ACETYLCHOLINESTERASE IMMUNOLESIONING - REGIONAL VULNERABILITY OF PREGANGLIONIC SYMPATHETIC NEURONS IN RAT SPINAL-CORD

Rats given antibodies against acetylcholinesterase (AChE) develop symp athetic dysfunction stemming from losses of preganglionic neurons in s pinal cord. Central effects of AChE antibodies are surprising since Ig G does not readily cross the blood-brain barrier, and lesions of perip heral terminals should not cause cell death. This study was designed t o explore the distribution of central neural damage and to investigate features that might account for vulnerability, Rat spinal cord and br ainstem were stained for choline acetyltransferase (ChAT) and nitric o xide synthase (NOS) immunoreactivity. Four months after administration of AChE antibodies, ChAT-positive neurons in the intermediolateral nu cleus (IML) were 61-66% fewer throughout the thoracolumbar cord (T1, T 2, T8,T12, L1). NOS-positive neurons in these loci were affected to th e same extent by antibody-treatment, although they were only two-third s as numerous. By contrast, neurons in the central autonomic nucleus o f the thoracolumbar cord were scarcely affected. These results point t o immunochemical differences in the central autonomic outflow, which m ay partially explain the puzzling selectivity of neural damage in AChE immunolesioning. Different results were obtained after guanethidine s ympathectomy, which ablated nearly all neurons in the superior cervica l ganglion without any effect on preganglionic neurons in the IML. The refore, if the central effects of antibodies are indirectly mediated b y loss of trophic support from the periphery, this support cannot aris e from adrenergic neurons but must come from other ganglionic cells. ( C) 1998 Academic Press.