Changes in synaptic inputs to sympathetic preganglionic neurons after spinal cord injury

Spinal cord injury (SCI) leads to plastic changes in organization that impa ct significantly on central nervous control of arterial pressure. SCI cause s hypotension and autonomic dysreflexia, an episodic hypertension induced b y spinal reflexes. Sympathetic preganglionic neurons (SPNs) respond to SCI by retracting and then regrowing their dendrites within 2 weeks of injury. We examined changes in synaptic input to SPNs during this time by comparing the density and amino acid content of synaptic input to choline acetyltran sferase (ChAT)-immunoreactive SPNs in the eighth thoracic spinal cord segme nt (T8) in unoperated rats and in rats at 3 days or at 14 days after spinal cord transection at T4. Postembedding immunogold labeling demonstrated imm unoreactivity for glutamate or gamma -aminobutyric acid (GABA) within presy naptic profiles. We counted the number of presynaptic inputs to measured le ngths of SPN somatic and dendritic membrane and identified the amino acid i n each input. We also assessed gross changes in the morphology of SPNs usin g retrograde labeling with cholera toxin B and light microscopy to determin e the structural changes that were present at the time of evaluation of syn aptic density and amino acid content. At 3 days after SCI, we found that re trogradely labeled SPNs had shrunken somata and greatly shortened dendrites . Synaptic density (inputs per 10-mum membrane) decreased on ChAT-immunorea ctive somata by 34% but increased on dendrites by 66%. Almost half of the i nputs to SPNs lacked amino acids. By 14 days, the density of synaptic input s to dendrites and somata decreased by 50% and 70%, respectively, concurren t with dendrite regrowth. The proportion of glutamatergic inputs to SPNs in spinal cord-transected rats (approximate to 40%) was less than that in uno perated rats, whereas the GABAergic proportion (60-68%) increased. In summa ry, SPNs participate in vasomotor control after SCI despite profound denerv ation. An altered balance of excitatory and inhibitory inputs may explain i njury-induced hypotension. (C) 2001 Wiley-Liss, Inc.