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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

Nitric oxide synthesis is blocked in the enteral nervous system during dormant periods of the snail Helix lucorum.

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 microM-1 mM), but decreased by the known NOS inhibitors 1 mM N(omega)-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.[1]


  1. Nitric oxide synthesis is blocked in the enteral nervous system during dormant periods of the snail Helix lucorum. Röszer, T., Czimmerer, Z., Szentmiklósi, A.J., Bánfalvi, G. Cell Tissue Res. (2004) [Pubmed]
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