title: Short-Term Ketamine Treatment Decreases Oxidative Stress Without Influencing TRPM2 and TRPV1 Channel Gating in the Hippocampus and Dorsal Root Ganglion of Rats.
abstract: Calcium ions (Ca2+) are important second messengers in neurons. Ketamine (KETAM) is an anesthetic and analgesic, with psychotomimetic effects and abuse potential. KETAM modulates the entry of Ca2+in neurons through glutamate receptors, but its effect on transient receptor potential melastatin 2 (TRPM2) and transient receptor potential vanilloid 1 (TRPV1) channels has not been clarified. This study investigated the short-term effects of KETAM on oxidative stress and TRPM2 and TRPV1 channel gating in hippocampal and dorsal root ganglion (DRG) neurons of rats. Freshly isolated hippocampal and DRG neurons were incubated for 24 h with KETAM (0.3 mM). The TRPM2 channel antagonist, N-(p-amylcinnamoyl)anthranilic acid (ACA), inhibited cumene hydroperoxide and ADP-ribose-induced TRPM2 currents in the neurons, and capsazepine (CPZ) inhibited capsaicin-induced TRPV1 currents. The TRPM2 and TRPV1 channel current densities and intracellular free calcium ion concentration of the neurons were lower in the neurons exposed to ACA and CPZ compared to the control neurons, respectively. However, the values were not further decreased by the KETAM + CPZ and KETAM + ACA treatments. KETAM decreased lipid peroxidation levels in the neurons but increased glutathione peroxidase activity. In conclusion, short-term KETAM treatment decreased oxidative stress levels but did not seem to influence TRPM2- and TRPV1-mediated Ca2+entry.
authors.affiliation: Department of Psychiatry, Faculty of Medicine, Suleyman Demirel University, Isparta, Turkey.
authors.forename: Arif
authors.initials: A
authors.lastname: Demirdaş
authors.affiliation: Department of Neuroscience, Health Science Institute, Suleyman Demirel University, Isparta, Turkey. mustafanaziroglu@sdu.edu.tr.|Neuroscience Research Center, Suleyman Demirel University, 32260, Isparta, Turkey. mustafanaziroglu@sdu.edu.tr.
authors.forename: Mustafa
authors.initials: M
authors.lastname: Nazıroğlu
authors.affiliation: Department of Neuroscience, Health Science Institute, Suleyman Demirel University, Isparta, Turkey.
authors.forename: Ishak Suat
authors.initials: IS
authors.lastname: Övey
mesh_terms: D000700:Analgesics / Q000008:administration & dosage; D000818:Animals; D020013:Calcium Signaling / Q000187:drug effects / Q000502:physiology; D004334:Drug Administration Schedule; D005727:Ganglia, Spinal / Q000187:drug effects / Q000378:metabolism*; D006624:Hippocampus / Q000187:drug effects / Q000378:metabolism*; D015640:Ion Channel Gating / Q000187:drug effects / Q000502:physiology; D007649:Ketamine / Q000008:administration & dosage*; D008297:Male; D018384:Oxidative Stress / Q000187:drug effects / Q000502:physiology*; D051381:Rats; D017208:Rats, Wistar; D050053:TRPM Cation Channels / Q000378:metabolism*; D050916:TRPV Cation Channels / Q000378:metabolism*; D016896:Treatment Outcome
chemical_list: D000700:Analgesics; D050053:TRPM Cation Channels; D050916:TRPV Cation Channels; C557080:Trpm2 protein, rat; C493922:Trpv1 protein, rat; D007649:Ketamine
keywords: Ketamine; Oxidative stress; Pain; TRPM2; TRPV1