Adenosine-induced inhibition of vagal motoneuron excitability: receptor subtype and mechanisms
Marks, J.D.; Donnelly, D.F.; Haddad, G.G.
American Journal of Physiology 264(2 Pt 1): L124-L132
1993
ISSN/ISBN: 0002-9513 PMID: 8383444 Document Number: 412610
With the use of intracellular techniques and a medullary slice preparation, we examined the changes in cellular and membrane properties of single adult rat vagal motoneurons during exposure to potent and specific agonists and antagonists of adenosine A-1 and A-2 receptors. A-1 receptor stimulation increased input resistance, but markedly reduced spontaneous neuroal firing and increased rheobase. A-1 agonists also increased the amplitude of the action potential afterhyperpolarization (AHP) in a dose-dependent manner. Prior treatment with A-1 antagonists blocked these electrophysiological effects. Blockade of Ca-2+ entry with Co-2+ abolished the AHP increase. Synaptic blockade with both tetrodotoxin and high Mg-2+, low Ca-2+ solutions prevented the increase in input resistance. A-2 receptor stimulation was without effect. Perfusion with adenosine in the presence of dipyridamole caused effects similar to A-1 agonist stimulation, but no effect in the absence of dipyridamole. These results show that adenosine decreases vagal motoneuron excitability by stimulating A-1 receptors. Our data also support the idea that the adenosine-induced decrease in excitability is presynaptic in nature. In addition, the AHP increase may be mediated by enhanced Ca-2+ entry into the postsynaptic neuron.