Research Article
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Investigation of Physiological Role of Mitochondrial KATP Channel’s on Penicillin G Induced Experimental Epilepsy Model in Rats

Year 2021, Volume: 16 Issue: 1, 19 - 29, 18.01.2021

Hayriye Soytürk Serif Demir Ömer Bozdoğan

Abstract

Epilepsy is one of the neurological diseases that is commonly seen in the world. It is characterized by excessive activation of neurons that can not be controlled by the central nervous system. ATP dependent potassium (KATP) channel modulation is related with the epilepsy. This study is intended to research the physiological role of mitochondrial KATP channels in epilepsy in electrophysiological perspective. And bepridil has been used for this purpose. Wistar albino rats have been used. Animals have been divided into three main groups; Control, bepridil applied groups in pre-seizure, and during seizure. As a result, bepridil once applied prior to seizure in 0.1 and 1mg/kg doses increased the latency period of the seizure. Bepridil showed anticonvulsant effect at doses of 0.1 and 1 mg/kg before and during seizure groups. Closure of sarcoplasmic channels and opening of mitochondrial channels may be important to decrease the convultion occurred during epilepy.

Keywords

Epilepsy Electrophysiology KATP Bepridil Mito KATP Channel

Supporting Institution

Bolu Abant İzzet Baysal Üniversitesi BAP birimi

Project Number

2012.03.01.521

Thanks

Bolu Abant İzzet Baysal Üniversitesi BAP birimine bu çalışmayı desteklediğinden dolayı teşekkür ederiz.

