Abstract
Glial cells comprise the majority of cells in the central nervous system and exhibit diverse functions including the development of persistent neuropathic pain. While earlier theories have proposed that the applied electric field specifically affects neurons, it has been demonstrated that electrical stimulation (ES) of neural tissue modulates gene expression of the glial cells. This study examines the effect of ES on the expression of eight genes related to oxidative stress and neuroprotection in cultured rodent glioma cells. Concentric bipolar electrodes under seven different ES types were used to stimulate cells for 30 min in the presence and absence of extracellular glutamate. ES consisted of rectangular pulses at 50 Hz in varying proportions of anodic and cathodic phases. Real-time reverse-transcribed quantitative polymerase chain reaction was used to determine gene expression using the ∆∆Cq method. The results demonstrate that glutamate has a significant effect on gene expression in both stimulated and non-stimulated groups. Furthermore, stimulation parameters have differential effects on gene expression, both in the presence and absence of glutamate. ES has an effect on glial cell gene expression that is dependent on waveform composition. Optimization of ES therapy for chronic pain applications can be enhanced by this understanding.
Highlights
The initiation, propagation, and perception of acute pain has been traditionally described in terms of the excitation of neuronal transmission pathways [1]
This shows that glioma cells were delivered with reproducibility (R2 = 0.976) and the consistency of the MTT value from experiment to experiment is a first approximation of use of same cell number and/or cell viability
A primary component of the central nervous system, have a diverse set of functions including their involvement in the development and maintenance of chronic pain [12,38]
Summary
The initiation, propagation, and perception of acute pain has been traditionally described in terms of the excitation of neuronal transmission pathways [1]. During the process of neural sensitization, which is central to the development of chronic pain, glial cells are activated, and undertake an immunoresponsive role characterized by the release of chemical signals such as cytokines and chemokines that induce neuronal hyperexcitability, inflammation, and apoptosis [4]. This process involves pro-inflammatory processes associated with the development of the chronic pain state, it is known that the activated glia can release anti-inflammatory modulators indicative of a neuroprotective role [5]
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
