PMID- 9527901
OWN - NLM
STAT- MEDLINE
DCOM- 19980522
LR  - 20190722
IS  - 0014-4886 (Print)
IS  - 0014-4886 (Linking)
VI  - 150
IP  - 2
DP  - 1998 Apr
TI  - NGF depletion reduces ipsilateral and contralateral trigeminal satellite cell 
      reactions after inferior alveolar nerve injury in adult rats.
PG  - 312-20
AB  - Following peripheral nerve injury, neuronal cell functions in sensory ganglia 
      shift from normal maintenance and neurotransmission toward survival and 
      regeneration. A rapid modulation of glial cell activity, which is related to 
      changes in neuronal-support cell interaction, also occurs after nerve injury. 
      Nerve growth factor (NGF) is required for the survival and maintenance of 
      specific populations of sensory and sympathetic neurons, and changes in neuronal 
      gene expression after axonal injury are due in part to a loss of NGF retrograde 
      transport from the periphery to the cell body. A similar role for NGF in 
      modulating support cell responses to peripheral nerve injury, however, has not 
      been demonstrated. Using an autoimmune model, we assessed the effects of NGF 
      depletion in adult rats on the injury-induced expression of glial fibrillary acid 
      protein immunoreactivity (GFAP-IR) in the ipsilateral and contralateral 
      trigeminal ganglia (TG). Unilateral inferior alveolar nerve crush resulted in a 
      bilateral, NGF-dependent trigeminal satellite cell response. In control rats 
      there was a widespread induction of GFAP-IR in the ipsilateral as well as the 
      contralateral TG. In contrast, GFAP-IR was reduced to the mandibular division of 
      the ipsilateral TG in NGF-depleted rats, and the contralateral up-regulation of 
      GFAP-IR was entirely abolished. Bilateral sympathectomy failed to mimic the 
      effects of autoimmunization. Our results provide evidence that NGF depletion 
      inhibits injury-induced satellite cell responses, independent of its effects on 
      sympathetic nerve function.
CI  - Copyright 1998 Academic Press.
FAU - Anderson, L C
AU  - Anderson LC
AD  - Department of Oral Biology, University of Washington, Seattle, Washington 98195, 
      USA.
FAU - von Bartheld, C S
AU  - von Bartheld CS
FAU - Byers, M R
AU  - Byers MR
LA  - eng
GR  - DE 05159/DE/NIDCR NIH HHS/United States
GR  - DE 12338/DE/NIDCR NIH HHS/United States
GR  - HD 29177/HD/NICHD NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Exp Neurol
JT  - Experimental neurology
JID - 0370712
RN  - 0 (Antibodies)
RN  - 0 (Glial Fibrillary Acidic Protein)
RN  - 0 (Immunoglobulin G)
RN  - 0 (Nerve Growth Factors)
RN  - EC 1.14.16.2 (Tyrosine 3-Monooxygenase)
SB  - IM
MH  - Animals
MH  - Antibodies/pharmacology
MH  - Functional Laterality
MH  - Glial Fibrillary Acidic Protein/analysis
MH  - Immunoglobulin G
MH  - Mandibular Nerve/*physiology
MH  - Nerve Crush
MH  - Nerve Growth Factors/immunology/*physiology
MH  - Neurons/cytology/*physiology
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Sympathectomy
MH  - Time Factors
MH  - Trigeminal Nerve/cytology/pathology/*physiology
MH  - Trigeminal Nerve Injuries
MH  - Tyrosine 3-Monooxygenase/analysis/biosynthesis
EDAT- 1998/05/30 00:00
MHDA- 1998/05/30 00:01
CRDT- 1998/05/30 00:00
PHST- 1998/05/30 00:00 [pubmed]
PHST- 1998/05/30 00:01 [medline]
PHST- 1998/05/30 00:00 [entrez]
AID - S0014488697967698 [pii]
AID - 10.1006/exnr.1997.6769 [doi]
PST - ppublish
SO  - Exp Neurol. 1998 Apr;150(2):312-20. doi: 10.1006/exnr.1997.6769.