Journal of Neurophysiology, Vol 76, Issue 4 2271-2279, Copyright © 1996 by APS

ARTICLES

Role of ventral respiratory group bulbospinal expiratory neurons in vestibular-respiratory reflexes

K. Shiba, M. S. Siniaia and A. D. Miller
Rockefeller University, New York City, New York 10021-6399, USA.

1. Activation of the vestibular system produces reflex modulation of expiratory muscle activity. The purpose of the present study was to investigate the possible role of bulbospinal expiratory (E) neurons located in the caudal ventral respiratory group (VRG) in mediating vestibulo-respiratory reflexes. Experiments were carried out in decerebrated, paralyzed, and artificially ventilated cats. 2. Electrical stimulation of the vestibular nerve (VN), using short trains of current pulses, elicited bilateral reflex responses on abdominal muscle nerves (ABDNs). This response was not affected by lesions of the cochlear nuclei made by kainic acid injections. The ABDN response typically consisted of a combination of short-latency excitation and long-latency inhibition on the ipsilateral side and, in contrast, a combination of short-latency inhibition and long-latency excitation on the contralateral side. 3. Extracellular recordings were made from 43 caudal VRG bulbospinal E neurons that were activated antidromically from the contralateral upper lumbar spinal cord. More than 80% of these neurons responded to either ipsi- and/or contralateral VN stimulation. The neuronal response consisted of either a combination of excitation and inhibition or only inhibition. The majority of neurons had response patterns appropriate to contribute to the response observed on the contralateral ABDN; however, the latency of the VRG E neuron response was too long to initiate the ABDN response. 4. To further evaluate the contribution of caudal VRG E neurons to the vestibulo-abdominal reflex, ABDN responses were compared before and after sectioning the axons of caudal VRG bulbospinal E neurons where they cross the midline between the obex and first cervical spinal segment. These midsagittal lesions abolished expiratory modulation of ABDN discharge. The lesions also decreased the amplitude of the vestibular-evoked ABDN response but could not abolish the response. The postlesion amplitude was decreased on average to approximately 70% of prelesion values. 5. In conclusion, although the present results indicate that the majority of caudal VRG bulbospinal E neurons respond appropriately to contribute to the vestibulo-abdominal reflex, the reflex largely is unaffected by the removal of caudal VRG E input. The additional descending inputs that are important for mediating the reflex remain to be investigated and may include vestibulospinal and/or reticulospinal tracts.

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