Identification of medullary loci critical for neurogenesis of gasping.
We hypothesized that a discrete medullary locus, critical for gasping neurogenesis, could be identified. In decerebrate, cerebellectomized, vagotomized, paralyzed, and ventilated cats, activities of phrenic, hypoglossal, and recurrent laryngeal nerves were monitored. Gasping was induced by freezing the brain stem, via a fork thermode, at the pontomedullary junction. By reversible cooling of the medulla, chemical lesions with kainic acid, and radio-frequency lesions, a critical area for gasping neurogenesis was localized bilaterally 2-3 mm rostral to obex, 2.0-2.5 mm lateral to midline, and 3-4 mm ventral to medullary surface. Electrical stimulation in this area elicited premature gasps, whereas unilateral lesions or lidocaine injections eliminated gasping activities in all nerves. These procedures did not cause similar changes during eupnea. In apneusis, however, lidocaine injections markedly altered the pattern or caused apnea. We conclude that discharge of neurons in a discrete portion of the lateral tegmental field of medulla is required for gasping neurogenesis. Our results are consistent with these neurons comprising the central pattern generator for gasping.
D000818:Animals; D001933:Brain Stem / Q000502:physiology; D002415:Cats; D003080:Cold Temperature; D004558:Electric Stimulation; D005260:Female; D007608:Kainic Acid / Q000494:pharmacology; D008012:Lidocaine / Q000494:pharmacology; D008297:Male; D008526:Medulla Oblongata / Q000502:physiology*; D012119:Respiration / Q000187:drug effects / Q000528:radiation effects; D012120:Respiration Disorders / Q000503:physiopathology
D008012:Lidocaine; D007608:Kainic Acid