Control of abdominal and expiratory intercostal muscle activity during vomiting: role of ventral respiratory group expiratory neurons

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Abstract
1. The role of ventral respiratory group (VRG) expiratory (E) neurons in the control of abdominal and internal intercostal (expiratory) muscle activity during vomiting was examined in decerebrate casts by 1) recording from these neurons during fictive vomiting in paralyzed animals and 2) comparing abdominal muscle activity during vomiting before and after sectioning the axons of these descending neurons. Fictive vomiting was defined by a series of bursts of coactivation of abdominal and phrenic nerves elicited by either subdiaphragmatic vagus nerve stimulation or emetic drugs. Such coordinated activity would be expected to produce vomiting if the animals were not paralyzed. 2. Data were recorded from 27 VRG E neurons that were antidromically activated from the lower thoracic (T13) or lumbar spinal cord. During fictive vomiting, almost two-thirds of these neurons (17/27) were mainly active in between periods of abdominal and phrenic nerve coactivation, when the internal intercostal motoneurons are known to be active. This group of neurons was termed INT neurons. INT neurons were subdivided according to whether they were active between every burst of phrenic and abdominal nerve coactivation (INTa neurons, n = 10) or only between some bursts (INTb neurons, n = 7). Another one-third of the VRG E neurons had normal or increased levels of activity when the abdominal nerves active during ficitive vomiting (ABD neurons). The one remaining neuron was mainly silent throughout fictive vomiting. 3. ABD neurons were indistinguishable from INT neurons on the basis of their location in the VRG, type of firing pattern (ramp versus step ramp), conduction velocity, or extent of projection in the lumbar cord. However, INTa neurons had a significantly higher discharge rate during respiration than either ABD or INTb neurons. 4. Abdominal muscle EMG and nerve activity were recorded from six unparalyzed cats before and after cutting the axons of VRG E neurons as they cross the midline between C1 and the obex. The lesions abolished or almost eliminated expiratory modulation of abdominal muscle activity. In contrast, the abdomininal muscles were always active during vomiting; however, the amplitude of postlesion abdominal activity varied from .apprx. 70-100% of prelesion values in three cats to 60-70% of normal in a fourth animal to only .apprx. 20% of prelesion values in two other cats. 5. In conclusion, about two-thirds of VRG E neurons that project at least as far caudally as the lower thoracic cord have the appropriate firing pattern to contribute to internal intercostal muscle activity during vomiting. The remaining one-third could contribute to abdominal muscle activation during vomiting. Other as yet unidentified inputs, either descending from the brain stem and/or arising from spinal reflexes, can also produce abdominal muscle activation during vomiting, as was shown by severing the axons of VRG E neurons.