References

  • Megiddo, I., Colson, A., Chisholm, D., Dua, T., Nandi, A., and Laxminarayan, R., (2016). Health and Economic Benefits of Public Financing of Epilepsy Treatment in India: An Agent-Based Simulation Model. Epilepsia, 57(3):464-474.
  • Ngugi, A.K., Bottomley, C., Kleinschmidt, I., Sander, J.W., and Newton, C.R., (2010). Estimation of the Burden of Active and Life-time Epilepsy: A Meta-analytic Approach. Epilepsia, 51(5):883-890.
  • Lasoń, W., Chlebicka, M., and Rejdak, K., (2013). Research Advances in Basic Mechanisms of Seizures and Antiepileptic Drug Action. Pharmacol Rep, 65(4):787-801.
  • Dhopeshwarkar, A. and Mackie, K., (2014). CB2 Cannabinoid Receptors as a Therapeutic Target-what does the Future Hold?. Mol Pharmacol, 86(4):430-437.
  • Noma, A., (1983). ATP-regulated K+ Channels in Cardiac Muscle. Nature, 305(5930):147-148.
  • Ashcroft, F.M., Harrison, D.E., and Ashcroft, S.J., (1984). Glucose Induces Closure of Single Potassium Channels in Isolated Rat Pancreatic Beta-Cells. Nature, 312(5993):446-448.
  • Bennett, K., James, C., and Hussain, K., (2010). Pancreatic β-Cell KATP Channels: Hypoglycaemia and Hyperglycaemia. Rev Endocr Metab Disord, 11(3):157-163.
  • Flanagan, S.E., Clauin, S., Bellanné-Chantelot, C., de Lonlay, P., Harries, L.W., Gloyn, A.L., et al., (2009). Update of Mutations in the Genes Encoding the Pancreatic Beta-cell K(ATP) channel Subunits Kir6.2 (KCNJ11) and Sulfonylurea Receptor 1 (ABCC8) in Diabetes Mellitus and Hyperinsulinism. Hum Mutat, 30(2):170-180.
  • Mannhold, R., (2004). KATP channel openers: structure-activity relationships and therapeutic potential. Med Res Rev, 24(2):213-266. doi:10.1002/med.10060.
  • Liss, B. and Roeper, J., (2001). A Role for Neuronal KATP Channels in Metabolic Control of the Seizure Gate. Trends in Pharmacological Science, 12-22.
  • Ardehali, H. and O’Rourke, B., (2005). Mitochondrial KATP Channels in Cell Survival and Death. J Mol Cell Cardiol, 39:7-16.
  • Olson, T.M. and Terzic, A., (2010). Human KATP Channelopathies: Dis-eases of Metabolic Homeostasis. Eur J Physiol, 460:295-306.
  • Jazayeri, A., Zolfaghari, S., and Ostadhad, S., (2013). Anticonvulsant Effect of Diazoxide against Dichlorvos- Induced Seizures in Mice. The Scientific World Journal, 1-4.
  • Heurteaux, C., Bertaina, V., Widmann, C., and Lazdunski, M., (1993). K+ Channel Openers Prevent Global Ischemia-induced Expression of c-fos, c-jun, Heat Shock Protein, and Amyloid Beta-Protein Precursor Genes and Neuronal Death in Rat Hippocampus. Proceeding of the National Academy of Science USA, 90:9431-9435.
  • Jiang, K., Shui, Q., Xia, Z., and Yu, Z., (2003). Changes in the Gene and Protein Expression of KATP Channel Subunits in the Hippocampus of Rats Subjected to Picrotoxin-induced Kindling. Progress in Biophysics & Molecular Biology, 81:133-176.
  • Yamada, K. and Inagaki, N., (2005). Neuroprotection by KATP Channels. The Journal of Molecular and Cellular Cardiology, 38:945-949.
  • Takanari, H., Honjo, H., Takemoto, Y., Suzuki, T., Kato, S., Harada, M., et al., (2011). Bepridil Facilitates Early Termination of Spiral-wave Reentry in Two-dimensional Cardiac Muscle through an Increase of Intercellular Electrical Coupling. Journal of Pharmacological Sciences, 115:15-26.
  • Gonca, E. and Bozdoğan, O., (2010). Both Mitochondrial KATP Channel Opening and Sarcolemmal KATP Channel Blockage Confer Protection Against Ischemia/reperfusion Induced Arrhythmia in Anesthetized Male Rats. Journal of Cardiovascular Pharmacology and Therapeutics, 15:403-11.
  • Wang, J., Li, Z., Feng, M., Ren, K., Shen, G., Zhao, C., et al., (2013). Opening of Astrocytic Mitochondrial ATP-Sensitive Potassium Channels Upregulates Electrical Coupling between Hippocampal Astrocytes in Rat. Brain Slices, 8:1-14.
  • Nichols, C.G., (2006). KATP Channels as Molecular Sensors of Cellular Metabolism. Nature, 440:470-476.
