Skip to main content
Erschienen in: Journal of Neural Transmission 1/2009

01.01.2009 | Basic Neurosciences, Genetics and Immunology - Original Article

Temporal expression of AMP-activated protein kinase activation during the kainic acid-induced hippocampal cell death

verfasst von: Ji Yeong Lee, Beong Tak Jeon, Hyun Joo Shin, Dong Hoon Lee, Jae Yoon Han, Hyun Joon Kim, Sang Soo Kang, Gyeong Jae Cho, Wan Sung Choi, Gu Seob Roh

Erschienen in: Journal of Neural Transmission | Ausgabe 1/2009

Einloggen, um Zugang zu erhalten

Abstract

Kainic acid (KA)-induced seizure induces the hippocampal cell death. There are reports that AMP-activated protein kinase (AMPK), which is an important regulator of energy homeostasis of cells, has been proposed as apoptotic molecule. In this study, we investigated the altered expression of AMPK cascade in the hippocampus of mice during KA-induced hippocampal cell death. Mice were killed at 2, 6, 24 or 48 h after KA (30 mg/kg) injection. Histological evaluation of KA-treated hippocampus revealed hippocampal cell death first at 6 h and appearing prominently by 48 h after KA injection. Immunoreactivity of Ca2+/calmodulin-dependent protein kinase kinaseβ (CaMKKβ) was increased after KA treatment. In Western blot analysis, AMPK activation was increased 2 h after KA treatment. The proteins of downstream AMPK, including those of glucose transporter1 (GLUT1) and phosphorylation of Acetyl CoA Carboxylase (ACC) were increased in the hippocampus after KA treatment. These results indicate that sustained AMPK activation might be a mechanism by which KA-induced seizure causes hippocampal cell death of mice.
Literatur
Zurück zum Zitat Andersson U, Filipsson K, Abbott CR et al (2004) AMP-activated protein kinase plays a role in the control of food intake. J Biol Chem 279:12005–12008PubMedCrossRef Andersson U, Filipsson K, Abbott CR et al (2004) AMP-activated protein kinase plays a role in the control of food intake. J Biol Chem 279:12005–12008PubMedCrossRef
Zurück zum Zitat Barnes K, Ingram JC, Porras OH et al (2002) Activation of GLUT1 by metabolic and osmotic stress: potential involvement of AMP-activated protein kinase (AMPK). J Cell Sci 115:2433–2442PubMed Barnes K, Ingram JC, Porras OH et al (2002) Activation of GLUT1 by metabolic and osmotic stress: potential involvement of AMP-activated protein kinase (AMPK). J Cell Sci 115:2433–2442PubMed
Zurück zum Zitat Blázquez C, Sánchez C, Velasco G et al (1998) Role of carnitine palmitoyltransferase I in the control of ketogenesis in primary cultures of rat astrocytes. J Neurochem 71:1597–1606PubMedCrossRef Blázquez C, Sánchez C, Velasco G et al (1998) Role of carnitine palmitoyltransferase I in the control of ketogenesis in primary cultures of rat astrocytes. J Neurochem 71:1597–1606PubMedCrossRef
Zurück zum Zitat Carling D (2004) The AMP-activated protein kinase cascade—a unifying system for energy control. Trends Biochem Sci 29:18–24PubMedCrossRef Carling D (2004) The AMP-activated protein kinase cascade—a unifying system for energy control. Trends Biochem Sci 29:18–24PubMedCrossRef
Zurück zum Zitat Corton JM, Gillespie JG, Hardie DG (1994) Role of the AMP-activated protein kinase in the cellular stress response. Curr Biol 4:315–324PubMedCrossRef Corton JM, Gillespie JG, Hardie DG (1994) Role of the AMP-activated protein kinase in the cellular stress response. Curr Biol 4:315–324PubMedCrossRef
Zurück zum Zitat Culmsee C, Monnig J, Kemp BE et al (2001) AMP-activated protein kinase is highly expressed in neurons in the developing rat brain and promotes neuronal survival following glucose deprivation. J Mol Neurosci 17:45–58PubMedCrossRef Culmsee C, Monnig J, Kemp BE et al (2001) AMP-activated protein kinase is highly expressed in neurons in the developing rat brain and promotes neuronal survival following glucose deprivation. J Mol Neurosci 17:45–58PubMedCrossRef
