Partial,selective survival of nitrergic neurons in chagasic megacolon |
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Authors: | Samir Jabari Alexandre B M da Silveira Enio C de Oliveira Salustiano G Neto Karl Quint Winfried Neuhuber Axel Brehmer |
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Institution: | 1.Institute of Anatomy I,University of Erlangen-Nuremberg,Erlangen,Germany;2.Human Anatomy Sector, ICBIM,Universidade Federal de Uberlandia,Uberlandia,Brazil;3.Department of Surgery, Medical School,Universidade Federal de Goiás,Goiania,Brazil;4.Institute for Surgical Research,University of Marburg,Marburg,Germany |
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Abstract: | One frequent chronic syndrome of Chagas’ disease is megacolon, an irreversible dilation of a colonic segment. Extensive enteric
neuron loss in the affected segment is regarded as key factor for deficient motility. Here, we assessed the quantitative balance
between cholinergic and nitrergic neurons representing the main limbs of excitatory and inhibitory colonic motor innervation,
respectively. From surgically removed megacolonic segments of four patients, each three myenteric wholemounts (from non-dilated
oral, megacolonic and non-dilated anal parts) was immunohistochemically triple-stained for choline acetyltransferase, neuronal
nitric oxide synthase (NOS) and the panneuronal human neuronal protein Hu C/D. Degenerative changes were most pronounced in
the megacolonic and anal regions, e.g. bulked, honeycomb-like ganglia with few neurons which were partly enlarged or atrophic
or vacuolated. Neuron counts from each 15 ganglia of 12 megacolonic wholemounts were compared with those of 12 age- and region-matched
controls. Extensive neuron loss, mainly in megacolonic and anal wholemounts, was obvious. In all three regions derived from
megacolonic samples, the proportion of NOS-positive neurons (control: 55%) was significantly increased: in non-dilated oral
parts to 61% (p = 0.003), in megacolonic regions to 72% (p < 0.001) and in non-dilated anal regions to 78% (p < 0.001). We suggest the chronic dilation of megacolonic specimens to be due to the preponderance of the nitrergic, inhibitory
input to the intestinal muscle. However, the observed neuronal imbalance was not restricted to the dilated regions: the non-dilated
anal parts may be innervated by ascending, cholinergic axons emerging from less affected, more anally located regions. |
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