Acetylcholinesterase Immunolesioning: Regional Vulnerability of Preganglionic Sympathetic Neurons in Rat Spinal Cord
Department of Pharmacology, Mayo Clinic, Mayo Foundation, 200 First Street S.W. Rochester, Minnesota, 55905Experimental Neurology (Impact Factor: 4.7). 09/1998; 152(2):167-176. DOI: 10.1006/exnr.1998.6822
Rats given antibodies against acetylcholinesterase (AChE) develop sympathetic dysfunction stemming from losses of preganglionic neurons in spinal cord. Central effects of AChE antibodies are surprising since IgG does not readily cross the blood–brain barrier, and lesions of peripheral terminals should not cause cell death. This study was designed to explore the distribution of central neural damage and to investigate features that might account for vulnerability. Rat spinal cord and brainstem were stained for choline acetyltransferase (ChAT) and nitric oxide synthase (NOS) immunoreactivity. Four months after administration of AChE antibodies, ChAT-positive neurons in the intermediolateral nucleus (IML) were 61–66% fewer throughout the thoracolumbar cord (T1, T2, T8, T12, L1). NOS-positive neurons in these loci were affected to the same extent by antibody-treatment, although they were only two-thirds as numerous. By contrast, neurons in the central autonomic nucleus of the thoracolumbar cord were scarcely affected. These results point to immunochemical differences in the central autonomic outflow, which may partially explain the puzzling selectivity of neural damage in AChE immunolesioning. Different results were obtained after guanethidine sympathectomy, which ablated nearly all neurons in the superior cervical ganglion without any effect on preganglionic neurons in the IML. Therefore, if the central effects of antibodies are indirectly mediated by loss of trophic support from the periphery, this support cannot arise from adrenergic neurons but must come from other ganglionic cells.
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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.Experimental Neurology 10/2002; 177(1):105-14. DOI:10.1006/exnr.2002.7974 · 4.70 Impact Factor
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ABSTRACT: Although Horner's syndrome is usually taken as an absolute indicator of avulsions of the C8 and T1 ventral roots in adult brachial plexus injury, its pathological basis in obstetric brachial plexus palsy (OBPP) is unclear. We therefore examined the morphological mechanism for the presence of Horner's syndrome in brachial plexus injury in infants and adults. Some axons of sympathetic preganglionic neurons in T1 innervate the superior cervical ganglion via the C7 ventral root in infants but not in adults. Therefore, the presence of Horner's syndrome may relate in part to avulsion of the C7 root in OBPP. These findings suggest that Horner's syndrome in OBPP is not necessarily indicative of avulsions of the C8 and T1 roots, as it can occur with avulsion of the C7 root.Muscle & Nerve 05/2008; 37(5):632-7. DOI:10.1002/mus.20960 · 2.28 Impact Factor
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