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Effects of a selective 5‐HT 2 agonist, DOI, on 5‐HT neuronal firing in the dorsal raphe nucleus and 5‐HT release and metabolism in the frontal cortex
Author(s) -
Wright Ian K.,
Garratt Jeni C.,
Marsden C.A.
Publication year - 1990
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/j.1476-5381.1990.tb14683.x
Subject(s) - dorsal raphe nucleus , raphe nuclei , microdialysis , agonist , 5 ht receptor , extracellular , serotonin , chemistry , neurotransmitter , raphe , median raphe nucleus , nucleus , cortex (anatomy) , neuroscience , endocrinology , medicine , pharmacology , receptor , biology , serotonergic , biochemistry
Systemic administration of the 5‐HT 2 agonist 1‐(2,5‐dimethoxy‐4‐iodophenyl)‐2‐aminopropane (DOI) (50 and 100 μg kg −1 , i.v.) inhibited dorsal raphe neuronal firing. DOI (100 μg kg −1 , i.v.) also produced a decrease in extracellular 5‐hydroxytryptamine (5‐HT) and 5‐hydroxyindoleacetic acid (5‐HIAA) in the frontal cortex measured by microdialysis. However, local administration of DOI into the frontal cortex produced no change in extracellular 5‐HT and 5‐HIAA at any dose given (1, 10 and 100 ng). The results demonstrate that DOI is a potent inhibitor of 5‐HT neuronal firing and terminal release and that the effects on release are not mediated by an action within the terminal region. The site of action and the receptor involved in the inhibition remains to be determined.