Zurück zum Zitat Dagon Y, Avraham Y, Berry EM (2006) AMPK activation regulates apoptosis, adipogenesis, and lipolysis by eIF2alpha in adipocytes. Biochem Biophys Res Commun 340:43–47PubMedCrossRef Dagon Y, Avraham Y, Berry EM (2006) AMPK activation regulates apoptosis, adipogenesis, and lipolysis by eIF2alpha in adipocytes. Biochem Biophys Res Commun 340:43–47PubMedCrossRef
Zurück zum Zitat Dasgupta B, Milbrandt J (2007) Resveratrol stimulates AMP kinase activity in neurons. Proc Natl Acad Sci USA 104:7217–7222PubMedCrossRef Dasgupta B, Milbrandt J (2007) Resveratrol stimulates AMP kinase activity in neurons. Proc Natl Acad Sci USA 104:7217–7222PubMedCrossRef
Zurück zum Zitat Evans MC, Griffiths T, Meldrum BS (1984) Kainic acid seizures and the reversibility of calcium loading in vulnerable neurons in the hippocampus. Neuropathol Appl Neurobiol 10:285–302PubMedCrossRef Evans MC, Griffiths T, Meldrum BS (1984) Kainic acid seizures and the reversibility of calcium loading in vulnerable neurons in the hippocampus. Neuropathol Appl Neurobiol 10:285–302PubMedCrossRef
Zurück zum Zitat Fryer LG, Foufelle F, Barnes K et al (2002) Characterization of the role of the AMP-activated protein kinase in the stimulation of glucose transport in skeletal muscle cells. Biochem J 363:167–174PubMedCrossRef Fryer LG, Foufelle F, Barnes K et al (2002) Characterization of the role of the AMP-activated protein kinase in the stimulation of glucose transport in skeletal muscle cells. Biochem J 363:167–174PubMedCrossRef
Zurück zum Zitat Garcia-Gil M, Pesi R, Perna S et al (2003) 5′-aminoimidazole-4-carboxamide riboside induces apoptosis in human neuroblastoma cells. Neuroscience 117:811–820PubMedCrossRef Garcia-Gil M, Pesi R, Perna S et al (2003) 5′-aminoimidazole-4-carboxamide riboside induces apoptosis in human neuroblastoma cells. Neuroscience 117:811–820PubMedCrossRef
Zurück zum Zitat Hu RQ, Koh S, Torgerson T et al (1998) Neuronal stress and injury in C57/BL mice after systemic kainic acid administration. Brain Res 810:229–240PubMedCrossRef Hu RQ, Koh S, Torgerson T et al (1998) Neuronal stress and injury in C57/BL mice after systemic kainic acid administration. Brain Res 810:229–240PubMedCrossRef
Zurück zum Zitat Hurley RL, Anderson KA, Franzone JM et al (2005) The Ca2+/calmodulin-dependent protein kinase kinases are AMP-activated protein kinase kinases. J Biol Chem 280:29060–29066PubMedCrossRef Hurley RL, Anderson KA, Franzone JM et al (2005) The Ca2+/calmodulin-dependent protein kinase kinases are AMP-activated protein kinase kinases. J Biol Chem 280:29060–29066PubMedCrossRef
Zurück zum Zitat Jung JE, Lee J, Ha J et al (2004) 5-Aminoimidazole-4-carboxamide-ribonucleoside enhances oxidative stress-induced apoptosis through activation of nuclear factor-kappaB in mouse Neuro 2a neuroblastoma cells. Neurosci Lett 354:197–200PubMedCrossRef Jung JE, Lee J, Ha J et al (2004) 5-Aminoimidazole-4-carboxamide-ribonucleoside enhances oxidative stress-induced apoptosis through activation of nuclear factor-kappaB in mouse Neuro 2a neuroblastoma cells. Neurosci Lett 354:197–200PubMedCrossRef
Zurück zum Zitat Kasischke KA, Vishwasrao HD, Fisher PJ et al (2004) Neural activity triggers neuronal oxidative metabolism followed by astrocytic glycolysis. Science 305:99–103PubMedCrossRef Kasischke KA, Vishwasrao HD, Fisher PJ et al (2004) Neural activity triggers neuronal oxidative metabolism followed by astrocytic glycolysis. Science 305:99–103PubMedCrossRef
