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[Q. Neuroscience-32]



             Alterations of intestinal neurotrophins in neurotoxin-induced


                                  Parkinson’s disease mouse models




            Jin Gyu Choi¹˙²˙³˙#, Ji-Hye Ahn¹˙²˙⁴˙#, Miran Jeong¹˙²˙³, Boh Rah Joo², Jeong-Hwa Woo², Dong-Hyun
                                   Kim¹˙²˙³, Myung Sook Oh¹˙²˙³˙*, Jung-Hye Choi¹˙²˙³˙*


           ¹Neurobiota Research Center (NRC),  Kyung Hee University, Seoul 02447, South Korea, ²College of Pharmacy,

          Kyung Hee University, Seoul 02447, South Korea, ³Department of Life and Nanopharmaceutical Sciences, Kyung
         Hee University, Seoul 02447, South Korea, ⁴College of Pharmacy, Woosuk University, Jeonbuk 55338, South Korea




        In several neurological disorders, a change in the levels of several gut neuropeptides has been shown. However, to

        the best of our knowledge, there is no report to demonstrate a remarkable change of intestinal neurotrophins in
        Parkinson’s disease (PD) animal model. In this study, we aimed to investigate the levels of four neurotrophins in the

        intestine of neurotoxin-induced PD mice. The PD mice were obtained by chronic injection of 1-methyl-4-phenyl-
        1,2,3,6 tetrahydropyridine (MPTP) or MPTP/probenecid (MPTP/p). The levels of mRNA and protein expression in

        mouse intestines were measured by using real-time reverse transcription polymerase chain reaction and Western
        blotting,  respectively.  We  found  that  the  mRNA  expression  of  two  neurotrophins  (neurotrophin  A  and  D)  was

        significantly decreased in the large intestine of MPTP group compared to the vehicle-treated group, but not in the
        small intestine. The protein levels of neurotrophin A, but not neurotrophin D, were reduced in the colon of MPTP

        or MPTP/p-treated mice compared to those of the vehicle-treated group. These data suggest that the intestinal
        expression of neurotrophin A was significantly reduced in PD animal models, and may play a role in the gut-brain

        axis in PD.
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