Abstract
The area postrema is well known to be a chemoreceptor trigger zone for emesis. Central administration of nicotine has been found to induce vomiting in cats (Beleslin & Krstic, 1987) and shrews (Rudd et al., 1999 ). Recently, emetic effects have been found in patients who were using M3 muscarinic receptor agonist for the treatment of dry mouth. To investigate the mechanism of emetic effects induced by cholinergic drugs, we performed the patch-clamp recording from area postrema neurons in the brain slices. Postsynaptic membrane currents and membrane potentials were recorded during the application of nicotine (10-50 μM) and carbachol (10-50 μM). Bath applied nicotine and carbachol caused excitatory responses in 21 of 27 cells and 3 of 14 cells, respectively. All three cells that responded to carbachol simultaneously responded to nicotine. Carbachol induced the mEPSCs without effects on the membrane potential in a cell. In the other cell, carbachol induced the marked depolarization of the membrane potential with generation of action potentials. In many cells that responded to nicotine, responses to carbachol were not observed. From these results, we considered the multiple mechanisms of muscarinic modulation of area postrema neuronal excitability. [J Physiol Sci. 2007;57 Suppl:S242]