Literature DB >> 7664817

P-type Ca2+ channels trigger stimulus-evoked [3H]acetylcholine release from mammalian motor endplates.

I Wessler1, D J Dooley, B Lohr.   

Abstract

In the present experiments it was tested whether omega-agatoxin-IVA, a peptide blocking P-type voltage-dependent Ca2+ channels, inhibits the evoked release of newly synthesized [3H]acetylcholine from the rat phrenic nerve. Release of [3H]acetylcholine was evoked by electrical stimulation of the isolated phrenic nerve (100 or 750 pulses at 5 Hz). omega-Agatoxin-IVA inhibited evoked [3H]acetylcholine release in a concentration-related manner; inhibition started at a concentration of 30 nM with complete block occurring at 500 nM. In conclusion, the present experiments demonstrate that omega-agatoxin-IVA-sensitive P-type Ca2+ channels are critically involved in the regulation of stimulus-induced transmitter release at mammalian motor endplates.

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Year:  1995        PMID： 7664817     DOI： 10.1016/0014-2999(95)00133-6

Source DB:  PubMed          Journal:  Eur J Pharmacol        ISSN： 0014-2999            Impact factor:   4.432


  3 in total

1.  Effect of subtype-specific Ca(2+)-antagonists and Ca(2+)-free media on the field stimulation-evoked release of ATP and [3H]acetylcholine from rat habenula slices.

Authors:  B Sperlágh; I András; S Vizi
Journal:  Neurochem Res       Date:  1997-08       Impact factor: 3.996

2.  Calcium channels involved in synaptic transmission at the mature and regenerating mouse neuromuscular junction.

Authors:  E Katz; P A Ferro; G Weisz; O D Uchitel
Journal:  J Physiol       Date:  1996-12-15       Impact factor: 5.182

3.  Tetanic depression is overcome by tonic adenosine A(2A) receptor facilitation of L-type Ca(2+) influx into rat motor nerve terminals.

Authors:  Laura Oliveira; M Alexandrina Timóteo; Paulo Correia-de-Sá
Journal:  J Physiol       Date:  2004-08-05       Impact factor: 5.182
  3 in total

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