Nicotinic Acetylcholine Receptors in Glial Cells as Molecular Target for Parkinson’s Disease
Érica Novaes Soares,
Ana Carla dos Santos Costa,
Gabriel de Jesus Ferrolho,
Rodrigo Portes Ureshino,
Bruk Getachew,
Silvia Lima Costa,
Victor Diogenes Amaral da Silva,
Yousef Tizabi
Affiliations
Érica Novaes Soares
Laboratory of Neurochemistry and Cell Biology, Department of Biochemistry and Biophysics, Institute of Health Sciences, Federal University of Bahia, Salvador 40110-902, BA, Brazil
Ana Carla dos Santos Costa
Laboratory of Neurochemistry and Cell Biology, Department of Biochemistry and Biophysics, Institute of Health Sciences, Federal University of Bahia, Salvador 40110-902, BA, Brazil
Gabriel de Jesus Ferrolho
Laboratory of Neurochemistry and Cell Biology, Department of Biochemistry and Biophysics, Institute of Health Sciences, Federal University of Bahia, Salvador 40110-902, BA, Brazil
Rodrigo Portes Ureshino
Department of Biological Sciences, Universidade Federal de São Paulo, Diadema 09961-400, SP, Brazil
Bruk Getachew
Department of Pharmacology, College of Medicine, Howard University, 520 W Street NW, Washington, DC 20059, USA
Silvia Lima Costa
Laboratory of Neurochemistry and Cell Biology, Department of Biochemistry and Biophysics, Institute of Health Sciences, Federal University of Bahia, Salvador 40110-902, BA, Brazil
Victor Diogenes Amaral da Silva
Laboratory of Neurochemistry and Cell Biology, Department of Biochemistry and Biophysics, Institute of Health Sciences, Federal University of Bahia, Salvador 40110-902, BA, Brazil
Yousef Tizabi
Department of Pharmacology, College of Medicine, Howard University, 520 W Street NW, Washington, DC 20059, USA
Parkinson’s disease (PD) is a progressive neurodegenerative disease characterized by resting tremor, bradykinesia, rigidity, and postural instability that also includes non-motor symptoms such as mood dysregulation. Dopamine (DA) is the primary neurotransmitter involved in this disease, but cholinergic imbalance has also been implicated. Current intervention in PD is focused on replenishing central DA, which provides remarkable temporary symptomatic relief but does not address neuronal loss and the progression of the disease. It has been well established that neuronal nicotinic cholinergic receptors (nAChRs) can regulate DA release and that nicotine itself may have neuroprotective effects. Recent studies identified nAChRs in nonneuronal cell types, including glial cells, where they may regulate inflammatory responses. Given the crucial role of neuroinflammation in dopaminergic degeneration and the involvement of microglia and astrocytes in this response, glial nAChRs may provide a novel therapeutic target in the prevention and/or treatment of PD. In this review, following a brief discussion of PD, we focus on the role of glial cells and, specifically, their nAChRs in PD pathology and/or treatment.