Zurück zum Zitat Kefas BA, Cai Y, Kerckhofs K et al (2004) Metformin-induced stimulation of AMP-activated protein kinase in beta-cells impairs their glucose responsiveness and can lead to apoptosis. Biochem Pharmacol 68:409–416PubMedCrossRef Kefas BA, Cai Y, Kerckhofs K et al (2004) Metformin-induced stimulation of AMP-activated protein kinase in beta-cells impairs their glucose responsiveness and can lead to apoptosis. Biochem Pharmacol 68:409–416PubMedCrossRef
Zurück zum Zitat Kemp BE, Mitchelhill KI, Stapleton D et al (1999) Dealing with energy demand: the AMP-activated protein kinase. Trends Biochem Sci 24:22–25PubMedCrossRef Kemp BE, Mitchelhill KI, Stapleton D et al (1999) Dealing with energy demand: the AMP-activated protein kinase. Trends Biochem Sci 24:22–25PubMedCrossRef
Zurück zum Zitat Kim MS, Park JY, Namkoong C et al (2004) Anti-obesity effects of alpha-lipoic acid mediated by suppression of hypothalamic AMP-activated protein kinase. Nat Med 10:727–733PubMedCrossRef Kim MS, Park JY, Namkoong C et al (2004) Anti-obesity effects of alpha-lipoic acid mediated by suppression of hypothalamic AMP-activated protein kinase. Nat Med 10:727–733PubMedCrossRef
Zurück zum Zitat Kondratyev A, Gale K (2000) Intracerebral injection of caspase-3 inhibitor prevents neuronal apoptosis after kainic acid-evoked status epilepticus. Brain Res Mol Brain Res 75:216–224PubMedCrossRef Kondratyev A, Gale K (2000) Intracerebral injection of caspase-3 inhibitor prevents neuronal apoptosis after kainic acid-evoked status epilepticus. Brain Res Mol Brain Res 75:216–224PubMedCrossRef
Zurück zum Zitat Li J, Coven DL, Miller EJ et al (2006) Activation of AMPK alpha- and gamma-isoform complexes in the intact ischemic rat heart. Am J Physiol Heart Circ Physiol 291:1927–1934CrossRef Li J, Coven DL, Miller EJ et al (2006) Activation of AMPK alpha- and gamma-isoform complexes in the intact ischemic rat heart. Am J Physiol Heart Circ Physiol 291:1927–1934CrossRef
Zurück zum Zitat Moore F, Weekes J, Hardie DG (1991) Evidence that AMP triggers phosphorylation as well as direct allosteric activation of rat liver AMP-activated protein kinase. A sensitive mechanism to protect the cell against ATP depletion. Eur J Biochem 199:691–697PubMedCrossRef Moore F, Weekes J, Hardie DG (1991) Evidence that AMP triggers phosphorylation as well as direct allosteric activation of rat liver AMP-activated protein kinase. A sensitive mechanism to protect the cell against ATP depletion. Eur J Biochem 199:691–697PubMedCrossRef
Zurück zum Zitat Narkilahti S, Pirttilä TJ, Lukasiuk K et al (2003) Expression and activation of caspase 3 following status epilepticus in the rat. Eur J Neurosci 18:1486–1496PubMedCrossRef Narkilahti S, Pirttilä TJ, Lukasiuk K et al (2003) Expression and activation of caspase 3 following status epilepticus in the rat. Eur J Neurosci 18:1486–1496PubMedCrossRef
Zurück zum Zitat Ramamurthy S, Ronnett GV (2006) Developing a head for energy sensing: AMP-activated protein kinase as a multifunctional metabolic sensor in the brain. J Physiol 574:85–93PubMedCrossRef Ramamurthy S, Ronnett GV (2006) Developing a head for energy sensing: AMP-activated protein kinase as a multifunctional metabolic sensor in the brain. J Physiol 574:85–93PubMedCrossRef
Zurück zum Zitat Ruderman NB, Dean D (1998) Malonyl CoA, long chain fatty acyl CoA and insulin resistance in skeletal muscle. J Basic Clin Physiol Pharmacol 9:295–308PubMed Ruderman NB, Dean D (1998) Malonyl CoA, long chain fatty acyl CoA and insulin resistance in skeletal muscle. J Basic Clin Physiol Pharmacol 9:295–308PubMed
Zurück zum Zitat Salt IP, Johnson G, Ashcroft SJ et al (1998) AMP-activated protein kinase is activated by low glucose in cell lines derived from pancreatic beta cells, and may regulate insulin release. Biochem J 335:533–539PubMed Salt IP, Johnson G, Ashcroft SJ et al (1998) AMP-activated protein kinase is activated by low glucose in cell lines derived from pancreatic beta cells, and may regulate insulin release. Biochem J 335:533–539PubMed
