Abstract
Tumor necrosis factor alpha (TNFα) is a potent modulator of autonomic reflex mechanisms that control the stomach. Evidence suggests that TNFα action directly on vago-vagal reflex control circuits causes the autonomic misregulation of digestion manifested as gastrointestinal stasis, nausea, and emesis associated with illness. Neurophysiological studies indicated that TNFα may have effects on vagal afferents in the solitary nucleus, as well as neurons of the solitary nucleus (NST) and dorsal motor nucleus (DMN) of the vagus. The aim of this study was to determine the location of the TNFR1 receptor (p55) in the medulla using immunocytochemical methods. We devised a technique for localizing the p55 receptor using heat-induced antigen recovery in fixed tissue sections. This protocol allowed us to demonstrate that dense p55-immunoreactivity (p55-ir) is constitutively present on central (but not peripheral) vagal afferents in the solitary tract (ST) and nucleus; p55-ir is also present on afferents entering the spinal trigeminal nucleus. Unilateral supra-nodose vagotomy eliminated p55-ir from ipsilateral central vagal afferents. Virtually all neurons in the brainstem appeared to express p55-ir at a low level, i.e., just above background. However, vagotomy caused a dramatic up-regulation of p55-ir in vagal motor neurons. This increase in p55-ir in axotomized neurons may play a pivotal role in the connection between the occurrence of the injury and the initiation of apoptotic processes resulting in elimination of damaged neurons.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 156-166 |
| Number of pages | 11 |
| Journal | Brain Research |
| Volume | 1004 |
| Issue number | 1-2 |
| DOIs | |
| State | Published - Apr 9 2004 |
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Keywords
- Apoptosis
- Cytokine
- Endocrine and autonomic regulation
- Immune-neural interaction
- Nerve injury
- Neural-immune interactions
- TNFR1
- Wallerian degeneration
Cite this
TNFα-p55 receptors : Medullary brainstem immunocytochemical localization in normal and vagus nerve-transected rats. / Hermann, Gerlinda E.; Hebert, Sadie L.; Van Meter, Montina J.; Holmes, Gregory M.; Rogers, Richard C.
In: Brain Research, Vol. 1004, No. 1-2, 09.04.2004, p. 156-166.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - TNFα-p55 receptors
T2 - Medullary brainstem immunocytochemical localization in normal and vagus nerve-transected rats
AU - Hermann, Gerlinda E.
AU - Hebert, Sadie L.
AU - Van Meter, Montina J.
AU - Holmes, Gregory M.
AU - Rogers, Richard C.
PY - 2004/4/9
Y1 - 2004/4/9
N2 - Tumor necrosis factor alpha (TNFα) is a potent modulator of autonomic reflex mechanisms that control the stomach. Evidence suggests that TNFα action directly on vago-vagal reflex control circuits causes the autonomic misregulation of digestion manifested as gastrointestinal stasis, nausea, and emesis associated with illness. Neurophysiological studies indicated that TNFα may have effects on vagal afferents in the solitary nucleus, as well as neurons of the solitary nucleus (NST) and dorsal motor nucleus (DMN) of the vagus. The aim of this study was to determine the location of the TNFR1 receptor (p55) in the medulla using immunocytochemical methods. We devised a technique for localizing the p55 receptor using heat-induced antigen recovery in fixed tissue sections. This protocol allowed us to demonstrate that dense p55-immunoreactivity (p55-ir) is constitutively present on central (but not peripheral) vagal afferents in the solitary tract (ST) and nucleus; p55-ir is also present on afferents entering the spinal trigeminal nucleus. Unilateral supra-nodose vagotomy eliminated p55-ir from ipsilateral central vagal afferents. Virtually all neurons in the brainstem appeared to express p55-ir at a low level, i.e., just above background. However, vagotomy caused a dramatic up-regulation of p55-ir in vagal motor neurons. This increase in p55-ir in axotomized neurons may play a pivotal role in the connection between the occurrence of the injury and the initiation of apoptotic processes resulting in elimination of damaged neurons.
AB - Tumor necrosis factor alpha (TNFα) is a potent modulator of autonomic reflex mechanisms that control the stomach. Evidence suggests that TNFα action directly on vago-vagal reflex control circuits causes the autonomic misregulation of digestion manifested as gastrointestinal stasis, nausea, and emesis associated with illness. Neurophysiological studies indicated that TNFα may have effects on vagal afferents in the solitary nucleus, as well as neurons of the solitary nucleus (NST) and dorsal motor nucleus (DMN) of the vagus. The aim of this study was to determine the location of the TNFR1 receptor (p55) in the medulla using immunocytochemical methods. We devised a technique for localizing the p55 receptor using heat-induced antigen recovery in fixed tissue sections. This protocol allowed us to demonstrate that dense p55-immunoreactivity (p55-ir) is constitutively present on central (but not peripheral) vagal afferents in the solitary tract (ST) and nucleus; p55-ir is also present on afferents entering the spinal trigeminal nucleus. Unilateral supra-nodose vagotomy eliminated p55-ir from ipsilateral central vagal afferents. Virtually all neurons in the brainstem appeared to express p55-ir at a low level, i.e., just above background. However, vagotomy caused a dramatic up-regulation of p55-ir in vagal motor neurons. This increase in p55-ir in axotomized neurons may play a pivotal role in the connection between the occurrence of the injury and the initiation of apoptotic processes resulting in elimination of damaged neurons.
KW - Apoptosis
KW - Cytokine
KW - Endocrine and autonomic regulation
KW - Immune-neural interaction
KW - Nerve injury
KW - Neural-immune interactions
KW - TNFR1
KW - Wallerian degeneration
UR - http://www.scopus.com/inward/record.url?scp=1642271629&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=1642271629&partnerID=8YFLogxK
U2 - 10.1016/j.brainres.2003.11.078
DO - 10.1016/j.brainres.2003.11.078
M3 - Article
VL - 1004
SP - 156
EP - 166
JO - Brain Research
JF - Brain Research
SN - 0006-8993
IS - 1-2
ER -