For function of the autonomic ganglia, acetylcholine and catecholamine provide the essential framework but other chemical messengers, such as amino acid, peptide, eicosanoides and a certain endogenous substance also participated. In the cardiac sympathetic ganglia, dopamine agonists inhibit the ganglionic transmission by reducing acetylcholine release via acting on DA1 receptor at the preganglionic terminals and by inhibiting postganglionic nicotinic and muscarinic stimulation via acting on DA2 receptor at the postganglionic sites. Endogenous γ-aminobutiric acid plays an inhibitory role in non-nicotinic transmission by acting on its receptors. Prostaglandin F2α facilitates the release of acetylcholine from preganglionic sites and prostaglandin E reduces epinephrine- and dopamine-induced inhibition of ganglionic transmission. Angiotensin II stimulates the ganglionic transmission at postganglionic sites via activation of AT1 receptor coupled to Ca2+/CaM- dependent protein kinase and Na+ channels activation. Endothelins inhibit ganglionic transmission by reducing acetylcholine release via increase of thromboxane A2 production at presynaptic sites and by activating low conductance calcium-activated potassium channel at postsynaptic sites. Long-term potentiation appears in non-nicotinic transmission after repetitive high frequency preganglionic stimulation and this potentiation involves an increase of CaM in the cytoplasmic fraction at postganglionic sites. The potential cognitive enhancer, nebracetam facilitates cholinergic transmission by accelerating the synthesis of acetycholine and its consequent release in the cardiac sympathetic ganglia.
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