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Inhibition of arachidonic acid cascade attenuates the induction of c-Fos proteins by DOI, 5-HT2A/2C receptor agonist, in the rat cortex.
Pol. J. Pharmacol. 2002: 54 (1) s.73-76, il., bibliogr. 9 poz.
Hasła klasyfikacyjne GBL:
Previous immunohistochemical studies have shown that c-Fos proteins induced by DOI, a 5-HT2A/2C agonist, are present in the population of cortical neurons, which are devoid of 5-HT2A receptors. A mechanism of the induction of c-Fos proteins expression by DOI is still unclear. However, the involvement of the 5-HT2A and AMPA, but not 5-HT2C receptors in this process has been reported. In the present study, we investigated whether arachidonic acid, a retrograde messenger, is involved in the above mechanism of c-Fos induction. Phospholipase A2 pathway, which leads to the subsequent generation of arachidonic acid and its metabolites, is known to be coupled to 5-HT2A receptor activation. The inhibition of arachidonic acid cascade both at the level of phospholipase A2 (by dexamethasone, 1.5 mg/kg0 or at the level of cyclooxygenases that catalyze arachidonic acid biotransformation (by indomethacin, 3 mg/kg), decreased the number of c-Fos immunopositive cells after induction by DOI (8 mg/kg). Our results suggest that arachidonic acid cascade may be involved in the induction of c-Fos proteins by DOI in the rat parietal cortex.
DOI, an agonist of 5-HT2A/2C serotonin receptor, alters the expression of cyclooxygenase-2 in the rat parietal cortex.
J. Physiol. Pharmacol. 2002: 53 (3) s.395-407, il., bibliogr. 41 poz.
Hasła klasyfikacyjne GBL:
The hallucinogenic effect of DOI, serotonin 5-HT2A/2C receptor agonist, is knownto be associated with the activation of cortical 5-HT2 receptors. However, the effect of DOI on excitability of cortical neurons and their subsequent function is still not quite understood. Previous immunohistochemical studies using Fos proteins expression as a marker of neuronal activity showed the involvement of arachidonic acid cascade, particularly cyclooxygenase metabolic pathway, in DOI-induced Fos proteins expression in the rat parietal cortex. DOI increases arachidonic acid release which is transformed itself via acceleration of cyclooxygenase metabolic pathway to biologically active metabolities, such as prostaglandins and tromboxanes. Since cyclooxygenase-2 (COX-2) expression correlates with neuronal activity, it was of interest to investigate whether DOI is capable of influencing the level of COX-2 protein and mRNA expression in the rat parietal cortex. It was observed that neurons which were positive for 5-HT2A receptors showed constitutive COX-2 immunoreactivity. It was found further, that COX-2 protein level was increased at 1h, and returned to the control level at 3 and 6 h after DOI (5mg/kg) administration. In contrast, DOI decreased the COX-2 mRNA expression at all tested time points (1h, 3h and 6h after DOI treatment). The obtained results further support the suggestion that COX-2 activation and possibility arachidonic acid metabolites generated by COX-2 may be considered as important mediators of functional responses generated by activation of cortical 5-HT2A/2C receptors.
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