Okadaic acid antagonizes the inhibitory action of internal GTP-gamma-S on the calcium current of dorsal raphe neurons but not that of 5-HT1A receptor activation.
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Biomedical subjects
Publications and source records attributed to H Hećimović.
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Serotonin syndrome usually occurs after treatment with monoamine oxydase inhibitors and drugs that enhance serotoninergic transmission. Serotonin agents, such as Proza, are commonly prescribed drugs; therefore, the serotonin syndrome appears more frequently than before. Clinicians must be able to prevent, recognize, and treat this syndrome in their practice. This review summarizes the literature of case reports of patients who developed the serotonin syndrome.
The whole-cell patch-clamp technique was used to examine the effect of substance P (SP) on glutamate-induced currents in freshly dissociated rat spinal dorsal horn neurons (LI-III). In 48% of examined cells SP (10(-10)-10(-6) M) at -70 mV, induced in inward current that desensitized in the continued presence of SP. When applied simultaneously with, or prior to L-glutamate, SP caused a potentiation of L-glutamate-induced current in 65% of the tested cells. Since glutamate activates both N-methyl-D-aspartate (NMDA) and non-NMDA receptors in rat dorsal horn neurons, selective agonists, kainate, quisqualate, alpha-amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid (AMPA) and NMDA were used to determine which subtype of excitatory amino acid receptors interacted with SP. We found that the responses to quisqualate, kainate, and AMPA were not significantly affected by SP (less than 20% increase). In contrast, the inward currents induced by NMDA (30-300 microM) appear to be reduced and potentiated after the administration of 2-200 nM of SP. These results suggest that post-synaptic mechanisms of action of tachykinins may contribute to the regulation of the strength of glutamate-mediated excitatory transmission in the rat spinal dorsal horn.