Acetylcholinesterase Inhibitor Elicits Muscarinic Receptor-Mediated Cholinergic Transmission in the Rat Adrenal Medulla
Both nicotinic and muscarinic receptors exist in the adrenal gland and their receptor agonists evoke catecholamine (CA) release from adrenal gland. The CA release induced by nerve stimulation is, however, predominantly suppressed by nicotinic antagonists and resistant to muscarinic antagonists.1,2 From these findings, it has been suggested that nicotinic receptors are primarily concentrated in the synaptic regions, with muscarinic receptors primarily localized on the extra-synaptic regions of chromaffin cells. We are interested in whether the differential anatomical localization can entirely explain the predominance of nicotinic receptors in cholinergic synaptic transmission and what conditions are relevant to muscarinic receptor-mediated synaptic transmission. We focused on the function of acetylcholinesterase (AChE), and hypothesized that the inhibition of AChE expanded the regions involved in cholinergic transmission to the extra-synaptic regions. To verify this hypothesis, we applied the microdialysis technique to the adrenal gland of anesthetized rats and investigated the influence of AChE inhibitor on cholinergic transmission in the adrenal gland.
KeywordsMuscarinic Receptor Chromaffin Cell Nicotinic Receptor AChE Inhibitor Cholinergic Transmission
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