Journal of Neuroscience, Vol 9, 2462-2467, Copyright © 1989 by Society for Neuroscience
Voltage-dependent calcium channels regulate melatonin output from cultured chick pineal cells
NL Harrison and M Zatz
Laboratory of Neurophysiology, NINCDS, Bethesda, Maryland 20892.
Chick pineal cells maintained in primary culture display a circadian rhythm
of melatonin production and release, and the nocturnal increase in
melatonin output is enhanced by elevating extracellular K+. The divalent
cations, Co2+, Cd2+, and Mn2+, each reduce nocturnal melatonin output.
Nitrendipine and nifedipine also prevent the nocturnal rise in melatonin
output, while Bay K 8644 increases it, suggesting a role for
voltage-dependent Ca2+ channels in regulating melatonin output. The
whole-cell patch-clamp technique was used to record from individual chick
pineal cells. Under conditions designed to isolate currents through
voltage-dependent Ca2+ channels, biphasic inward currents are elicited by
large depolarizing commands (e.g., to 0 mV) from a holding potential of -90
mV; from a holding potential of -40 mV, only a sustained inward current is
elicited by steps to 0 mV. Both components of the inward current are
blocked by Co2+ or Cd2+. The sustained current is increased in amplitude by
Bay K 8644 and blocked by nifedipine, while the transient current is
unaffected. Since there is no evidence for vesicular release of melatonin,
the "L-type" calcium channels mediating the sustained calcium current
appear to be involved in the pathways regulating melatonin synthesis in
chick pineal cells.
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