Sympathetic (SYMP) activity is not abolished by high spinal transection. It is possible that sensory inputs transmitted through dorsal root ganglia can retain activity via intraspinal reflex circuits. In Saffan anesthetized, vagotomized, paralyzed and artificially ventilated (100% Oxygen) piglets, recordings were obtained from phrenic and lumbar SYMP nerves before and after spinal cord transection (SCT). Intact animals displayed modulation of SYMP activity by both baroreceptor and central respiratoryrelated inputs. Following SCT, modulation of SYMP activity related to lung inflation emerged. SYMP activity was maximum during inflation and at a minimum during deflation. The relationship of SYMP to lung inflation was quantified by autopower and coherence spectra. Prominent peaks (ca. 1 Hz), were highly correlated in coherence spectra (>0.1). These results suggest pulmonary afferent modulation of SYMP discharge may account for the observed vasomotor changes occurring in SCT mammals. Cfos gene expression was used to monitor functional responses of spinal cord neurons to spinal injury. After 2.53 hrs, animals were prepared for immunocytochemistry. After SCT, larger numbers of intensely labeled nuclei were concentrated in C3C5 (laminae V, VIII and X) and thoracic gray (laminae I, V, VIII, X, including intermediolateral cell column). Neurons expressing Fos after SCT occupy laminae that harbor SYMP in response to spinal cord injury. It appears that the activity present in efferent preganlionic discharge in developing animals is less dependent on supraspinal mechanisms, possibly because funtional synaptic contacts with brain stem SYMP neurons are not yet fully expressed. (Supported by NIH grants HL20864, HD28931 [P.M.G., A.L.S.] and HL18974, NS28200[D.A.R.]).