  • Xue, Y., Xie, N., Lin, Y., Xu, J., Han, Y., Wang, S., et al., (2011). Role of PI3K/Akt in Diazoxide Preconditioning against Rat Hippocampal Neuronal Death in Pilocarpine-induced Seizures Brain Research, 1383:135–140.
  • Ghasemi, M., Shafaroodi, H., Karimollah, A.R., Gholipour, T., Nezami, B.G., Ebrahimi, F., et al., (2010). ATP-sensitive Potassium Channels Contribute to the Time-dependent Alteration in the Pentylenetetrazole-induced Seizure Threshold in Diabetic Mice. Seizure, 19:53–58.
  • Haj-Mirzaian, A., Ramezanzadeh, K., Afshari, K., Mousapour, P., Abbasi, N., Haj-Mirzaian, A., et al., (2019). Activation of ATP-sensitive K-channel Promotes the Anticonvulsant Properties of Cannabinoid Receptor agonist through Mitochondrial ATP Level Reduction. Epilepsy & Behavior, 93:1–6.
  • Terzic, A., Dzeja, P.P., and Holmuhamedov, E.L., (2000). Mitochondrial KATP Channels: Probing Molecular Identity and Pharmacology, J Mol Cell Cardiol, 32:1911-5.
  • Jan, L.Y. and Jan, Y.N., (1994). Potassium Channels and Their Evolving Gates. Nature, 371:119–22.
  • Mathie, A., Wooltorton, J.R., and Watkins, C.S., (1998). Voltage-activated Potassium Channels in Mammalian Neurons and their Block by Novel Pharmacological Agents. Gen Pharmacol, 30:13–24.
  • Storm, J.F., (1990). Potassium Currents in Hippocampal Pyramidal Cells. Prog Brain Res. 83:161–87.
  • Köhling, R. and Wolfart, J., (2016). Potassium Channels in Epilepsy. Cold Spring Harb Perspect Med, 6:a022871.
  • Niaki, S.E.A., Shafaroodi, H., Ghasemi, M., Shakiba, B., Fakhimi, A., and Dehpour, A.R., (2008). Mouth Breathing Increases the Pentylenetetrazole-induced Seizure Threshold in Mice: a Role for ATP-sensitive Potassium Channels. Epilepsy Behav, 13:284–9.
  • Shafaroodi, H., Asadi, S., Sadeghipour, H., Ghasemi, M., Ebrahimi, F., Tavakoli, S., et al., (2007). Role of ATP-Sensitive Potassium Channels in the Biphasic Effects of Morphine on Pentylenetetrazole-induced Seizure Threshold in Mice. Epilepsy Res, 75:63–9.
  • Franke, H., Grummich, B., Härtig, W., Grosche, J., Regenthal, R., Edwards, R.H., et al., (2006). Changes in Purinergic Signaling after Cerebral Injury – involvement of Glutamatergic Mechanisms? Int. J. Dev Neurosci, 24:123–132.
  • Melani, A., Turchi, D., Vannucchi, M.G., Cipriani, S., Gianfriddo, M., and Pedata, F., (2005). ATP Extracellular Concentrations are Increased in the Rat Striatum during in Vivo Ischemia. Neurochem Int, 47:442–448.
  • Burnstock, G., (2016). An Introduction to the Roles of Purinergic Signalling in Neurodegeneration, Neuroprotection and Neuroregeneration. Neuropharmacology, 104:4–17.
  • Enge, T., Gomez-Villafuertes, R., Tanaka, K., Mesuret, G., Sanz-Rodriguez, A., Garcia-Huerta, P., et al., (2012a). Seizure Suppression and Neuroprotection by Targeting the Purinergic P2x7 Receptor During Status Epilepticus in mice. FASEB J, 26:1616–1628.
  • Jimenez-Pacheco, A., Diaz-Hernandez, M., Arribas-Blazquez, M., Sanz-Rodriguez, A., Olivos-Oré, LA., Artalejo, AR., et al., (2016). Transient P2x7 Receptor Antagonism Produces Lasting Reductions in Spontaneous Seizures and Gliosis in Experimental Temporal Lobe Epilepsy. J. Neurosci, 36:5920–5932.
  • Doná, F., Conceição, I.M., Ulrich, H., Ribeiro, E.B., Freitas, T.A., Nencioni, A.L.A., et al., (2016). Variations of Atp and İts Metabolites in the Hippocampus Of Rats Subjected to Pilocarpine-induced Temporal Lobe Epilepsy. Purinergic Signal, 12:295–302.
  • Engel, T., Alves, M., Sheedy, C., and Henshall, D.C., (2016). ATP Ergic Signalling During Seizures and Epilepsy. Neuropharmacology, 104:140–153.
  • Engel, T., Alves, M., Sheedy, C., and Henshall., D.C., (2012a). Seizure Suppression and Neuroprotection by Targeting the Purinergic P2x7 Receptor During Status Epilepticus in Mice. FASEB J, 26:1616–1628.
  • Beamer, E., Gölöncsér, F., Horváth, G., Bekő, K., Otrokocsi, L., Koványi, B., et al., (2016). Purinergic Mechanisms in Neuroinflammation: an Update from Molecules to Behavior. Neuropharmacology, 104:94–104.

