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Calcium signaling in single peripheral sensory nerve terminals
Tony D Gover1, Joseph P Y Kao, Daniel Weinreich
1The Neuroscience Program, University of Maryland, Baltimore, Maryland 21201-1559, USA.
Summary
Peripheral sensory nerve terminals (PSNTs) in the cornea utilize calcium signaling (Ca2+ transients) in response to nerve impulses and chemical stimuli. This study reveals Ca2+ entry into PSNTs, including pain-sensing nociceptors.
Area of Science:
- Neuroscience
- Cell Biology
- Ophthalmology
Background:
- Peripheral sensory nerve terminals (PSNTs) have vital roles in sensation and epithelial maintenance.
- Intracellular calcium (Ca2+) is crucial for PSNT function, but its signaling in these small, inaccessible terminals remains unstudied.
Purpose of the Study:
- To investigate the role and mechanisms of Ca2+ signaling in rat corneal PSNTs.
- To determine if nerve activity and chemical stimuli evoke Ca2+ transients in PSNTs.
Main Methods:
- Epifluorescence microscopy with a Ca2+ indicator was used to measure intracellular Ca2+ levels.
- Electrical stimulation of ciliary nerves and corneal electrical field stimulation were employed.
- Pharmacological agents including lidocaine, saxitoxin (STX), diltiazem, nifedipine, and capsazepine were used to probe Ca2+ channels and receptors.
Main Results:
- Action potentials and chemical irritation induced Ca2+ transients in corneal PSNTs.
- Ca2+ transients were proportional to stimulation intensity and blocked by lidocaine, STX, and L-type Ca2+ channel antagonists.
- Capsaicin, a nociceptive agonist, evoked Ca2+ transients blocked by capsazepine but not by STX or nifedipine, indicating TRPV1 channel involvement.
Conclusions:
- Nerve impulses and chemical stimuli trigger Ca2+ entry into corneal PSNTs.
- This study provides the first evidence of Ca2+ signaling in PSNTs, including nociceptors.
- The findings highlight the importance of Ca2+ in sensory nerve terminal function in the cornea.