Lesion or muscimol in the rostral ventral medulla reduces ventilatory output and the CO(2) response in decerebrate piglets.

Developmental abnormalities have been described in the arcuate nucleus of sudden infant death syndrome (SIDS) victims. The arcuate nucleus has putative homologues in chemosensitive areas of the ventral medulla in animals. We refer to some of these areas collectively as the rostral ventral medulla (RVM). In the RVM of decerebrate piglets 2-15 days of age, we studied the effects of electrolytic lesions (n=7) or microdialysis of muscimol (n=15), a GABAA receptor agonist, on ventilatory output and the response to hypercapnia. Lesions caused a 66.7+/-17.3% reduction in eupneic phrenic minute activity (MA) and abolished the response to hypercapnia. Muscimol dialysis caused a 32.4+/-10.4% reduction in MA with a significant downward displacement of the response to hypercapnia with no significant effect on the slope. We conclude that the piglet RVM contains neurons of vital importance in the maintenance of normal breathing and the response to systemic CO(2). We hypothesize that dysfunction of homologous regions in the human infant could lead to impaired ability to respond to hypercapnia and could potentially be involved in the pathogenesis of SIDS.