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Calcium channels involved in synaptic transmission at the mature and regenerating mouse neuromuscular junction.
Author(s) -
Katz E,
Ferro P A,
Weisz G,
Uchitel O D
Publication year - 1996
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.1996.sp021800
Subject(s) - nitrendipine , neuromuscular transmission , chemistry , neuromuscular junction , voltage dependent calcium channel , neurotransmission , motor nerve , pharmacology , calcium , medicine , neuroscience , receptor , anatomy , biology , biochemistry , organic chemistry
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 omega‐agatoxin IVA (omega‐AgaIVA), a P/Q‐type VDCC blocker, both in normal and reinnervating endplates (100 nM omega‐AgaIVA caused > 90% inhibition). The N‐type VDCC antagonist omega‐conotoxin GVIA (omega‐CgTX; 1 and 5 microM), as occurs in normal preparations, did not significantly affect this type of release during reinnervation. Nitrendipine (1‐10 microM), an L‐type VDCC blocker, strongly antagonized release in reinnervating muscles (approximately 40‐69% 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 omega‐AgaIVA nor 10 microM 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 omega‐AgaIVA reduced approximately 70% of the K(+)‐evoked MEPP frequency). L‐type VDCCs were found not to participate in this type of release (10 microM nitrendipine lacked any effect). 5. In reinnervating muscles, the L‐type VDCC blocker, nitrendipine (10 microM), provoked a significant increase (approximately 25%) in the latency of the evoked endplate potential (EPP). This drug also caused an increase (approximately 0.3 ms) in the latency of the presynaptic currents. The P/Q‐ and Ny‐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.