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Short-Term Ketamine Treatment Decreases Oxidative Stress Without Influencing TRPM2 and TRPV1 Channel Gating in the Hippocampus and Dorsal Root Ganglion of Rats.
Cell Mol Neurobiol. 2017 Jan; 37(1):133-144.CM

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+Show Affiliations

Department of Psychiatry, Faculty of Medicine, Suleyman Demirel University, Isparta, Turkey.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.Department of Neuroscience, Health Science Institute, Suleyman Demirel University, Isparta, Turkey.

Pub Type(s)

Journal Article

Language

eng

PubMed ID

26935063

Citation

Demirdaş, Arif, et al. "Short-Term Ketamine Treatment Decreases Oxidative Stress Without Influencing TRPM2 and TRPV1 Channel Gating in the Hippocampus and Dorsal Root Ganglion of Rats." Cellular and Molecular Neurobiology, vol. 37, no. 1, 2017, pp. 133-144.
Demirdaş A, Nazıroğlu M, Övey IS. Short-Term Ketamine Treatment Decreases Oxidative Stress Without Influencing TRPM2 and TRPV1 Channel Gating in the Hippocampus and Dorsal Root Ganglion of Rats. Cell Mol Neurobiol. 2017;37(1):133-144.
Demirdaş, A., Nazıroğlu, M., & Övey, I. S. (2017). Short-Term Ketamine Treatment Decreases Oxidative Stress Without Influencing TRPM2 and TRPV1 Channel Gating in the Hippocampus and Dorsal Root Ganglion of Rats. Cellular and Molecular Neurobiology, 37(1), 133-144. https://doi.org/10.1007/s10571-016-0353-4
Demirdaş A, Nazıroğlu M, Övey IS. Short-Term Ketamine Treatment Decreases Oxidative Stress Without Influencing TRPM2 and TRPV1 Channel Gating in the Hippocampus and Dorsal Root Ganglion of Rats. Cell Mol Neurobiol. 2017;37(1):133-144. PubMed PMID: 26935063.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Short-Term Ketamine Treatment Decreases Oxidative Stress Without Influencing TRPM2 and TRPV1 Channel Gating in the Hippocampus and Dorsal Root Ganglion of Rats. AU - Demirdaş,Arif, AU - Nazıroğlu,Mustafa, AU - Övey,Ishak Suat, Y1 - 2016/03/02/ PY - 2016/01/16/received PY - 2016/02/22/accepted PY - 2016/3/5/pubmed PY - 2017/2/14/medline PY - 2016/3/4/entrez KW - Ketamine KW - Oxidative stress KW - Pain KW - TRPM2 KW - TRPV1 SP - 133 EP - 144 JF - Cellular and molecular neurobiology JO - Cell Mol Neurobiol VL - 37 IS - 1 N2 - 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. SN - 1573-6830 UR - https://www.unboundmedicine.com/medline/citation/26935063/Short_Term_Ketamine_Treatment_Decreases_Oxidative_Stress_Without_Influencing_TRPM2_and_TRPV1_Channel_Gating_in_the_Hippocampus_and_Dorsal_Root_Ganglion_of_Rats_ L2 - https://doi.org/10.1007/s10571-016-0353-4 DB - PRIME DP - Unbound Medicine ER -