Year 2021, Volume: 16 Issue: 1, 19 - 29, 18.01.2021

Hayriye Soytürk Serif Demir Ömer Bozdoğan

Abstract

Keywords

Epilepsy

Project Number

2012.03.01.521

References

  • Megiddo, I., Colson, A., Chisholm, D., Dua, T., Nandi, A., and Laxminarayan, R., (2016). Health and Economic Benefits of Public Financing of Epilepsy Treatment in India: An Agent-Based Simulation Model. Epilepsia, 57(3):464-474.
  • Ngugi, A.K., Bottomley, C., Kleinschmidt, I., Sander, J.W., and Newton, C.R., (2010). Estimation of the Burden of Active and Life-time Epilepsy: A Meta-analytic Approach. Epilepsia, 51(5):883-890.
  • Lasoń, W., Chlebicka, M., and Rejdak, K., (2013). Research Advances in Basic Mechanisms of Seizures and Antiepileptic Drug Action. Pharmacol Rep, 65(4):787-801.
  • Dhopeshwarkar, A. and Mackie, K., (2014). CB2 Cannabinoid Receptors as a Therapeutic Target-what does the Future Hold?. Mol Pharmacol, 86(4):430-437.
  • Noma, A., (1983). ATP-regulated K+ Channels in Cardiac Muscle. Nature, 305(5930):147-148.
  • Ashcroft, F.M., Harrison, D.E., and Ashcroft, S.J., (1984). Glucose Induces Closure of Single Potassium Channels in Isolated Rat Pancreatic Beta-Cells. Nature, 312(5993):446-448.
  • Bennett, K., James, C., and Hussain, K., (2010). Pancreatic β-Cell KATP Channels: Hypoglycaemia and Hyperglycaemia. Rev Endocr Metab Disord, 11(3):157-163.
  • Flanagan, S.E., Clauin, S., Bellanné-Chantelot, C., de Lonlay, P., Harries, L.W., Gloyn, A.L., et al., (2009). Update of Mutations in the Genes Encoding the Pancreatic Beta-cell K(ATP) channel Subunits Kir6.2 (KCNJ11) and Sulfonylurea Receptor 1 (ABCC8) in Diabetes Mellitus and Hyperinsulinism. Hum Mutat, 30(2):170-180.
  • Mannhold, R., (2004). KATP channel openers: structure-activity relationships and therapeutic potential. Med Res Rev, 24(2):213-266. doi:10.1002/med.10060.
  • Liss, B. and Roeper, J., (2001). A Role for Neuronal KATP Channels in Metabolic Control of the Seizure Gate. Trends in Pharmacological Science, 12-22.
  • Ardehali, H. and O’Rourke, B., (2005). Mitochondrial KATP Channels in Cell Survival and Death. J Mol Cell Cardiol, 39:7-16.
  • Olson, T.M. and Terzic, A., (2010). Human KATP Channelopathies: Dis-eases of Metabolic Homeostasis. Eur J Physiol, 460:295-306.
  • Jazayeri, A., Zolfaghari, S., and Ostadhad, S., (2013). Anticonvulsant Effect of Diazoxide against Dichlorvos- Induced Seizures in Mice. The Scientific World Journal, 1-4.
  • Heurteaux, C., Bertaina, V., Widmann, C., and Lazdunski, M., (1993). K+ Channel Openers Prevent Global Ischemia-induced Expression of c-fos, c-jun, Heat Shock Protein, and Amyloid Beta-Protein Precursor Genes and Neuronal Death in Rat Hippocampus. Proceeding of the National Academy of Science USA, 90:9431-9435.
  • Jiang, K., Shui, Q., Xia, Z., and Yu, Z., (2003). Changes in the Gene and Protein Expression of KATP Channel Subunits in the Hippocampus of Rats Subjected to Picrotoxin-induced Kindling. Progress in Biophysics & Molecular Biology, 81:133-176.
  • Yamada, K. and Inagaki, N., (2005). Neuroprotection by KATP Channels. The Journal of Molecular and Cellular Cardiology, 38:945-949.
  • Takanari, H., Honjo, H., Takemoto, Y., Suzuki, T., Kato, S., Harada, M., et al., (2011). Bepridil Facilitates Early Termination of Spiral-wave Reentry in Two-dimensional Cardiac Muscle through an Increase of Intercellular Electrical Coupling. Journal of Pharmacological Sciences, 115:15-26.
  • Gonca, E. and Bozdoğan, O., (2010). Both Mitochondrial KATP Channel Opening and Sarcolemmal KATP Channel Blockage Confer Protection Against Ischemia/reperfusion Induced Arrhythmia in Anesthetized Male Rats. Journal of Cardiovascular Pharmacology and Therapeutics, 15:403-11.
  • Wang, J., Li, Z., Feng, M., Ren, K., Shen, G., Zhao, C., et al., (2013). Opening of Astrocytic Mitochondrial ATP-Sensitive Potassium Channels Upregulates Electrical Coupling between Hippocampal Astrocytes in Rat. Brain Slices, 8:1-14.
  • Nichols, C.G., (2006). KATP Channels as Molecular Sensors of Cellular Metabolism. Nature, 440:470-476.
