Electrophysiological evidence for a functional interaction between 5‐HT1A and 5‐HT2A receptors in the rat medial prefrontal cortex: An lontophoretic study

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Abstract
In this study, we examined the interaction of 5‐HT1A and 5‐HT2A receptors in the rat medial prefrontal cortex (mPFc) using the techniques of extracellular single unit recording and microiontophoresis. The iontophoresis of the selective 5‐HT1A receptor agonist (±)‐8‐hydroxy‐2‐(di‐n‐propylamino) tetralin (8‐OHDPAT) produced a current‐dependent suppression (2.5‐20 nA) of the basal firing rate of spontaneously active mPFc cells. The iontophoretic (5‐10 nA) and systemic administration (0.1‐0.5 mg/kg, i.v. ) of the 5‐HT2A/5‐HT2C receptor antagonist ritanserin and the selective 5 HT2A receptor antagonist MDL 28727 significantly potentiated and prolonged 8‐OHDPATs suppressant action. In addition, the systemic administration of another selective 5‐HT2A antagonist MDL 100907, but not its less active enantiomer MDL 100009, also potentiated and prolonged 8‐OHDPATs action. The potentiating effect of the 5‐HT2A receptor antagonists on the action of 8‐OHDPAT is specific in that neither the iontophoresis of ritanserin nor MDL 28727 altered the suppressant action produced by the iontophoresis of the 5‐HT3 receptor agonist 2‐methylserotonin onto mPFc cells. Moreover, the suppressant action of 8‐OHDPAT was not altered by the systemic administration of the selective 5‐HT3 receptor antagonist granisetron (0.1‐0.5 mg/kg, i.v.). On the other hand, the iontophoresis of a low current (0.5 nA) of the 5‐HT2A,2C receptor agonist (±)‐1‐(2,5‐dimethoxy‐4‐iodophenyl)‐2‐aminopropane (DOI) potentiated the excitation induced by the iontophoresis of 1‐glutamate on quiescent mPFc cells. The iontophoresis of 8‐OHD‐PAT at a current that had no effect on the firing rate of 1‐glutamate activated when administered alone significantly attenuated the excitatory action produced by the iontophoresis of DOI. Overall these results confirm and extend the hypothesis that there is an interaction between 5‐HT1A and 5‐HT2A receptors in the mPFc at the neuronal level.

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