The NO‐cGMP pathway in the rat locus coeruleus: electrophysiological, immunohistochemical and in situ hybridization studies
Identifieur interne : 000E60 ( Main/Exploration ); précédent : 000E59; suivant : 000E61The NO‐cGMP pathway in the rat locus coeruleus: electrophysiological, immunohistochemical and in situ hybridization studies
Auteurs : Zhi-Qing David Xu [Pays-Bas] ; Jan De Vente [Pays-Bas] ; Harry Steinbusch [Pays-Bas] ; Sten Grillner [Pays-Bas] ; Tomas Hökfelt [Pays-Bas]Source :
- European Journal of Neuroscience [ 0953-816X ] ; 1998-11.
English descriptors
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Abstract
The effect of two nitric oxide (NO) donors, SIN‐1 and DEA/NO, as well as of the inactive SIN‐1 derivative molsidomin, was studied on locus coeruleus (LC) neurons in a slice preparation using intracellular recordings. In addition, the effect of the guanylate cyclase inhibitor ODQ was analysed. Furthermore, the effect of NO donors on cyclic guanosine monophosphate (GMP) levels in the LC was studied using the indirect immunofluorescence technique, and the expression of soluble guanylyl cyclase with in situ hybridization. In 36 of 66 LC neurons extracellular application of SIN‐1 and DEA/NO caused a hyperpolarization and a decrease in apparent input resistance. In almost 20% of neurons SIN‐1 increased the firing rate. No effect could be recorded with the brain‐inactive SIN‐1 derivative molsidomin. The membrane permeable cGMP analogue 8‐bromo‐cGMP imitated the action of SIN‐1. The hyperpolarizing effect of SIN‐1 and DEA/NO was attenuated by preincubation with the guanylyl cyclase inhibitor ODQ. The immunohistochemical analysis revealed lack of cGMP immunostaining in non‐stimulated slices, whereas SIN‐1 dramatically increased this staining in about 40% of the LC neurons, and these neurons were all tyrosine hydroxylase positive, that is noradrenergic. A large proportion of the LC neurons expressed soluble guanylyl cyclase mRNA. The present and previous results suggest that NO, released from a small number of non‐noradrenergic neurons in the LC, mainly has an inhibitory influence on many noradrenergic neurons, by upregulating cGMP levels via stimulation of soluble guanylyl cyclase. As nitric oxide synthase is present only in a small number of non‐noradrenergic neurons ( Xu et al. 1994 ), a few neurons may influence a large population of noradrenergic LC neurons, which in turn may control activity in many regions of the central nervous system.
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DOI: 10.1046/j.1460-9568.1998.00359.x
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In addition, the effect of the guanylate cyclase inhibitor ODQ was analysed. Furthermore, the effect of NO donors on cyclic guanosine monophosphate (GMP) levels in the LC was studied using the indirect immunofluorescence technique, and the expression of soluble guanylyl cyclase with in situ hybridization. In 36 of 66 LC neurons extracellular application of SIN‐1 and DEA/NO caused a hyperpolarization and a decrease in apparent input resistance. In almost 20% of neurons SIN‐1 increased the firing rate. No effect could be recorded with the brain‐inactive SIN‐1 derivative molsidomin. The membrane permeable cGMP analogue 8‐bromo‐cGMP imitated the action of SIN‐1. The hyperpolarizing effect of SIN‐1 and DEA/NO was attenuated by preincubation with the guanylyl cyclase inhibitor ODQ. The immunohistochemical analysis revealed lack of cGMP immunostaining in non‐stimulated slices, whereas SIN‐1 dramatically increased this staining in about 40% of the LC neurons, and these neurons were all tyrosine hydroxylase positive, that is noradrenergic. A large proportion of the LC neurons expressed soluble guanylyl cyclase mRNA. The present and previous results suggest that NO, released from a small number of non‐noradrenergic neurons in the LC, mainly has an inhibitory influence on many noradrenergic neurons, by upregulating cGMP levels via stimulation of soluble guanylyl cyclase. As nitric oxide synthase is present only in a small number of non‐noradrenergic neurons ( Xu et al. 1994 ), a few neurons may influence a large population of noradrenergic LC neurons, which in turn may control activity in many regions of the central nervous system.</div></front></TEI><affiliations><list><country><li>Pays-Bas</li></country></list><tree><country name="Pays-Bas"><noRegion><name sortKey="Xu, Zhi Ing David" sort="Xu, Zhi Ing David" uniqKey="Xu Z" first="Zhi-Qing David" last="Xu">Zhi-Qing David Xu</name></noRegion><name sortKey="De Vente, Jan" sort="De Vente, Jan" uniqKey="De Vente J" first="Jan" last="De Vente">Jan De Vente</name><name sortKey="Grillner, Sten" sort="Grillner, Sten" uniqKey="Grillner S" first="Sten" last="Grillner">Sten Grillner</name><name sortKey="Hokfelt, Tomas" sort="Hokfelt, Tomas" uniqKey="Hokfelt T" first="Tomas" last="Hökfelt">Tomas Hökfelt</name><name sortKey="Steinbusch, Harry" sort="Steinbusch, Harry" uniqKey="Steinbusch H" first="Harry" last="Steinbusch">Harry Steinbusch</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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