RGD Reference Report - Involvement of a spinal brain-derived neurotrophic factor/full-length TrkB pathway in the development of nerve injury-induced thermal hyperalgesia in mice.

General

Involvement of a spinal brain-derived neurotrophic factor/full-length TrkB pathway in the development of nerve injury-induced thermal hyperalgesia in mice.
Authors:	Yajima, Y Narita, M Narita, M Matsumoto, N Suzuki, T
Citation:	Yajima Y, etal., Brain Res. 2002 Dec 27;958(2):338-46.
RGD ID:	8657091
Pubmed:	PMID:12470870 (View Abstract at PubMed)
Partial sciatic nerve ligation in mice caused a marked and persistent decrease in the latency of paw withdrawal from a thermal stimulus only on the ipsilateral side. This thermal hyperalgesia was abolished by repeated intrathecal pretreatment with a specific antibody to brain-derived neurotrophic factor (BDNF), but not neurotrophin-4, just before and after the nerve ligation. These results provide direct evidence that BDNF within the spinal cord may contribute to the development of thermal hyperalgesia caused by nerve injury in mice. We previously reported that protein level of full-length TrkB, which contains the cytoplasmic protein tyrosine kinase domain, were clearly increased on the ipsilateral side of spinal cord membranes obtained from sciatic nerve-ligated mice. In the present study, we further demonstrated that the increased in the protein level of full-length TrkB is completely reversed by concomitant intrathecal injection of BDNF antibody. Furthermore, thermal hyperalgesia induced by nerve ligation was completely suppressed by repeated intrathecal injection of a specific antibody to full-length TrkB and an inhibitor of the protein tyrosine kinase activity for the neurotrophin receptor, K-252a. However, repeated intrathecal injection of a specific antibody to truncated TrkB, which lacks the cytoplasmic protein tyrosine kinase domain, failed to reverse thermal hyperalgesia observed in nerve-ligated mice. These findings suggest the possibility that the binding of BDNF to full-length TrkB and subsequent its activation may play a critical role in the development of neuropathic pain-like thermal hyperalgesia induced by nerve injury in mice.

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Term	Qualifier	Evidence	With	Reference	Notes	Source	Original Reference(s)
Hyperalgesia		ISO	Bdnf (Mus musculus)	8657091; 8657091	associated with Sciatic Neuropathy	RGD
Hyperalgesia		IMP		8657091	associated with Sciatic Neuropathy	RGD
Hyperalgesia		ISO	Ntrk2 (Mus musculus)	8657091; 8657091		RGD
Hyperalgesia		IMP		8657091		RGD

Objects Annotated

Genes (Rattus norvegicus)

Bdnf (brain-derived neurotrophic factor)

Ntrk2 (neurotrophic receptor tyrosine kinase 2)

Genes (Mus musculus)

Bdnf (brain derived neurotrophic factor)

Ntrk2 (neurotrophic tyrosine kinase, receptor, type 2)

Genes (Homo sapiens)

BDNF (brain derived neurotrophic factor)

NTRK2 (neurotrophic receptor tyrosine kinase 2)

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Involvement of a spinal brain-derived neurotrophic factor/full-length TrkB pathway in the development of nerve injury-induced thermal hyperalgesia in mice.