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C‐type natriuretic peptide (CNP) regulates cocaine‐induced dopamine increase and immediate early gene expression in rat brain
Author(s) -
Thiriet Nathalie,
Jouvert Peggy,
Gobaille Serge,
Solov'Eva Olga,
Gough Bobby,
Aunis Dominique,
Ali Syed,
Zwiller Jean
Publication year - 2001
Publication title -
european journal of neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.346
H-Index - 206
eISSN - 1460-9568
pISSN - 0953-816X
DOI - 10.1046/j.0953-816x.2001.01791.x
Subject(s) - dopaminergic , dopamine , medicine , endocrinology , nucleus accumbens , immediate early gene , substantia nigra , chemistry , biology , gene expression , biochemistry , gene
The neuropeptide C‐type natriuretic peptide (CNP) is the primary biologically active natriuretic peptide in brain. Using in situ hybridization, the present report demonstrates that CNP regulates egr‐1 , c‐fos and junB immediate early gene expression in rat brain. In the frontal cortex, CNP induced immediate early gene expression whereas it inhibited dose‐dependently the cocaine‐induced early gene expression in the dopaminergic projection fields nucleus accumbens and caudate–putamen. CNP may produce its effect directly on dopaminergic neurons because we found that its receptor, guanylyl cyclase GC‐B, was expressed in the mesencephalon where dopaminergic neurons originate, as well as in their projection fields. The inhibition by CNP of the early gene expression elicited by cocaine in the caudate–putamen is correlated with a CNP‐evoked decrease in cocaine‐induced rise in extracellular dopamine, measured by in vivo microdialysis experiments. The significance of the inhibition of cocaine‐induced dopamine release and early gene induction by the endogenous peptide CNP is demonstrated by data indicating that CNP reduced the cocaine‐induced spontaneous locomotor activation. By inhibiting dopaminergic neuronal activity, CNP represents a potential negative regulator of related behavioural effects of cocaine.