NMDA-R inhibition affects cellular process formation in Tilapia Melanocytes; a model for pigmented adrenergic neurons in process formation and retraction

• Published in: Metabolic brain disease 2014-06, Vol.29 (2), p.541-551
• Main Authors: Ogundele, Olalekan Michael, Okunnuga, Adetokunbo Adedotun, Fabiyi, Temitope Deborah, Olajide, Olayemi Joseph, Akinrinade, Ibukun Dorcas, Adeniyi, Philip Adeyemi, Ojo, Abiodun Ayodele
• Format: Article
• Language: English
• Subjects: Adrenergic Neurons - drug effects; Adrenergic Neurons - physiology; Animals; Biochemistry; Biomedical and Life Sciences; Biomedicine; Cells, Cultured; Excitatory Amino Acid Antagonists - pharmacology; Ketamine - pharmacology; Melanocytes - drug effects; Melanocytes - physiology; Metabolic Diseases; Neurology; Neurosciences; Oncology; Original Paper; Pigmentation - drug effects; Pigmentation - physiology; Receptors, N-Methyl-D-Aspartate - antagonists & inhibitors; Receptors, N-Methyl-D-Aspartate - physiology; Tilapia
• ISSN: 0885-7490; 1573-7365
• DOI: 10.1007/s11011-013-9447-6

Parkinson’s disease has long been described to be a product of dopamine and (or) melanin loss in the substanstia nigra (SN). Although most studies have focused on dopaminergic neurons, it is important to consider the role of pigment cells in the etiology of the disease and to create an in vitro live cell model for studies involving pigmented adrenergic cells of the SN in Parkinsonism. The Melanocytes share specific features with the pigmented adrenergic neurons as both cells are pigmented, contain adrenergic receptors and have cellular processes. Although the melanocyte cellular processes are relatively short and observable only when stimulated appropriately by epinephrine and other factors or molecules. This study employs the manipulation of N-Methyl-D-Aspartate Receptor (NMDA-R), a major receptor in neuronal development, in the process formation pattern of the melanocyte in order to create a suitable model to depict cellular process elongation and shortening in pigmented adrenergic cells. NMDA-R is an important glutamate receptor implicated in neurogenesis, neuronal migration, maturation and cell death, thus we investigated the role of NMDA-R potentiation by glutamate/KCN and its inhibition by ketamine in the behavior of fish scale melanocytes in vitro. This is aimed at establishing the regulatory role of NMDA-R in this cell type (melanocytes isolated form Tilapia) in a similar manner to what is observable in the mammalian neurons. In vitro live cell culture was prepared in modified Ringer’s solution following which the cells were treated as follows; Control, Glutamate, Ketamine, Glutamate + Ketamine, KCN + Ketamine and KCN. The culture was maintained for 10 min and the changes were captured in 3D-Time frame at 0, 5 and 10 min for the control and 5, 7 and 10 min for each of the treatment category. Glutamate treatment caused formation of short cellular processes localized directly on the cell body while ketamine treatment (inhibition of NMDA-R) facilitated elongation of secondary cellular processes (highly branched) from primary major processes (Less branched); co-incubation of glutamate and ketamine induced short and highly branched process formation. Cyanide toxicity induced degeneration and reduction of cell size while co-treatment of cyanide and ketamine gave changes similar to that observed in glutamate-ketamine co-incubation. NMDA-R is present in the melanocytes. Activation of the receptor reduced elongation process, while inhibition of the receptor