Death of Preganglionic Sympathetic Neurons after Surgical or Immunologic Lesion of Peripheral Processes

Abstract

Three months after systemic injection of antibody to acetylcholinesterase (AChE), there is a 60% decrease in the population of preganglionic sympathetic neurons expressing choline acetyltransferase (ChAT) in the intermediolateral (IML) nucleus of the rat spinal cord. In principle, the disappearance of identifiable cholinergic neurons might reflect either outright cell death or severe atrophy with downregulation of cholinergic markers. To distinguish between these possibilities, preganglionic neurons were labeled with the retrograde tracer dye, Fast Blue, 1 week before antibody injection or surgical transection of the cervical sympathetic trunk. Three months after either treatment, the thoracic IML contained 40–60% fewer Fast Blue-labeled neurons than in controls. Therefore, preganglionic sympathetic neurons do degenerate after antibody injection or axotomy. To clarify the role of axonal damage in this process, the effects of three different mechanical lesions were examined. A lumbar ganglionectomy designed to interrupt most sympathetic axons emanating from L2 IML caused 92% loss of ChAT-positive cells observed 10 weeks later at that site. In comparison, transection of the cervical sympathetic trunk, which spared some distally directed axonal branches from the thoracic IML, caused only a 46% loss of ChAT-positive neurons at T1. Still smaller effects were seen after the same nerve was crushed, a lesion that is less destructive. Thus, the ability of central sympathetic neurons to survive a peripheral lesion may be related to the degree of axonal damage and to the opportunity for axonal regrowth.