Hostname: page-component-cd9895bd7-mkpzs Total loading time: 0 Render date: 2024-12-26T05:25:03.943Z Has data issue: false hasContentIssue false
  • English
  • Français

Na+,K+-ATPase activity is increased in rats subjected to chronic administration of ketamine

Published online by Cambridge University Press:  24 June 2014

Renata D. De Luca ,
Daiane de B. Fraga ,
Fernando V. Ghedim ,
Janaína Kolling ,
Andrea G. K. Ferreira ,
Aline A. Cunha ,
Angela T. S. Wyse  and
Alexandra I. Zugno
Renata D. De Luca
Affiliation:
Laboratório de Neurociências and Instituto Nacional de Ciência e Tecnologia Translacional em Medicina (INCT-TM), Programa de Pós-Graduação em Ciências da Saúde, Unidade Acadêmica de Ciências da Saúde, Universidade do Extremo Sul Catarinense, 88806-000, Criciúma, SC, Brazil
Daiane de B. Fraga
Affiliation:
Laboratório de Neurociências and Instituto Nacional de Ciência e Tecnologia Translacional em Medicina (INCT-TM), Programa de Pós-Graduação em Ciências da Saúde, Unidade Acadêmica de Ciências da Saúde, Universidade do Extremo Sul Catarinense, 88806-000, Criciúma, SC, Brazil
Fernando V. Ghedim
Affiliation:
Laboratório de Neurociências and Instituto Nacional de Ciência e Tecnologia Translacional em Medicina (INCT-TM), Programa de Pós-Graduação em Ciências da Saúde, Unidade Acadêmica de Ciências da Saúde, Universidade do Extremo Sul Catarinense, 88806-000, Criciúma, SC, Brazil
Janaína Kolling
Affiliation:
Laboratório de Erros Inatos do Metabolismo, Programa de Pós-Graduação em Ciências Biológicas – Bioquímica, Universidade Federal do Rio Grande do Sul, Porto Alegre, RS, Brazil
Andrea G. K. Ferreira
Affiliation:
Laboratório de Erros Inatos do Metabolismo, Programa de Pós-Graduação em Ciências Biológicas – Bioquímica, Universidade Federal do Rio Grande do Sul, Porto Alegre, RS, Brazil
Aline A. Cunha
Affiliation:
Laboratório de Erros Inatos do Metabolismo, Programa de Pós-Graduação em Ciências Biológicas – Bioquímica, Universidade Federal do Rio Grande do Sul, Porto Alegre, RS, Brazil
Angela T. S. Wyse
Affiliation:
Laboratório de Erros Inatos do Metabolismo, Programa de Pós-Graduação em Ciências Biológicas – Bioquímica, Universidade Federal do Rio Grande do Sul, Porto Alegre, RS, Brazil
Alexandra I. Zugno*
Affiliation:
Laboratório de Neurociências and Instituto Nacional de Ciência e Tecnologia Translacional em Medicina (INCT-TM), Programa de Pós-Graduação em Ciências da Saúde, Unidade Acadêmica de Ciências da Saúde, Universidade do Extremo Sul Catarinense, 88806-000, Criciúma, SC, Brazil
*
Professor Alexandra Ioppi Zugno, Laboratório de Neurociências, Programa de Pós-Graduação em Ciências da Saúde, Unidade Acadêmica de Ciências da Saúde, Universidade do Extremo Sul Catarinense, 88806-000 Criciúma, SC, Brazil. Tel: +55 48 3431 2792; Fax: +55 48 3431 2759; E-mail: [email protected]
Get access Rights & Permissions [Opens in a new window]

Extract

De Luca RD, Fraga DB, Ghedim FV, Kolling J, Ferreira AGK, Cunha AA, Wyse ATS, Zugno AI. Na+,K+-ATPase activity is increased in rats subjected to chronic administration of ketamine.

Objective: Schizophrenia is a devastating psychiatric disorder. Symptoms of schizophrenia can be divided into positive, negative and cognitive, and the physiopathology is still been unknown. Na+,K+-ATPase is a protein in its role as a maintainer of fluid balance in all mammals and alterations in this enzyme could cause brain abnormalities. The aim of our study was to investigate the activity of this enzyme in rats submitted to chronic administration of ketamine.

Methods: Adult male Wistar rats were submitted to sub-anaesthetic doses of the 25 mg/kg ketamine by seven consecutive days and the Na+,K+-ATPase activity was analysed in prefrontal and hippocampus of rats.

Results: We observed an increase in Na+,K+-ATPase activity in prefrontal cortex administration of 25 mg/kg ketamine. However, ketamine has no effect in hippocampus.

Conclusion: This evidence indicates that the alteration in Na+,K+-ATPase may be related with glutamatergic system and consequently could be related to the development of schizophrenia.

Keywords

Na+,K+-ATPasehippocampusprefrontal cortexschizophrenia
Type
Rapid Communications
Information
Acta Neuropsychiatrica , Volume 23 , Issue 5 , October 2011 , pp. 215 - 218
Copyright
Copyright © Cambridge University Press 2011

Access options

Get access to the full version of this content by using one of the access options below. (Log in options will check for institutional or personal access. Content may require purchase if you do not have access.)