Zurück zum Zitat Schurr A, Miller JJ, Payne RS et al (1999) An increase in lactate output by brain tissue serves to meet the energy needs of glutamate-activated neurons. J Neurosci 19:34–39PubMed Schurr A, Miller JJ, Payne RS et al (1999) An increase in lactate output by brain tissue serves to meet the energy needs of glutamate-activated neurons. J Neurosci 19:34–39PubMed
Zurück zum Zitat Schwechter EM, Velísková J, Velísek L (2003) Correlation between extracellular glucose and seizure susceptibility in adult rats. Ann Neurol 53:91–101PubMedCrossRef Schwechter EM, Velísková J, Velísek L (2003) Correlation between extracellular glucose and seizure susceptibility in adult rats. Ann Neurol 53:91–101PubMedCrossRef
Zurück zum Zitat Shibata R, Sato K, Pimentel DR et al (2005) Adiponectin protects against myocardial ischemia-reperfusion injury through AMPK-and COX-2-dependent mechanisms. Nat Med 11:1096–1103PubMedCrossRef Shibata R, Sato K, Pimentel DR et al (2005) Adiponectin protects against myocardial ischemia-reperfusion injury through AMPK-and COX-2-dependent mechanisms. Nat Med 11:1096–1103PubMedCrossRef
Zurück zum Zitat Stahmann N, Woods A, Carling D et al (2006) Thrombin activates AMP-activated protein kinase in endothelial cells via a pathway involving Ca2+/calmodulin-dependent protein kinase kinase beta. Mol Cell Biol 26:5933–5945PubMedCrossRef Stahmann N, Woods A, Carling D et al (2006) Thrombin activates AMP-activated protein kinase in endothelial cells via a pathway involving Ca2+/calmodulin-dependent protein kinase kinase beta. Mol Cell Biol 26:5933–5945PubMedCrossRef
Zurück zum Zitat Sztriha L, Joó F, Szerdahelyi P (1985) Accumulation of calcium in the rat hippocampus during kainic acid seizures. Brain Res 360:51–57PubMedCrossRef Sztriha L, Joó F, Szerdahelyi P (1985) Accumulation of calcium in the rat hippocampus during kainic acid seizures. Brain Res 360:51–57PubMedCrossRef
Zurück zum Zitat Sztriha L, Joo F (1986) Intraendothelial accumulation of calcium in the hippocampus and thalamus of rats after systemic kainic acid administration. Acta Neuropathol 72:111–116PubMedCrossRef Sztriha L, Joo F (1986) Intraendothelial accumulation of calcium in the hippocampus and thalamus of rats after systemic kainic acid administration. Acta Neuropathol 72:111–116PubMedCrossRef
Zurück zum Zitat Terai K, Hiramoto Y, Masaki M et al (2005) AMP-activated protein kinase protects cardiomyocytes against hypoxic injury through attenuation of endoplasmic reticulum stress. Mol Cell Biol 25:9554–9575PubMedCrossRef Terai K, Hiramoto Y, Masaki M et al (2005) AMP-activated protein kinase protects cardiomyocytes against hypoxic injury through attenuation of endoplasmic reticulum stress. Mol Cell Biol 25:9554–9575PubMedCrossRef
Zurück zum Zitat Vavvas D, Apazidis A, Saha AK et al (1997) Contraction-induced changes in acetyl-CoA carboxylase and 5′-AMP-activated kinase in skeletal muscle. J Biol Chem 272:13255–13261PubMedCrossRef Vavvas D, Apazidis A, Saha AK et al (1997) Contraction-induced changes in acetyl-CoA carboxylase and 5′-AMP-activated kinase in skeletal muscle. J Biol Chem 272:13255–13261PubMedCrossRef
Metadaten
Titel
Temporal expression of AMP-activated protein kinase activation during the kainic acid-induced hippocampal cell death
verfasst von
Ji Yeong Lee
Beong Tak Jeon
Hyun Joo Shin
Dong Hoon Lee
Jae Yoon Han
Hyun Joon Kim
Sang Soo Kang
Gyeong Jae Cho
Wan Sung Choi
Gu Seob Roh
Publikationsdatum
01.01.2009
Verlag
Springer Vienna
Erschienen in
Journal of Neural Transmission / Ausgabe 1/2009
Print ISSN: 0300-9564
Elektronische ISSN: 1435-1463
DOI
https://doi.org/10.1007/s00702-008-0158-9

