Calcium channels involved in synaptic transmission at the mature and regenerating mouse neuromuscular junction
1. The involvement of the different types of voltage-dependent calcium channels (VDCCs) in synaptic transmission at the mature and newly formed mammalian neuromuscular junction was studied by evaluating the effects of L-, P/Q- and N-type VDCC antagonists on transmitter release in normal and reinnerv...
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| Autores principales: | , , , |
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| Formato: | JOUR |
| Materias: | |
| Acceso en línea: | http://hdl.handle.net/20.500.12110/paper_00223751_v497_n3_p687_Katz |
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| Sumario: | 1. The involvement of the different types of voltage-dependent calcium channels (VDCCs) in synaptic transmission at the mature and newly formed mammalian neuromuscular junction was studied by evaluating the effects of L-, P/Q- and N-type VDCC antagonists on transmitter release in normal and reinnervating levator auris preparations of adult mice. 2. Nerve-evoked transmitter release was blocked by ω-agatoxin IVA (ω-AgaIVA), a P/Q-type VDCC blocker, both in normal and reinnervating endplates (100 nM ω-AgaIVA caused > 90% inhibition). The N-type VDCC antagonist ω-conotoxin GVIA (ω-CgTX; 1 and 5 μM), as occurs in normal preparations, did not significantly affect this type of release during reinnervation. Nitrendipine (1-10 μM), an L-type VDCC blocker, strongly antagonized release in reinnervating muscles (~ 40-60% blockade) and lacked any effect in normal preparations. 3. In reinnervating muscles, spontaneous release was not dependent on Ca2+ entry through either P- or L-type VDCCs. Neither 100 nM ω-AgaIVA nor 10 μM nitrendipine affected the miniature endplate potential (MEPP) frequency or amplitude. 4. At the newly formed endplates, K+-evoked release was dependent on Ca2+ entry through VDCCs of the P-type family (100 nM ω-AgaIVA reduced ~ 70% of the K+-evoked MEPP frequency). L-type VDCCs were found not to participate in this type of release (10 μM nitrendipine lacked any effect). 5. In reinnervating muscles, the L-type VDCC blocker, nitrendipine (10 μM), provoked a significant increase (~ 25%) in the latency of the evoked endplate potential (EPP). This drug also caused an increase (~ 0.3 ms) in the latency of the presynaptic currents. The P/Q- and N-type VDCC) blockers did not affect the latency of the EPP. 6. These results show that at newly formed mouse neuromuscular junctions, as occurs in mature preparations, VDCCs of the P-type family play a prominent role in evoked transmitter release whereas N-type channels are not involved in this process. In addition, signal conduction and transmitter release become highly sensitive to nitrendipine during reinnervation. This suggests that L-type VDCCs may play a role in synaptic transmission at the immature mammalian neuromuscular junction. |
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