Abstract
5-HTt1A receptor agonists reduce the neuronal release of 5-hydroxytryptamine (5-HT) by activation of raphe 5-HT1A autoreceptors. Using in vivo microdialysis in unanesthetized rats, we show that the local application of the selective 5-HT1A receptor agonist 8-OH-DPAT decreased the 5-HT output to approximately 50% of controls in medial prefrontal cortex (mPFC) but not in dorsal hippocampus. The decrease in 5-HT output was counteracted by the concurrent application of the selective 5-HT1A receptor antagonist WAY-100635. This agent also reversed the decrease in 5-HT output elicited by the novel 5-HT1A receptor agonist BAY x 3702 (30 microM) in mPFC and dorsal raphe nucleus. These results indicate that postsynaptic 5-HT1A receptors in mPFC also participate in the control of serotonergic activity.
Publication types
-
Research Support, Non-U.S. Gov't
MeSH terms
-
8-Hydroxy-2-(di-n-propylamino)tetralin / pharmacology
-
Analysis of Variance
-
Animals
-
Benzopyrans / pharmacology
-
Male
-
Neurons / drug effects
-
Neurons / metabolism*
-
Piperazines / pharmacology
-
Prefrontal Cortex / cytology
-
Prefrontal Cortex / drug effects
-
Prefrontal Cortex / metabolism*
-
Pyridines / pharmacology
-
Rats
-
Rats, Wistar
-
Receptors, Serotonin / drug effects
-
Receptors, Serotonin / physiology*
-
Serotonin / metabolism*
-
Serotonin Antagonists / pharmacology
-
Serotonin Receptor Agonists / pharmacology
-
Synapses / drug effects
-
Synapses / physiology*
-
Thiazoles / pharmacology
Substances
-
Benzopyrans
-
Piperazines
-
Pyridines
-
Receptors, Serotonin
-
Serotonin Antagonists
-
Serotonin Receptor Agonists
-
Thiazoles
-
repinotan hydrochloride
-
Serotonin
-
N-(2-(4-(2-methoxyphenyl)-1-piperazinyl)ethyl)-N-(2-pyridinyl)cyclohexanecarboxamide
-
8-Hydroxy-2-(di-n-propylamino)tetralin