Function in ventilatory control of respiratory neurons at the pontomedullary junction.
Previous studies have demonstrated that electrolytic lesions placed in the midline at the pontomedullary junction result in increased respiratory frequency. The increase in frequency is greater during hypercapnia. The present study sought to determine whether the effects of the lesions were mediated, at least in part, by destruction of neurons. Alternatively, the lesions may have interrupted fiber tracts. Both destruction by kainic acid and inhibition by selective cooling of neurons on the midline at the pontomedullary junction in decerebrate, vagotomized, paralyzed and artificially ventilated cats produced results similar to those engendered by the lesions; i.e., an increased respiratory frequency. Microinjections of glutamate produced a slowing of respiration. In additional cats, extracellular single unit recordings were obtained from 48 neurons located in the medial areas (0-1 mm lateral to midline) at the pontomedullary junction. Of these, 41 neurons were tonically active and 38 were judged to be respiratory-modulated by both the F-test and the Friedman test. The activity of these neurons was sensitive to changes in CO2. Therefore, neurons located at the pontomedullary junction may play a primary role in the integration of central chemoreceptor afferent stimuli.
D000818:Animals; D002415:Cats; D003080:Cold Temperature; D005971:Glutamates / Q000494:pharmacology; D007608:Kainic Acid / Q000494:pharmacology; D008526:Medulla Oblongata / Q000187:drug effects / Q000502:physiology*; D009474:Neurons / Q000187:drug effects / Q000502:physiology*; D010791:Phrenic Nerve / Q000502:physiology; D011149:Pons / Q000187:drug effects / Q000502:physiology*; D012119:Respiration
D005971:Glutamates; D007608:Kainic Acid