Evaluation of chemical mediator-induced respiratory center inhibition in medulla

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Membrane potential and resistance (Rm) were measured in inspiratory neurons in rostral ventrolateral medulla (RVLM) of the isolated brainstem - spinal cord preparation from newborn rats during bath application of opioids (μ-,κ-, and δ- receptor agonists), cytokine (TNF-alfa), and NSAID (salicylate).μ-andκ-opioid receptor agonists caused reduction of final motor outputs by mainly inhibiting medullary inspiratory neuron network. This inhibition of inspiratory neurons seems to be due to both a pre - and postsynaptic inhibition. The central respiratory rhythm as reflected by the preinspiratory neuron burst rate was essentially unaltered by the agonists.TNF-alfa induced respiratory depression. Resting membrane potential hyperpolarized and Rm decreased. These results mean that TNF-alfa-induced respiratory depression seems to be a postsynaptic action.Low dose salicylate increased in inspiratory neuron burst. While the burst rates of inspiratory neuron were decreased after application of high dose salicylate. While the depressant effects by 10 mM salicylate were antagonized by GABA receptor antagonist. Resting membrane potential did not change. Salicylate effects on the medullary inspiratory neurons seem to be due to presynaptic effect. GABAergic mechanisms are probably involved in the salicylate-induced central respiratory depression.