Michael et al., Cell Dev Biol 2013, 2:4 DOI: 10.4172/2168-9296.1000127 Volume 2 • Issue 4 • 1000127 Cell Dev Biol ISSN: 2168-9296 CDB, an open access journal Open Access Research Article VDR Potentiation and NMDA R Inhibition Facilitates Axo-Dendritic Process Formation in Melanocyte Model for Pigmented Cells in Parkinsonism Ogundele Olalekan Michael 1 *, Ajonijebu 2 , Duyilemi Chris 3 , Okunnuga Adedotun Adetokunbo 4 , Adekeye Adeshina Oloruntoba 1 and Ojo Abiodun Ayodele 4 1 Department of Anatomy, College of Medicine and Health Sciences, Afe Babalola University, Nigeria 2 Department of Physiology, College of Medicine and Health Sciences, Afe Babalola University, Nigeria 3 Department of Morbid Anatomy and Histopathology, Federal Medical Centre, Nigeria 4 Department of Chemical Sciences, College of Sciences, Afe Babalola University, Nigeria Abstract Background: A major cellular change in dopaminergic neurons leading to Parkinsonism is the alteration of microtubule proteins that causes accumulation of tau protein, α-syn and β-amyloid plaque in the cells. In this study we investigate the role of Vitamin D 3 in relieving the symptoms of Parkinsonism as it is capable of stimulating polymerization of microtubules. The Microtubules (MT) system in the fsh scale melanocytes has been modeled for the dopaminergic neurons of the Substantia Nigra (SN). These cells are capable of forming cellular processes similar to what is seen in the dopaminergic neurons; in this study, we investigate the protective effect of Vitamin D 3 Receptor Agonist (VDRA) and N-Methyl-D-Aspartate Receptor (NMDA R) inhibition in process formation, synaptic denervation and melanin loss in fsh scale melanocytes modeled as pigmented adrenergic cells. Method: The Tilapia scale was isolated and sub cultured in Ringer’s solution following which the cells were prepared for imaging. We incubated the cells with VDRA, Ketamine and a combination of Ketamine and VDRA in separate set ups for 60 minutes. Using brightfeld imaging techniques, the cells were viewed during the incubation period and recorded using a Cameroscope connected to a computer interface. Results/Conclusion: The cells incubated with VDRA and NMDA R inhibitor, showed an increase in the number of process and extent of the process formation; the increased number of process is an indication of a rapid rate of polymerization of microtubules. Also, the processes formed are combined long processes peculiar to the NMDA R1 inhibition and short processes characteristic of VDR potentiation as seen in VDRA treatment only. Most of the effects of the VDRA were restricted to process formation around the cell body; this is similar to the microtubule cytoskeletal system found in the dendritic nucleation assembly. This fnding confrms the presence of VDR and its likely restriction to d cell body plus its role in facilitating short dendrite-like process formation while NMDA R is located on the processes and facilitates long process formation. *Corresponding author: Ogundele OM, Department of Anatomy, College of Medicine and Health Sciences, Afe Babalola University, Nigeria, Tel: +234(0)7031022702; E-mail: ola.ogundele@abuad.edu.ng Received September 01, 2013; Accepted October 24, 2013; Published October 26, 2013 Citation: Michael OO, Ajonijebu, Chris D, Adetokunbo OA, Oloruntoba AA, et al. (2013) VDR Potentiation and NMDA R Inhibition Facilitates Axo-Dendritic Process Formation in Melanocyte Model for Pigmented Cells in Parkinsonism. Cell Dev Biol 2: 127. doi:10.4172/2168-9296.1000127 Copyright: © 2013 Michael OO, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Keywords: Parkinsonism; Melanocytes; Microtubules; Pigment; Dopamine; Neurons; Vitamin D; Neurodegeneration Abbreviations: ACSF: Artifcial Cerebrospinal Fluid; VDR: Vitamin D 3 Receptor; VDRA: Vitamin D 3 Receptor Agonist; ATP: Adenosine Trios Phosphate; DNA: Deoxyribonucleic Acid; NMDA R: N-Methyl- D-Aspartate Receptor; PD: Parkinson Disease; SN: Substantia Nigra; MT: Microtubule; MTOC: Microtubule Organization Centre; NDD: Neurodegenerative Disease Introduction Selective vulnerability of the dopaminergic neurons and pigment cells of the SN cannot be over emphasized in the etiology and progression of PD. Defciency of Vitamin D 3 or genetic mutations involving the VDR have been described in multi array organ malfunction especially in the SN, parathyroid gland, bone and gastrointestinal tract [1,2]. Vitamin D 3 Receptors (VDR) have been observed in the Substantia Nigra (SN) [3,4]; as well as in the skin and liver of the fsh [5]. Our choice of the VDR and VDRA, in this study, is to establish in part, the cellular mechanism of Vitamin D 3 as a neuroprotective agent in PD especially as it involves process formation and prevention of synaptic denervation via signaling pathways that facilitates polymerization of MT. Te model used for this study involved melanocytes in Ringer’s solution containing NMDA R blocker ketamine; to induce process and synapse-like structure formation in these cells in vitro. Tus co-treatment, in vitro, with ketamine and Vitamin D 3 (VDRA) describes the pharmacological action of NMDA R inhibition and VDR potentiation. Te mechanism of the VDRA involves calcium signaling pathways that facilitate polymerization of MT such that the αβ-tubulin sub-units assemble and convey melanosomes and other vesicles to the periphery of the cell using the kinesin motor assembly [6]. Tis is believed to be complimentary to the inhibition of NMDA R; prevention of glutamate toxicity [7], as such movement of vesicles, away from the nucleus prevents cell death by autophagy. Te VDRA binds to a cytoplasmic receptor VDR having two domains; frst is the hormone binding domain and second is the DNA binding domain. A VDR-VDRA receptor complex is formed and can bind to the promoter region of genes, thus increasing the rate of gene transcription and cellular activity [8]. Several studies have also shown that VDRAs are members of neuroactive steroids capable of regulating C e l l & D e v e l o p m e n t a l B i o l o g y ISSN: 2168-9296 Cell & Developmental Biology