Ca2+ channels and synaptic transmission at the adult, neonatal, and P/Q-type deficient neuromuscular junction
Different types of voltage-activated Ca2+ channels have been established based on their molecular structure and pharmacological and biophysical properties. One of them, the P/Q-type, is the main channel involved in nerve-evoked neurotransmitter release at neuromuscular junctions and the immunologica...
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| Autores principales: | , , , |
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| Publicado: |
2003
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| Acceso en línea: | https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_00778923_v998_n_p11_Nudler http://hdl.handle.net/20.500.12110/paper_00778923_v998_n_p11_Nudler |
| Aporte de: |
| Sumario: | Different types of voltage-activated Ca2+ channels have been established based on their molecular structure and pharmacological and biophysical properties. One of them, the P/Q-type, is the main channel involved in nerve-evoked neurotransmitter release at neuromuscular junctions and the immunological target in Eaton-Lambert Syndrome. At adult neuromuscular junctions, L- and N-type Ca2+ channels become involved in transmitter release only under certain experimental or pathological conditions. In contrast, at neonatal rat neuromuscular junctions, nerve-evoked synaptic transmission depends jointly on both N- and P/Q-type channels. Synaptic transmission at neuromuscular junctions of the ataxic P/Q-type Ca2+ channel knockout mice is also dependent on two different types of channels, N- and R-type. At both neonatal and P/Q knockout junctions, the K +-evoked increase in miniature endplate potential frequency was not affected by N-type channel blockers, but strongly reduced by both P/Q- and R-type channel blockers. These differences could be accounted for by a differential location of the channels at the release site, being either P/Q- or R-type Ca2+ channels located closer to the release site than N-type Ca2+ channels. Thus, Ca2+ channels may be recruited to mediate neurotransmitter release where P/Q-type channels seem to be the most suited type of Ca2+ channel to mediate exocytosis at neuromuscular junctions. |
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