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Catecholamine secretion in trout chromaffin cells experiencing nicotinic receptor desensitization is maintained by

Brian McNeill1, Colin J Montpetit, Steve F Perry

  • 1Department of Biology, University of Ottawa, 30 Marie Curie, Ottawa, Ontario K1N 6N5, Canada.

The Journal of Experimental Biology
|October 29, 2003
PubMed

Insights

Rainbow trout chromaffin cells maintain catecholamine secretion via non-cholinergic pathways when nicotinic receptors desensitize. This study reveals alternative release mechanisms, including peptidergic pathways, are crucial for sustained secretion.

Area of Science:

  • Neuroendocrinology
  • Fish Physiology
  • Cellular Signaling

Background:

  • Chromaffin cells are key in stress response, secreting catecholamines.
  • Nicotinic receptor desensitization can impair catecholamine release.
  • Non-cholinergic pathways may compensate for compromised cholinergic signaling.

Purpose of the Study:

  • To investigate catecholamine secretion from rainbow trout Oncorhynchus mykiss chromaffin cells during nicotinic receptor desensitization.
  • To determine if non-cholinergic pathways can maintain catecholamine release under desensitized conditions.
  • To identify specific non-cholinergic pathways involved in this compensatory secretion.

Main Methods:

  • Developed an in situ model of chromaffin cell nicotinic receptor desensitization using perfused posterior cardinal vein.
  • Applied electrical stimulation at varying frequencies (1 Hz and 20 Hz) to assess secretory response.
  • Utilized receptor antagonists (hexamethonium, atropine, VIP(6-28)) and agonists (cod VIP, angiotensin II, methylcholine) to probe signaling pathways.
  • Measured catecholamine secretion in response to different stimuli under desensitized and control conditions.

Main Results:

  • Nicotinic receptor desensitization rendered cells unresponsive to high-frequency electrical stimulation.
  • Low-frequency (1 Hz) electrical stimulation maintained catecholamine secretion, unaffected by nicotinic desensitization or cholinergic blockade.
  • VPAC receptor antagonist VIP(6-28) partially reduced the 1 Hz stimulation-evoked secretion, indicating a role for peptidergic pathways.
  • Secretion evoked by cod VIP and angiotensin II was significantly enhanced in desensitized cells.
  • Muscarinic receptor agonist methylcholine did not alter secretion, suggesting distinct pathways.

Conclusions:

  • Rainbow trout chromaffin cells can maintain catecholamine secretion through non-cholinergic mechanisms during nicotinic receptor desensitization.
  • Peptidergic pathways, activated by low-frequency stimulation, are important for compensatory catecholamine release.
  • Angiotensin II and VIP signaling pathways are upregulated or more effective in desensitized chromaffin cells.
  • These findings highlight the adaptability of the chromaffin cell secretory machinery to maintain vital functions under stress.

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