PMID- 10404406
OWN - NLM
STAT- MEDLINE
DCOM- 19990908
LR  - 20220317
IS  - 0021-9967 (Print)
IS  - 0021-9967 (Linking)
VI  - 410
IP  - 3
DP  - 1999 Aug 2
TI  - Effects of aging and axotomy on the expression of neurotrophin receptors in 
      primary sensory neurons.
PG  - 368-86
AB  - Aging is accompanied by declined sensory perception, paralleled by widespread 
      dystrophic and degenerative changes in both central and peripheral sensory 
      pathways. Several lines of evidence indicate that neurotrophic interactions are 
      of importance for a maintained plasticity in the adult and aging nervous system, 
      and that changes in the expression of neurotrophins and/or their receptors may 
      underpin senile neurodegeneration. We have here examined the expression of 
      neurotrophin receptor (p75NTR, trkA, trkB, and trkC) mRNA and protein in intact 
      and axotomized primary sensory neurons of young adult (3 months) and aged (30 
      months) rats. To examine possible differences among primary sensory neuron 
      populations, we have studied trigeminal ganglia (TG) as well as cervical and 
      lumbar dorsal root ganglia (DRG). In intact aged rats, a decrease in trk (A/B/C) 
      mRNA labeling densities and protein-like immunoreactivities was observed. The 
      decrease was most pronounced in lumbar DRG. In contrast, a small, not 
      statistically significant, increase of p75NTR expression was observed in aged DRG 
      neuron profiles. After axotomy, a down-regulation of mRNA and protein levels was 
      observed for all neurotrophin receptors (p75NTR, trkA, trkB and trkC) in both 
      young adult and aged rats. Consistent with the higher expression levels of 
      neurotrophin receptors in unlesioned young adult primary sensory neurons, the 
      relative effect of axotomy was more pronounced in the young adult than aged rats. 
      Although a decrease in mean cell profile cross-sectional areas was found during 
      aging and after axotomy, the characteristic distribution of neurotrophin receptor 
      expression in different populations of NRG neurons was conserved. The present 
      findings suggest an attenuation of neurotrophic signaling in primary sensory 
      neurons with advancing age and that the expression of p75NTR and trks is 
      regulated differently during aging. A similar dissociation of p75NTR and trk 
      regulation has previously been reported in other neuronal systems during aging, 
      suggesting that there may be a common underlying mechanism. Decreased access to 
      ligands, disturbed axon function and systemic changes in androgen/estrogen levels 
      are discussed as inducing and/or contributing factors.
FAU - Bergman, E
AU  - Bergman E
AD  - Department of Neuroscience, Karolinska Institutet, Stockholm, Sweden. 
      esbjorn.bergman@neuro.ki.se
FAU - Fundin, B T
AU  - Fundin BT
FAU - Ulfhake, B
AU  - Ulfhake B
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - J Comp Neurol
JT  - The Journal of comparative neurology
JID - 0406041
RN  - 0 (Proto-Oncogene Proteins)
RN  - 0 (RNA, Messenger)
RN  - 0 (Receptor, Ciliary Neurotrophic Factor)
RN  - 0 (Receptor, Nerve Growth Factor)
RN  - 0 (Receptors, Nerve Growth Factor)
RN  - EC 2.7.10.1 (Receptor Protein-Tyrosine Kinases)
RN  - EC 2.7.10.1 (Receptor, trkA)
RN  - EC 2.7.10.1 (Receptor, trkC)
SB  - IM
MH  - Aging/*physiology
MH  - Animals
MH  - Axotomy
MH  - Female
MH  - Ganglia, Spinal/growth & development/*metabolism
MH  - *Gene Expression Regulation
MH  - Gene Expression Regulation, Developmental
MH  - Neurons, Afferent/*physiology
MH  - Proto-Oncogene Proteins/*genetics
MH  - RNA, Messenger/genetics
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Receptor Protein-Tyrosine Kinases/*genetics
MH  - Receptor, Ciliary Neurotrophic Factor
MH  - Receptor, Nerve Growth Factor
MH  - Receptor, trkA
MH  - Receptor, trkC
MH  - Receptors, Nerve Growth Factor/*genetics
MH  - Transcription, Genetic
MH  - Trigeminal Ganglion/growth & development/*metabolism
EDAT- 1999/07/15 10:00
MHDA- 2000/06/20 09:00
CRDT- 1999/07/15 10:00
PHST- 1999/07/15 10:00 [pubmed]
PHST- 2000/06/20 09:00 [medline]
PHST- 1999/07/15 10:00 [entrez]
AID - 10.1002/(SICI)1096-9861(19990802)410:3<368::AID-CNE2>3.0.CO;2-I [pii]
AID - 10.1002/(sici)1096-9861(19990802)410:3<368::aid-cne2>3.0.co;2-i [doi]
PST - ppublish
SO  - J Comp Neurol. 1999 Aug 2;410(3):368-86. doi: 
      10.1002/(sici)1096-9861(19990802)410:3<368::aid-cne2>3.0.co;2-i.