Activation of 5-HT2 receptors enhances the release of acetylcholine in the prefrontal cortex and hippocampus of the rat.
Sunila G Nair, Gary A. Gudelsky
Synapse September 15, 2004 DOI: 10.1002/syn.20054 (opens in new tab)
Study at a glance
AI-extracted from the abstract| Characteristics | Experimental animal study using in vivo microdialysis Peer reviewed |
|---|---|
| Population | Rats |
| Interventions | DOI LY-53 857 MK-212 mescaline |
| Dose | DOI 1 and 2 mg/kg i.p.; LY-53,857 3 mg/kg i.p.; MK-212 5 mg/kg i.p.; mescaline 10 mg/kg i.p.; intracortical or intrahippocampal infusion of DOI or LY-53,857 at 100 microM |
| Topics | Serotonin |
| Key findings | DOI, MK-212, and mescaline increased acetylcholine release in the medial prefrontal cortex and/or dorsal hippocampus, effects attenuated by the 5-HT2 antagonist LY-53,857. The authors suggest acetylcholine release in these regions is influenced by 5-HT2 receptor mechanisms, with the prefrontal cortex appearing more sensitive than the dorsal hippocampus to 5-HT2 agonist stimulation. |
Abstract
The role of 5-HT2 receptors in the regulation of acetylcholine (ACh) release was examined in the medial prefrontal cortex and dorsal hippocampus using in vivo microdialysis. The 5-HT(2A/2C) agonist +/-1-(2,5-dimethoxy-4-iodophenyl) -2- aminopropane hydrochloride (DOI) (1 and 2 mg/kg, i.p.) significantly increased the extracellular concentration of ACh in both brain regions, and this response was attenuated in rats treated with the 5-HT(2A/2B/2C) antagonist LY-53,857 (3 mg/kg, i.p.). Treatment with LY-53,857 alone did not significantly alter ACh release in either brain region The 5-HT(2C) agonist 6-chloro-2-(1-piperazinyl)-pyrazine) (MK-212) (5 mg/kg, i.p.) significantly enhanced the release of ACh in both the prefrontal cortex and hippocampus, whereas the 5-HT2 agonist mescaline (10 mg/kg, i.p.) produced a 2-fold increase in ACh release only in the prefrontal cortex. Intracortical, but not intrahippocampal, infusion of DOI (100 microM) significantly enhanced the release of ACh, and intracortical infusion of LY-53,857 (100 microM) significantly attenuated this response. These results suggest that the release of ACh in the prefrontal cortex and hippocampus is influenced by 5-HT2 receptor mechanisms. The increase in release of ACh induced by DOI in the prefrontal cortex, but not in the hippocampus, appears to be due to 5-HT2 receptor mechanisms localized within this brain region. Furthermore, it appears that the prefrontal cortex is more sensitive than the dorsal hippocampus to the stimulatory effect of 5-HT2 agonists on ACh release.
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