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Calcium-dependent depolarizations originating in lizard motor nerve terminals
1Department of Physiology and Biophysics, University of Miami School of Medicine, Florida 33101.
Summary
Motor nerve terminal afterpotentials are calcium-dependent, influenced by calcium influx and sensitive to dihydropyridines. These findings shed light on calcium channel function in nerve terminals.
Area of Science:
- Neuroscience
- Neurophysiology
- Molecular Biology
Background:
- Motor axons innervate multiple muscle terminals.
- Action potentials are followed by afterpotentials in motor axons.
Purpose of the Study:
- To investigate the nature and ionic basis of Ca-dependent afterpotentials in motor nerve terminals.
- To explore the role of calcium influx and specific calcium channels in these afterpotentials.
Main Methods:
- Microelectrode recordings of action potentials and afterpotentials in lizard motor axons.
- Intra-axonal injection of Lucifer yellow dye to map terminal innervation.
- Pharmacological manipulation using tetraethylammonium (TEA), omega-conotoxin, Cd, Mn, tetrodotoxin, Bay K 8644, nimodipine, and nitrendipine.
Main Results:
- Depolarizing afterpotentials in motor nerve terminals are Ca-dependent.
- These afterpotentials are abolished by calcium channel blockers and restored by calcium perfusion near terminals.
- Dihydropyridines like Bay K 8644 and nimodipine modulate afterpotential components, suggesting sensitivity of terminal calcium channels.
Conclusions:
- Intra-axonally recorded Ca-dependent afterpotentials result from electrotonic spread of terminal calcium influx.
- Specific motor nerve terminal calcium channels exhibit sensitivity to dihydropyridine drugs.