Abstract
Melatonin production by isolated pineal glands from guinea pigs was examined under conditions that affect membrane potential or the firing of action potential-like spikes. In glands from superior cervical ganglionectomized animals, depolarization resulting from increasing extracellular potassium concentration to 100 mM did not initiate melatonin production, and it delayed the response to the β-adrenoceptor agonist orciprenaline. In glands from intact animals, melatonin production was initiated by exposure to 100 mM potassium with a time-course similar to the response to orciprenaline. A proportion of this response was propanol resistant, suggesting that the normal control of melatonin production may involve a neurotransmitter in addition to norepinephrine. Exposure to verapamil or nifedipine, or removal of extracellular calcium, previously shown to eliminate action potential-like spikes, did not substantially affect the increase in melatonin production induced by orciprenaline. Phenylephrine, which stimulates spiking, produced only a slight increase in melatonin production. It is concluded that the depolarization and the spiking are not closely related to the stimulation of melatonin production, but may relate principally to the secretion of a substance other than melatonin.
| Original language | English |
|---|---|
| Pages (from-to) | 80-90 |
| Number of pages | 11 |
| Journal | Journal of Pineal Research |
| Volume | 21 |
| Issue number | 2 |
| DOIs | |
| Publication status | Published - 1 Jan 1996 |
Keywords
- Action potential-like spikes
- Calcium entry
- Depolarization
- Melatonin production
- β-adrenoceptor agonist
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