References

1. Schultz, SH, North, SW, Shields, CG. Schizophrenia: a review. Am Fam Physician 2007;75:1821–1829. Google Scholar
2. Hunt, MJ, Raynaud, B, Garcia, R. Ketamine dose-dependently unduces high-frequency oscillations in the nucleus accumbens in freely moving rats. Biol Psychiatry 2006;60:1206–1214. Google Scholar
3. Littlewood, CL, Jones, N, O'neill, MJ. Mapping the central effects of ketamine in the rat using pharmacological MRI. Psychopharmacology 2006;186:64–81. CrossRefGoogle ScholarPubMed
4. Grace, AA. Cortical regulation of subcortical dopamine systems and its possible relevance to schizophrenia. J Neural Transm 1993;91:111–134. CrossRefGoogle ScholarPubMed
5. Aperia, A. New roles for an old enzyme: Na,K-ATPase emerges as an interesting drug target. J Intern Med 2007;261:44–52. Google Scholar
6. Wyse, AT, Streck, EL, Worm, P, Wajner, A, Ritter, F, Netto, CA. Preconditioning prevents the inhibition of Na+,K+-ATPase activity after brain ischemia. Neurochem Res 2000;25:971–975. Google Scholar
7. Nanitsos, EK, Nguyen, KT, St'astný, F, Balcar, VJ. Glutamatergic hypothesis of schizophrenia: involvement of Na+/K+-dependent glutamate transport. J Biomed Sci 2005;12:9712. CrossRefGoogle ScholarPubMed
8. Hattori, N, Kitagawa, K, Higashida, T et al. CI-ATPase and Na+/K(+)-ATPase activities in Alzheimer's disease brains. Neurosci Lett 1998;2:54141–54144. Google Scholar
9. Zugno, AI, Valvassori, SS, Scherer, EB et al. Na+,K+-ATPase activity in an animal model of mania. J Neural Transm 2009;116:431–446. CrossRefGoogle Scholar
10. Canever, L, Oliveira, L, De Luca, R et al. A rodent model of schizophrenia reveals increase in creatine kinase activity with associated behavior changes. Oxid Med and Cell Longevity 2010;3:421–427. Google Scholar
11. Oliveira, L, Fraga, DB, De Luca, RD et al. Behavioral changes and mitochondrial dysfunction in a rat model of schizophrenia induced by ketamine. Metab Brain Dis 2011;26:69–77. Google Scholar
12. Imre, G, Fokkema, DS, Den Boer, JA, Ter Horst, GJ. Dose-response characteristics of ketamine effect on locomotion, cognitive function and central neuronal activity. Brain Res Bull 2006;69:338–346. Google Scholar
13. Chan, KM, Delfert, DM, Koepnick, SL, McDonald, JM. Effect of W7 on Ca2+ uptake and Ca2+-ATPase activities of the endoplasmic reticulum of rat liver. Arch Biochem Biophys 1987;256:472–479. Google Scholar
14. Verma, A, Moghaddam, B. NMDA receptor antagonists impair prefrontal cortex function as accessed via spatial delayed alternation performance in rats: modulation by dopamine. J Neurosci 1996;16:373–379. CrossRefGoogle Scholar
15. Yamaguchi, I, Walk, SF, Jose, PA, Felder, RA. Dopamine D2L receptors stimulate Na+/K(+)-ATPase activity in murine LTK- cells. Mol Pharmacol 1996;49:373–378. Google Scholar
16. Snyder, GL, Fienberg, AA, Huganir, RL, Greengard, P. A dopamine/D1 receptor/protein kinase A/dopamine- and cAMP-regulated phosphoprotein (Mr 32 kDa)/protein phosphatase-1 pathway regulates dephosphorylation of the NMDA receptor. J Neurosci 1998;18:10297–10303. Google Scholar
17. Ben-Shachar, D, Zuk, R, Gazawi, H, Ljubuncic, P. Dopamine toxicity involves mitochondrial complex I inhibition: implications to dopamine-related neuropsychiatric disorders. Biochem Pharmacol 2004;67:1965–1974. Google Scholar
18. Volz, HR, Riehemann, S, Maurer, I et al. Reduced phosphodiesters and high-energy phosphates in the frontal lobe of schizophrenic patients: a (31) P chemical shift spectroscopic-imaging study. Biol Psychiatry 2000;47:954–961. CrossRefGoogle ScholarPubMed
19. Ben-Shachar, D, Nadri, C, Karry, G, Agam, G. Mitochondrial complex I subunits are altered in rats with neonatal ventral hippocampal damage but not in rats exposed to oxygen restriction at neonatal age. J Mol Neurosci 2009;38:143–151. Google Scholar
20. Kurup, Rk, Kurup, PA. Schizoid neurochemical pathology-induced membrane Na(+)-K+ ATPase inhibition in relation to neurological disorders. Int J Neurosci 2003;113:1705–1717. CrossRefGoogle ScholarPubMed
21. Del Arco, A, Ronzoni, G, Mora, F. Prefrontal stimulation of GABAA receptors counteracts the corticolimbic hyperactivity produced by NMDA antagonists in the prefrontal cortex of the rat. Psychopharmacology 2011;214:525–536. CrossRefGoogle ScholarPubMed
22. Del Arco, A, Mora, F. Glutamate-dopamine in vivo interaction in the prefrontal cortex modulates the release of dopamine and acetylcholine in the nucleus accumbens of the awake rat. J Neural Transm 2005;112:97–109. Google Scholar
23. Corti, C, Xuereb, JH, Crepaldi, L, Corsi, M, Michielin, F, Ferraguti, F. Altered levels of glutamatergic receptors and Na+/K+ ATPase α1 in the prefrontal cortex of subjects with schizophrenia. Schizophr Res 2011;128:7–14. Google Scholar