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PEDIATRIC ANESTHESIA

Salicylate Action on Medullary Inspiratory Neuron Activity in a Brainstem-Spinal Cord Preparation from Newborn Rats

Department of Anesthesiology and Intensive Care, Nippon Medical School, Tokyo, Japan

Address correspondence and reprint requests to Shinhiro Takeda, MD, PhD, Department of Anesthesiology and Intensive Care, Nippon Medical School, 1-1-5 Sendagi, Bunkyo-ku, Tokyo 113-8603, Japan. Address e-mail to shinhiro{at}nms.ac.jp

Salicylate affects central respiratory control. The inspiratory neurons are the most important component of the medullary respiratory control center because they modulate the final motor output via the phrenic nerve. We investigated changes in burst rate, intraburst firing frequency, and membrane properties of inspiratory neurons in the isolated brainstem after the administration of salicylate. Newborn rat brainstem-spinal cord preparations were superfused with salicylate. Whole-cell recordings were performed from inspiratory neurons. Application of 1 mM salicylate caused an increase in the inspiratory neuronal burst rate from 6.9 ± 1.6 bursts/min to 8.2 ± 1.9 bursts/min (P < 0.05). The inspiratory neuron burst rate decreased from 8.3 ± 0.7 bursts/min to 4.5 ± 1.1 bursts/min after the application of 10 mM salicylate (P < 0.01). The depressant effect of 10 mM salicylate was antagonized by the -aminobutyric acid (GABA) receptor antagonist bicuculline (1 µM). Resting membrane potential and intraburst firing frequency did not change with the application of salicylate and bicuculline even when the burst rate did change. We conclude that the effects of salicylate on the medullary inspiratory neurons are mainly due to a presynaptic action. GABAergic mechanisms are probably involved in the salicylate-induced central respiratory depression.

IMPLICATIONS: We investigated salicylate effects on the medullary respiratory center. Small-dose salicylate (1 mM) directly stimulated the respiratory center. Large-dose salicylate (10 mM) caused central respiratory depression involving a GABAergic mechanism.

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