Modulation in expression of neurokinin receptor NK1 in the striatum of 6-hydroxydopamine-lesioned rats

Parkinson’s disease (PD) is a serious motor disorder which caused by a degeneration of dopaminergic neurons in the substantia nigra (SN) of the basal ganglia. Neurokinins (NK) are a group of neuropeptides that are affected after and/or involved in the pathogenesis of Parkinson’s disease. Objectives of the present study were to investigate the changes in expression of NK1 receptor in different neuronal elements of the striatum after the onset of PD using 6-hydroxydopamine-lesioned rat as an animal model. In lesioned rats, up-regulation of NK1 proteins was generally observed in the striatum by western blotting and immunofluorescence. In addition, double immunofluorescence revealed that NK1 immunoreactivity was primarily found in perikarya of striatal interneurons, namely the cholinergic, nitric oxide synthasepositive striatal interneurons. Interestingly, after lesion, a marked internalization of NK1 immunoreactivity was found in cholinergic interneurons in the lesioned striatum. The intensity of NK1 immunofluorescence was found to be increased in cholinergic and NOS-immunoreactive striatal interneurons in the lesioned striatum. The present results indicate that expression of NK1 receptor is modulated in the striatum of the lesioned rats. The patterns of expression of NK1 receptor in striatal interneuron subpopulations are also modulated after dopamine denervation. NK1 receptor may therefore involve in the neuroprotection of Parkinson’s disease. Acknowledgement: Support contributed by: Joint Research Scheme, National Natural Science Foundation of China and Research Grants Council of Hong Kong, 30218002 and N_HKBU202/02.link_to_subscribed_fulltex