and abolished or even reversed the light-ON response (OR), which is caused by histamine-gated chloride conductance, as the chloride equilibrium potential (ECl) was increased beyond the Erp, i.e., 50 mV upward. Ionophoretic sodium injections were found to mimic the action of the ionophoretic chloride injections and thus also to cause chloride accumulation inside the cell. 3. Ionophoretic injections of bicarbonate only had the effect of hyperpolarizing the Erp by 5-15 mV for 1-25 s, but chloride gradient, i.e., ECl remained unchanged. Intracellular proton load caused depolarization of the Erp by 15 +/- 5 mV (mean +/- SE) for 20-25 s and a slight 15 +/- 5-mV decrease of the peak OR. Ionophoretic injections of potassium, acetate, and furosemide failed to cause any physiological effect. 4. The time constant for the recovery of the peak OR after sodium load increased linearly as a function of injected charge whereby the time constant for the recovery after chloride accumulation increased slowly up to 50 nC of injected charge, after which it increased rapidly, possibly indicating substrate inhibition. The time constant for the recovery of peak OR after sodium load was from 5 to 65 nC greater than that of chloride.(ABSTRACT TRUNCATED AT 250 WORDS)