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Regulation of the intracellular free calcium concentration in acutely dissociated neurones from rat nucleus basalis.

1. Neurones were acutely dissociated from the rat nucleus basalis. Whole‐cell patch clamp recordings of calcium currents (ICa) and fura‐2 microfluorimetric recordings of intracellular free Ca2+ concentration ([Ca2+]i) were made simultaneously. 2. Depolarization from ‐60 to 0 mV elicited ICa and a gradual increase in [Ca2+]i. After repolarization, ICa terminated in 0.7 ms, and [Ca2+]i recovered to control exponentially (1‐5 s). 3. Both ICa and the transient [Ca2+]i increase in response to step depolarizations, were abolished in Ca2+ free extracellular solution and in Cd(2+)‐containing solution. 4. Depolarizations from ‐90 mV to membrane potentials less negative than ‐40 mV induced ICa and an increase in [Ca2+]i. Depolarization to 0 mV elicited the maximum ICa, and produced the largest increase in [Ca2+]i. There was a parallel relationship between the [Ca2+]i increase and the magnitude of the ICa. 5. The [Ca2+]i increase was associated with an increase in total Ca2+ influx when the duration of the step depolarization was varied. The relationship between the total Ca2+ influx and the peak of [Ca2+]i transient reached an asymptote as total Ca2+ influx exceeded 200 pC. A similar finding was made when more than thirty action potentials were used in increasing [Ca2+]i. 6. The process of the [Ca2+]i recovery was slowed down by lowering the temperature, by an intracellular dialysis with vanadate, by extracellular application of a mitochondrial inhibitor, carbonyl cyanide m‐chlorophenyl‐hydrazone (CCCP), and by Na(+)‐free external solution. It was unaffected by membrane potential (‐50 to ‐130 mV). 7. When pipette solution contained a high concentration of fura‐2 (200 microM), the [Ca2+]i increase per 1 pC of Ca2+ influx decreased, and the [Ca2+]i recovery was slowed. 8. The results indicate that the ICa through voltage‐dependent Ca2+ channels elevates [Ca2+]i. The neurones possess a large capacity for Ca2+ buffering, and the recovery of [Ca2+]i requires both the Ca2+ pump and membrane Na(+)‐Ca2+ exchange.