RESUMEN
Neurotrophic factor activates signal pathways of intracellular phosphoinositide 3-kinase and extracellular signal-regulated kinase after acting on Trk receptor tyrosine kinase.It promotes the survival and differentiation of neurons.The development of small molecule Trk agonists of non-peptides and neurotrophic factor simulants can avoid a number of shortcomings of neurotrophic factors while agitating trk receptor signal transduction.It may provide a novel therapeutic approach for the treatment of nervous system diseases.
RESUMEN
Immunofluorescence histochemistry combined with retrograde tracing technique was employed to observe the effects of masseteric nerve transection on the expression of Trk ( tropomyosin-related kinase) receptor proteins, namely TrkA, TrkB and TrkC in the trigeminal mesencephalic nucleus ( Me5 ) of the rat. At 7 and 14 days following transection of masseteric nerve through which Fluorogold (FG) was applied to identify the Me5 neurons innervating masseter, brain sections were immunohistochemically processed to detect the three Trk isoforms in FG-labeled Me5 neurons. With the percentage of double-labeled neurons to the total number of FG-labeled neurons as the index,we demonstrated ( 1 ) a significant increase in the percentage of TrkA-immunoreactive (IR) Me5 neurons at both 7 and 14 days after nerve transection, (2) no significant, but gradual, increase in the percentage of TrkB-IR Me5 neruons with longer survival time post transection and ( 3 ) little change of TrkC expression. The current findings indicate that axotomy differently affected the expression of the individual Trk receptors and these expression patterns may reflect an adaptation of the Me5 neurons to the peripheral nerve injury.