Loading…
Nitric oxide-containing neurons in the nervous ganglia of Helix aspersa during rest and activity: Immunocytochemical and enzyme histochemical detection
Nitric oxide synthase (NOS) immunoreactivity and staining for nicotinamide adenine dinucleotide phosphate‐diaphorase (NADPH‐diaphorase) activity are two cytochemical markers for nitric oxide (NO)‐containing neurons. The authors examined the changes in the distribution of NOS immunolabeling and NADPH...
Saved in:
Published in: | Journal of comparative neurology (1911) 1999-06, Vol.409 (2), p.274-284 |
---|---|
Main Authors: | , , , , , |
Format: | Article |
Language: | English |
Subjects: | |
Online Access: | Get full text |
Tags: |
Add Tag
No Tags, Be the first to tag this record!
|
Summary: | Nitric oxide synthase (NOS) immunoreactivity and staining for nicotinamide adenine dinucleotide phosphate‐diaphorase (NADPH‐diaphorase) activity are two cytochemical markers for nitric oxide (NO)‐containing neurons. The authors examined the changes in the distribution of NOS immunolabeling and NADPH‐diaphorase reactivity in the cerebral and buccal ganglia of the terrestrial snail Helix aspersa during resting and active phases. During inactivity and after 1 day of activity, in the mesocerebrum and metacerebrum of the snails, there were several reactive neurons for both markers; after 7 days of activity, the number of reactive neurons was lower. Opposite results were obtained in the buccal ganglia, in which increased staining and numbers of reactive neurons were present in the active snails (after 1 day and 7 days of activity). Although the staining patterns for the two reactions were similar, colocalization was not always observed. The comparison between inactive and active animals provided a more precise survey of NOS‐containing neurons in the snail cerebral ganglia than previously described. Moreover, it suggested that not only is NO involved in distinct nervous circuits, but, as a ubiquitous molecule, it also plays a role in neuroprotection and neuropeptide release. J. Comp. Neurol. 409:274–284, 1999. © 1999 Wiley‐Liss, Inc. |
---|---|
ISSN: | 0021-9967 1096-9861 |
DOI: | 10.1002/(SICI)1096-9861(19990628)409:2<274::AID-CNE8>3.0.CO;2-E |