  • Xue, Y., Xie, N., Lin, Y., Xu, J., Han, Y., Wang, S., et al., (2011). Role of PI3K/Akt in Diazoxide Preconditioning against Rat Hippocampal Neuronal Death in Pilocarpine-induced Seizures Brain Research, 1383:135–140.
  • Ghasemi, M., Shafaroodi, H., Karimollah, A.R., Gholipour, T., Nezami, B.G., Ebrahimi, F., et al., (2010). ATP-sensitive Potassium Channels Contribute to the Time-dependent Alteration in the Pentylenetetrazole-induced Seizure Threshold in Diabetic Mice. Seizure, 19:53–58.
  • Haj-Mirzaian, A., Ramezanzadeh, K., Afshari, K., Mousapour, P., Abbasi, N., Haj-Mirzaian, A., et al., (2019). Activation of ATP-sensitive K-channel Promotes the Anticonvulsant Properties of Cannabinoid Receptor agonist through Mitochondrial ATP Level Reduction. Epilepsy & Behavior, 93:1–6.
  • Terzic, A., Dzeja, P.P., and Holmuhamedov, E.L., (2000). Mitochondrial KATP Channels: Probing Molecular Identity and Pharmacology, J Mol Cell Cardiol, 32:1911-5.
  • Jan, L.Y. and Jan, Y.N., (1994). Potassium Channels and Their Evolving Gates. Nature, 371:119–22.
  • Mathie, A., Wooltorton, J.R., and Watkins, C.S., (1998). Voltage-activated Potassium Channels in Mammalian Neurons and their Block by Novel Pharmacological Agents. Gen Pharmacol, 30:13–24.
  • Storm, J.F., (1990). Potassium Currents in Hippocampal Pyramidal Cells. Prog Brain Res. 83:161–87.
  • Köhling, R. and Wolfart, J., (2016). Potassium Channels in Epilepsy. Cold Spring Harb Perspect Med, 6:a022871.
  • Niaki, S.E.A., Shafaroodi, H., Ghasemi, M., Shakiba, B., Fakhimi, A., and Dehpour, A.R., (2008). Mouth Breathing Increases the Pentylenetetrazole-induced Seizure Threshold in Mice: a Role for ATP-sensitive Potassium Channels. Epilepsy Behav, 13:284–9.
  • Shafaroodi, H., Asadi, S., Sadeghipour, H., Ghasemi, M., Ebrahimi, F., Tavakoli, S., et al., (2007). Role of ATP-Sensitive Potassium Channels in the Biphasic Effects of Morphine on Pentylenetetrazole-induced Seizure Threshold in Mice. Epilepsy Res, 75:63–9.
  • Franke, H., Grummich, B., Härtig, W., Grosche, J., Regenthal, R., Edwards, R.H., et al., (2006). Changes in Purinergic Signaling after Cerebral Injury – involvement of Glutamatergic Mechanisms? Int. J. Dev Neurosci, 24:123–132.
  • Melani, A., Turchi, D., Vannucchi, M.G., Cipriani, S., Gianfriddo, M., and Pedata, F., (2005). ATP Extracellular Concentrations are Increased in the Rat Striatum during in Vivo Ischemia. Neurochem Int, 47:442–448.
  • Burnstock, G., (2016). An Introduction to the Roles of Purinergic Signalling in Neurodegeneration, Neuroprotection and Neuroregeneration. Neuropharmacology, 104:4–17.
  • Enge, T., Gomez-Villafuertes, R., Tanaka, K., Mesuret, G., Sanz-Rodriguez, A., Garcia-Huerta, P., et al., (2012a). Seizure Suppression and Neuroprotection by Targeting the Purinergic P2x7 Receptor During Status Epilepticus in mice. FASEB J, 26:1616–1628.
  • Jimenez-Pacheco, A., Diaz-Hernandez, M., Arribas-Blazquez, M., Sanz-Rodriguez, A., Olivos-Oré, LA., Artalejo, AR., et al., (2016). Transient P2x7 Receptor Antagonism Produces Lasting Reductions in Spontaneous Seizures and Gliosis in Experimental Temporal Lobe Epilepsy. J. Neurosci, 36:5920–5932.
  • Doná, F., Conceição, I.M., Ulrich, H., Ribeiro, E.B., Freitas, T.A., Nencioni, A.L.A., et al., (2016). Variations of Atp and İts Metabolites in the Hippocampus Of Rats Subjected to Pilocarpine-induced Temporal Lobe Epilepsy. Purinergic Signal, 12:295–302.
  • Engel, T., Alves, M., Sheedy, C., and Henshall, D.C., (2016). ATP Ergic Signalling During Seizures and Epilepsy. Neuropharmacology, 104:140–153.
  • Engel, T., Alves, M., Sheedy, C., and Henshall., D.C., (2012a). Seizure Suppression and Neuroprotection by Targeting the Purinergic P2x7 Receptor During Status Epilepticus in Mice. FASEB J, 26:1616–1628.
  • Beamer, E., Gölöncsér, F., Horváth, G., Bekő, K., Otrokocsi, L., Koványi, B., et al., (2016). Purinergic Mechanisms in Neuroinflammation: an Update from Molecules to Behavior. Neuropharmacology, 104:94–104.
There are 39 citations in total.

