2006 Fiscal Year Final Research Report Summary
What is the mechanism for paresthesia following nerve injury?
Grant-in-Aid for Scientific Research (C)
|Allocation Type||Single-year Grants |
|Research Institution||Niigata University |
SEO Kenji Niigata University, Institute of Medicine and Dentistry, Associate professor -> 新潟大学, 医歯学系, 助教授 (40242440)
FUJIWARA Naoshi Niigata University, Institute of Medicine and Dentistry, Professor, 医歯学系, 教授 (70181419)
MAEDA Takeyasu Niigata University, Institute of Medicine and Dentistry, Professor, 医歯学系, 教授 (40183941)
|Project Period (FY)
2005 – 2006
|Keywords||nerve injury / trigeminal / paresthesia / peptide / substance p / optical imaging / capsaicin / mice|
1.Immuno-histochemical study : Temporo-spatial changes of substance P distribution in the trigeminal caudalis after nerve injury
(1)Neonatal capsaicin treatment induces a disappearance of substance p in deep part of the trigeminal caudalis (Vc) in adult and a transient decrease of substance p in superficial layers of the Vc recovered at 2 weeks of age.
(2)This emerged substance p in superficial layers of the Vc does not have any immunoreactivity either for N-200 (the marker for myelinated fiber) or IB4 (the marker for non-peptidergic neuron).
These results suggest that neonatal capsaicin treatment induces a long term deficit in nociceptive transmission in the Vc and it is caused by unavailability of neurotransmitter releasing but not by an disappearance of neural transmitters.
2.Behavioral study : Long term observation of changes in the mechanical-touch threshold after partial injury of mental nerve
(1)Ligation of the mental nerve in mice induces an apparent elevation of mechanical touch threshold just after nerve injury and this state lasts for 1 week.
(2)This elevation of the threshold decreases around 1 weeks and relative high level of the threshold remains for 4 weeks. After that, this elevation decreases and reaches to the control level.
(3)Changes in the threshold of this animal model look similar to clinical observation of peripheral nerve injury.
Combined with these results, it was suggested that peripheral nerve injury relates to neuropeptide from the afferent terminals in the Vc and mechanism for sensory impairment following nerve injury and its recovery has some relationships to change in the neuropeptide.
Research Products (3 results)