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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todo:paper_00223751_v497_n3_p687_Katz2023-10-03T14:32:27Z Calcium channels involved in synaptic transmission at the mature and regenerating mouse neuromuscular junction Katz, E. Ferro, P.A. Weisz, G. Uchitel, O.D. calcium channel conotoxin nitrendipine potassium ion toxin animal tissue article calcium transport controlled study endplate potential latent period male membrane current miniature endplate potential mouse muscle reinnervation nervous system development neuromuscular synapse neurotransmitter release nonhuman presynaptic nerve priority journal synaptic transmission 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. Fil:Katz, E. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. Fil:Weisz, G. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. Fil:Uchitel, O.D. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. JOUR info:eu-repo/semantics/openAccess http://creativecommons.org/licenses/by/2.5/ar http://hdl.handle.net/20.500.12110/paper_00223751_v497_n3_p687_Katz |
institution |
Universidad de Buenos Aires |
institution_str |
I-28 |
repository_str |
R-134 |
collection |
Biblioteca Digital - Facultad de Ciencias Exactas y Naturales (UBA) |
topic |
calcium channel conotoxin nitrendipine potassium ion toxin animal tissue article calcium transport controlled study endplate potential latent period male membrane current miniature endplate potential mouse muscle reinnervation nervous system development neuromuscular synapse neurotransmitter release nonhuman presynaptic nerve priority journal synaptic transmission |
spellingShingle |
calcium channel conotoxin nitrendipine potassium ion toxin animal tissue article calcium transport controlled study endplate potential latent period male membrane current miniature endplate potential mouse muscle reinnervation nervous system development neuromuscular synapse neurotransmitter release nonhuman presynaptic nerve priority journal synaptic transmission Katz, E. Ferro, P.A. Weisz, G. Uchitel, O.D. Calcium channels involved in synaptic transmission at the mature and regenerating mouse neuromuscular junction |
topic_facet |
calcium channel conotoxin nitrendipine potassium ion toxin animal tissue article calcium transport controlled study endplate potential latent period male membrane current miniature endplate potential mouse muscle reinnervation nervous system development neuromuscular synapse neurotransmitter release nonhuman presynaptic nerve priority journal synaptic transmission |
description |
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. |
format |
JOUR |
author |
Katz, E. Ferro, P.A. Weisz, G. Uchitel, O.D. |
author_facet |
Katz, E. Ferro, P.A. Weisz, G. Uchitel, O.D. |
author_sort |
Katz, E. |
title |
Calcium channels involved in synaptic transmission at the mature and regenerating mouse neuromuscular junction |
title_short |
Calcium channels involved in synaptic transmission at the mature and regenerating mouse neuromuscular junction |
title_full |
Calcium channels involved in synaptic transmission at the mature and regenerating mouse neuromuscular junction |
title_fullStr |
Calcium channels involved in synaptic transmission at the mature and regenerating mouse neuromuscular junction |
title_full_unstemmed |
Calcium channels involved in synaptic transmission at the mature and regenerating mouse neuromuscular junction |
title_sort |
calcium channels involved in synaptic transmission at the mature and regenerating mouse neuromuscular junction |
url |
http://hdl.handle.net/20.500.12110/paper_00223751_v497_n3_p687_Katz |
work_keys_str_mv |
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_version_ |
1807317620806909952 |