Nishimura T
Department of Physiology, Tokai University School of Medicine, Kanagawa, Japan.
Tokai J Exp Clin Med. 1997 Mar;22(1):1-5.
Intracellular recordings were made from mammalian vesical parasympathetic ganglia. A fast excitatory postsynaptic potential (EPSP) was abolished by hexamethonium (200 microM) in rabbit and feline ganglia. A slow inhibitory postsynaptic potential (IPSP) and a following slow EPSP were abolished by atropine (1 microM) in the feline ganglia. Bath application of adenosine (300 microM) depressed the amplitude of nicotinic fast EPSP by 48 +/- 4% in the rabbit ganglia. The action of adenosine was dose-dependent. An antagonist of A1-purinoceptors, 8-cyclopentyltheophylline (1-10 microM), inhibited the adenosine-induced depression but not the amplitude of fast EPSP. Adenosine (2-3 mM) did not significantly affect either the muscarinic slow IPSP, or the slow EPSP, in the feline ganglia. Adenosine also caused a hyperpolarization (1-5 mV) in 40% of the rabbit neurons and 66% of the feline neurons. However a purinergic IPSP was not recorded from either species. These data suggest diverse actions of adenosine in modulating cholinergic transmission in rabbit and feline vesical ganglia.
