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Control of serotonergic neurons in rat brain by dopaminergic receptors outside the dorsal raphe nucleus
Author(s) -
MartínRuiz Raúl,
Ugedo Luisa,
Honrubia María A.,
Mengod Guadalupe,
Artigas Francesc
Publication year - 2001
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1046/j.1471-4159.2001.00275.x
Subject(s) - dorsal raphe nucleus , serotonergic , serotonergic cell groups , neuroscience , dopaminergic , raphe nuclei , dorsum , raphe , dopaminergic pathways , biology , serotonin , receptor , anatomy , dopamine , biochemistry
We studied the control of dorsal raphe (DR) serotonergic neurons by dopaminergic transmission in rat brain using microdialysis and single unit extracellular recordings. Apomorphine (0.5–3.0 mg/kg s.c.) and quinpirole (0.5 mg/kg s.c.) increased serotonin (5‐HT) output in the DR and (only apomorphine) in striatum. These effects were antagonized by 0.3 mg/kg s.c. SCH 23390 (in DR and striatum) and 1 mg/kg s.c. raclopride (in DR). 5‐HT 1A receptor blockade potentiated the 5‐HT increase produced by apomorphine in the DR. Apomorphine (50–400 µg/kg i.v.) increased the firing rate of most 5‐HT neurons, an effect prevented by SCH 23390 and raclopride. Quinpirole (40–160 µg/kg i.v.) also enhanced the firing rate of 5‐HT neurons. When applied in the DR, neither drug increased the 5‐HT output in the DR or striatum. Likewise, micropressure injection of quinpirole (0.2–8 pmol) failed to increase the firing rate of 5‐HT neurons. In situ hybridization showed that the dopamine (DA) D 2 receptor transcript was almost absent in the DR and abundant in the substantia nigra (SN) and the periaqueductal grey matter (PAG). Using dual probe microdialysis, the application of tetrodotoxin or apomorphine in SN significantly increased the DR 5‐HT output. Thus, the discrepancy between local and systemic effects of dopaminergic agonists and the absence of DA D 2 receptor transcript in 5‐HT neurons suggest that DA D 2 receptors outside the DR control serotonergic activity.