Weitere Artikel der Ausgabe 1/2009

Journal of Neural Transmission 1/2009 Zur Ausgabe

Biological Child and Adolescent Psychiatry - Short Communication

Emotional memory in ADHD patients with and without comorbid ODD/CD

Biological Child and Adolescent Psychiatry - Short Communication

Reduced serotonergic functioning changes heart rate in ADHD

Leitlinien kompakt für die Neurologie

Mit medbee Pocketcards sicher entscheiden.

Seit 2022 gehört die medbee GmbH zum Springer Medizin Verlag

Nicht Creutzfeldt Jakob, sondern Abführtee-Vergiftung

29.05.2024 Hyponatriämie Nachrichten

Eine ältere Frau trinkt regelmäßig Sennesblättertee gegen ihre Verstopfung. Der scheint plötzlich gut zu wirken. Auf Durchfall und Erbrechen folgt allerdings eine Hyponatriämie. Nach deren Korrektur kommt es plötzlich zu progredienten Kognitions- und Verhaltensstörungen.

Schutz der Synapsen bei Alzheimer

29.05.2024 Morbus Alzheimer Nachrichten

Mit einem Neurotrophin-Rezeptor-Modulator lässt sich möglicherweise eine bestehende Alzheimerdemenz etwas abschwächen: Erste Phase-2-Daten deuten auf einen verbesserten Synapsenschutz.

Sozialer Aufstieg verringert Demenzgefahr

24.05.2024 Demenz Nachrichten

Ein hohes soziales Niveau ist mit die beste Versicherung gegen eine Demenz. Noch geringer ist das Demenzrisiko für Menschen, die sozial aufsteigen: Sie gewinnen fast zwei demenzfreie Lebensjahre. Umgekehrt steigt die Demenzgefahr beim sozialen Abstieg.

Hirnblutung unter DOAK und VKA ähnlich bedrohlich

17.05.2024 Direkte orale Antikoagulanzien Nachrichten

Kommt es zu einer nichttraumatischen Hirnblutung, spielt es keine große Rolle, ob die Betroffenen zuvor direkt wirksame orale Antikoagulanzien oder Marcumar bekommen haben: Die Prognose ist ähnlich schlecht.

Update Neurologie

Bestellen Sie unseren Fach-Newsletter und bleiben Sie gut informiert.