Selective loss of NGF-sensitive neurons following experimental colitis.

Abstract:

:Nerve growth factor (NGF) enhances neuronal survival during injury to the mature central and peripheral nervous systems, but its potential as a neuroprotective factor in the enteric nervous system (ENS) has not been examined. We used the trinitrobenzene sulfonic acid (TNBS)-induced model of colitis to examine if NGF-sensitive neurons were selectively spared from inflammation-induced cell loss. Immunocytochemistry of whole mounts of the rat colon showed that total myenteric neuronal number decreased by 32.9% +/- 1.4% by 35 days after inflammation. At this time, the proportion of neurons expressing both the p75 and trkA receptor decreased to 38.4% from a control value of 62.0%. The distribution of expression of neural phenotypes among the NGF receptor-expressing population was differentially affected by inflammation, with selective decrease among cholinergic excitatory neurons and calbindin-expressing neurons, and a trend to increase among inhibitory nitrergic neurons. This is evidence of a novel mechanism whereby intestinal inflammation can give rise to a permanent imbalance between excitatory and inhibitory neural pathways, thus tending to compromise intestinal function.

journal_name

Exp Neurol

journal_title

Experimental neurology

authors

Lin A,Lourenssen S,Stanzel RD,Blennerhassett MG

doi

10.1016/j.expneurol.2004.10.003

keywords:

subject

Has Abstract

pub_date

2005-02-01 00:00:00

pages

337-43

issue

2

eissn

0014-4886

issn

1090-2430

pii

S0014-4886(04)00392-9

journal_volume

191

pub_type

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