Literature DB >> 1382809

Effect of neurotransmitters on axoplasmic transport: acetylcholine effect on superior cervical ganglion cells.

T Takenaka1, T Kawakami, N Hikawa, Y Bandou, H Gotoh.   

Abstract

The effect of acetylcholine (ACh) on particle movements along axons of cultured superior cervical ganglion cells was analyzed with a computer-assisted video-enhanced differential interference contrast microscope system. ACh suppressed the axoplasmic transport reversibly in both anterograde and retrograde directions. A muscarinic agonist, arecoline, mimicked the ACh effect, but nicotine did not. An experiment with the Ca(2+)-indicator dye, fura-2, revealed that ACh suppressed the transport without any change of intracellular Ca2+ concentration. ACh also suppressed the axoplasmic transport in Ca(2+)-free medium. Islet-activating protein (IAP), pertussis toxin, blocked the ACh effect. These results indicate that ACh activates muscarinic receptors and suppresses fast axoplasmic transport through the activation of IAP-sensitive GTP-binding protein, irrespective of Ca2+ ions.

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Year:  1992        PMID: 1382809     DOI: 10.1016/0006-8993(92)91577-2

Source DB:  PubMed          Journal:  Brain Res        ISSN: 0006-8993            Impact factor:   3.252


  2 in total

1.  Signal transduction mechanism responsible for changes in axoplasmic transport caused by neurotransmitters.

Authors:  T Takenaka; T Kawakami
Journal:  Neurochem Res       Date:  1996-05       Impact factor: 3.996

2.  Kinesin superfamily protein 3 (KIF3) motor transports fodrin-associating vesicles important for neurite building.

Authors:  S Takeda; H Yamazaki; D H Seog; Y Kanai; S Terada; N Hirokawa
Journal:  J Cell Biol       Date:  2000-03-20       Impact factor: 10.539

  2 in total

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