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Nitric oxide synthesis is blocked in the enteral nervous system during dormant periods of the snail<Emphasis Type="Italic"> Helix lucorum</Emphasis>
Authors:Email author" target="_blank">Tamás?R?szerEmail author  Zsolt?Czimmerer  A?József?Szentmiklósi  Gáspár?Bánfalvi
Institution:(1) Workgroup of Neurochemistry, Department of Animal Anatomy and Physiology, Faculty of Science, Debrecen University, 4010 Debrecen, Hungary;(2) Department of Pharmacology and Pharmacotherapy, Medical and Health Science Center, Debrecen University, 4028 Debrecen, Hungary;(3) Department of Animal Anatomy and Physiology, Faculty of Science, Debrecen University, PO Box 15, 4010 Debrecen , Hungary
Abstract:During dormancy of terrestrial snails, the whole neuromodulation of the nervous system is deeply modified. In this work we studied the adaptation of a previously described, putatively nitric oxide (NO) forming enteral network to the long-term resting periods of the snail Helix lucorum. The standard NADPH diaphorase (NADPHd) technique, which is an accepted method for histochemical NO synthase (NOS) detection, labeled the same enteric neurons of the midintestine in active or hibernated snails. Quantification of the NO-derived nitrite by the Griess reaction established that the nitrite formation is confined to the NADPHd-reactive network containing the midintestinal segment. In active snails, the nitrite formation could be enhanced by the NOS substrate l-arginine (10 mgrM–1 mM), but decreased by the known NOS inhibitors 1 mM Nohgr-nitro-l-arginine (NOARG) and 10 mM aminoguanidine (AG). Application of 1 mM l-arginine and 1 mM NOARG decreased the amplitude of the midintestinal muscle contractile activity, but did not affect the rectal motility. In dormancy, the nitrite formation was reduced in the NADPHd-reactive midintestinal network. Application of l-arginine could not provoke nitrite production and did not influence the midintestinal motility. Our findings indicate that NO is involved in the neural transmission to intestinal muscles of gastropods, but enteric release of NO is blocked during dormancy. The decreased NO synthesis is possibly due to an as yet undefined mechanism, by which the l-arginine/NO conversion ability of NOS could temporarily be inhibited in the long-term resting period of H. lucorum.T. Röszer and Zs. Czimmerer contributed equally to this work as lead authors. This research was supported by OTKA grant no. T42762 (G.B.) and PRCH Student Science Foundation grants 2000, 2002 (T.R.) and 2003 (Zs. Cz). The study is dedicated to Borbála Vecsei-Czimmerer, Elemér Czimmerer, Ágnes M. Fodor-Röszer and József S. Röszer.
Keywords:NADPH diaphorase  Nitric oxide synthase  Hibernation  Estivation  Enteric nervous system  Helix lucorum L  (Mollusca)
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