Details

Primary Language English
Subjects Health Care Administration
Journal Section Articles
Authors

Hayriye Soytürk 0000-0002-0000-3768

Serif Demir 0000-0002-2548-1969

Ömer Bozdoğan 0000-0001-5073-0691

Project Number 2012.03.01.521
Publication Date January 18, 2021
Published in Issue Year 2021 Volume: 16 Issue: 1

Cite

APA Soytürk, H., Demir, S., & Bozdoğan, Ö. (2021). Investigation of Physiological Role of Mitochondrial KATP Channel’s on Penicillin G Induced Experimental Epilepsy Model in Rats. Medical Sciences, 16(1), 19-29.
AMA Soytürk H, Demir S, Bozdoğan Ö. Investigation of Physiological Role of Mitochondrial KATP Channel’s on Penicillin G Induced Experimental Epilepsy Model in Rats. Medical Sciences. January 2021;16(1):19-29.
Chicago Soytürk, Hayriye, Serif Demir, and Ömer Bozdoğan. “Investigation of Physiological Role of Mitochondrial KATP Channel’s on Penicillin G Induced Experimental Epilepsy Model in Rats”. Medical Sciences 16, no. 1 (January 2021): 19-29.
EndNote Soytürk H, Demir S, Bozdoğan Ö (January 1, 2021) Investigation of Physiological Role of Mitochondrial KATP Channel’s on Penicillin G Induced Experimental Epilepsy Model in Rats. Medical Sciences 16 1 19–29.
IEEE H. Soytürk, S. Demir, and Ö. Bozdoğan, “Investigation of Physiological Role of Mitochondrial KATP Channel’s on Penicillin G Induced Experimental Epilepsy Model in Rats”, Medical Sciences, vol. 16, no. 1, pp. 19–29, 2021.
ISNAD Soytürk, Hayriye et al. “Investigation of Physiological Role of Mitochondrial KATP Channel’s on Penicillin G Induced Experimental Epilepsy Model in Rats”. Medical Sciences 16/1 (January 2021), 19-29.
JAMA Soytürk H, Demir S, Bozdoğan Ö. Investigation of Physiological Role of Mitochondrial KATP Channel’s on Penicillin G Induced Experimental Epilepsy Model in Rats. Medical Sciences. 2021;16:19–29.
MLA Soytürk, Hayriye et al. “Investigation of Physiological Role of Mitochondrial KATP Channel’s on Penicillin G Induced Experimental Epilepsy Model in Rats”. Medical Sciences, vol. 16, no. 1, 2021, pp. 19-29.
Vancouver Soytürk H, Demir S, Bozdoğan Ö. Investigation of Physiological Role of Mitochondrial KATP Channel’s on Penicillin G Induced Experimental Epilepsy Model in Rats. Medical Sciences. 2021;16(1):19-2.