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Brain creatine kinase activity in an animal model of mania.

Abstract

There is evidence pointing to dysfunction at the mitochondrial level as an important target for the understanding of the pathophysiology of bipolar disorder (BD). We assessed creatine kinase (CK) activity in rats submitted to an animal model of mania which included the use of lithium and valproate. In the acute treatment, amphetamine (AMPH) or saline was administered to rats for 14 days, and between day 8 and 14, rats were treated with either lithium, valproate or saline. In the maintenance treatment, rats were pretreated with lithium, valproate or saline, and between day 8 and 14, AMPH or saline were administered. In both experiments, locomotor activity was assessed by open-field test and CK activity was evaluated in hippocampus, striatum, cerebellum, whole cortex and prefrontal cortex. Our results showed that mood stabilizers reversed AMPH-induced behavioral effects. Moreover, AMPH (acute treatment) inhibited CK activity in hippocampus, striatum and cortex, but not in cerebellum and prefrontal cortex, and administration of lithium or valproate did not reverse the enzyme inhibition. In the maintenance treatment, AMPH decreased CK activity in saline-pretreated rats in hippocampus, striatum and cortex, but not in cerebellum and prefrontal cortex. AMPH administration in lithium- or valproate-pretreated animals decreased CK activity in hippocampus, striatum and cortex. Our results showed that AMPH inhibited CK activity and that mood stabilizers were not able to reverse and/or prevent the enzyme inhibition. These findings reinforce the hypothesis that mitochondrial dysfunction plays an important role in the pathophysiology of BD.

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  • Authors+Show Affiliations

    ,

    Laboratório de Fisiopatologia Experimental, Programa de Pós-Graduação em Ciências da Saúde, Universidade do Extremo Sul Catarinense, 88806-000 Criciúma, SC, Brazil. emiliostreck@terra.com.br

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    Source

    Life sciences 82:7-8 2008 Feb 13 pg 424-9

    MeSH

    Amphetamine
    Animals
    Antimanic Agents
    Bipolar Disorder
    Brain
    Central Nervous System Stimulants
    Creatine Kinase
    Disease Models, Animal
    Drug Therapy, Combination
    Injections, Intraperitoneal
    Lithium Compounds
    Male
    Motor Activity
    Rats
    Rats, Wistar
    Valproic Acid

    Pub Type(s)

    Journal Article
    Research Support, Non-U.S. Gov't

    Language

    eng

    PubMed ID

    18191157

    Citation

    Streck, Emilio L., et al. "Brain Creatine Kinase Activity in an Animal Model of Mania." Life Sciences, vol. 82, no. 7-8, 2008, pp. 424-9.
    Streck EL, Amboni G, Scaini G, et al. Brain creatine kinase activity in an animal model of mania. Life Sci. 2008;82(7-8):424-9.
    Streck, E. L., Amboni, G., Scaini, G., Di-Pietro, P. B., Rezin, G. T., Valvassori, S. S., ... Quevedo, J. (2008). Brain creatine kinase activity in an animal model of mania. Life Sciences, 82(7-8), pp. 424-9. doi:10.1016/j.lfs.2007.11.026.
    Streck EL, et al. Brain Creatine Kinase Activity in an Animal Model of Mania. Life Sci. 2008 Feb 13;82(7-8):424-9. PubMed PMID: 18191157.
    * Article titles in AMA citation format should be in sentence-case
    TY - JOUR T1 - Brain creatine kinase activity in an animal model of mania. AU - Streck,Emilio L, AU - Amboni,Graziela, AU - Scaini,Giselli, AU - Di-Pietro,Priscila B, AU - Rezin,Gislaine T, AU - Valvassori,Samira S, AU - Luz,Gabrielle, AU - Kapczinski,Flávio, AU - Quevedo,João, Y1 - 2007/12/14/ PY - 2007/05/25/received PY - 2007/07/24/revised PY - 2007/11/30/accepted PY - 2008/1/15/pubmed PY - 2008/4/23/medline PY - 2008/1/15/entrez SP - 424 EP - 9 JF - Life sciences JO - Life Sci. VL - 82 IS - 7-8 N2 - There is evidence pointing to dysfunction at the mitochondrial level as an important target for the understanding of the pathophysiology of bipolar disorder (BD). We assessed creatine kinase (CK) activity in rats submitted to an animal model of mania which included the use of lithium and valproate. In the acute treatment, amphetamine (AMPH) or saline was administered to rats for 14 days, and between day 8 and 14, rats were treated with either lithium, valproate or saline. In the maintenance treatment, rats were pretreated with lithium, valproate or saline, and between day 8 and 14, AMPH or saline were administered. In both experiments, locomotor activity was assessed by open-field test and CK activity was evaluated in hippocampus, striatum, cerebellum, whole cortex and prefrontal cortex. Our results showed that mood stabilizers reversed AMPH-induced behavioral effects. Moreover, AMPH (acute treatment) inhibited CK activity in hippocampus, striatum and cortex, but not in cerebellum and prefrontal cortex, and administration of lithium or valproate did not reverse the enzyme inhibition. In the maintenance treatment, AMPH decreased CK activity in saline-pretreated rats in hippocampus, striatum and cortex, but not in cerebellum and prefrontal cortex. AMPH administration in lithium- or valproate-pretreated animals decreased CK activity in hippocampus, striatum and cortex. Our results showed that AMPH inhibited CK activity and that mood stabilizers were not able to reverse and/or prevent the enzyme inhibition. These findings reinforce the hypothesis that mitochondrial dysfunction plays an important role in the pathophysiology of BD. SN - 0024-3205 UR - https://www.unboundmedicine.com/medline/citation/18191157/Brain_creatine_kinase_activity_in_an_animal_model_of_mania_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0024-3205(07)00858-2 DB - PRIME DP - Unbound Medicine ER -