PMID- 19911114
OWN - NLM
STAT- MEDLINE
DCOM- 20100412
LR  - 20211020
IS  - 1435-1463 (Electronic)
IS  - 0300-9564 (Linking)
VI  - 117
IP  - 2
DP  - 2010 Feb
TI  - Evaluation of brain creatine kinase activity in an animal model of mania induced 
      by ouabain.
PG  - 149-53
LID - 10.1007/s00702-009-0337-3 [doi]
AB  - Bipolar disorder (BD) is a common and severe mood disorder associated with higher 
      rates of suicide and disability. The development of new animal models, and the 
      investigation employing those available have extensively contributed to 
      understand the pathophysiological mechanisms of BD. Intracerebroventricular 
      (i.c.v.) administration of ouabain, a specific Na+,K+-ATPase inhibitor, has been 
      used as an animal model for BD. It has been demonstrated that Na+,K+-ATPase is 
      altered in psychiatric disorders, especially BD. Creatine kinase (CK) is 
      important for brain energy homeostasis by exerting several integrated functions. 
      In the present study,we evaluated CK activity in the striatum, prefrontal cortex 
      and hippocampus of rats subjected to i.c.v. administration of ouabain. Adult male 
      Wistar rats received a single i.c.v. administration of ouabain (10(-2) and 10(-3) 
      M) or vehicle (control group). Locomotor activity was measured using the open 
      field test. CK activity was measured in the brain of rats immediately (1 h) and 7 
      days after ouabain administration. Our results showed that spontaneous locomotion 
      was increased 1 h after ouabain administration and that hyperlocomotion was also 
      observed 7 days after that.Moreover, CK activity was inhibited immediately after 
      the administration of ouabain in the striatum, hippocampus and prefrontal cortex. 
      Moreover, the enzyme was not affected in the striatum and hippocampus 7 days 
      after ouabain administration. On the other hand, an inhibition in CK activity in 
      the prefrontal cortex was observed. If inhibition of CK also occurs in BD 
      patients, it will be tempting to speculate that the reduction of brain metabolism 
      may be related probably to the pathophysiology of this disease.
FAU - Freitas, Tiago P
AU  - Freitas TP
AD  - Laboratorio de Fisiopatologia Experimental, Programa de Pos-graduacao em Ciencias 
      da Saude, Universidade do Extremo Sul Catarinense, Criciuma, SC, Brazil.
FAU - Scaini, Giselli
AU  - Scaini G
FAU - Correa, Cristiane
AU  - Correa C
FAU - Santos, Patricia M
AU  - Santos PM
FAU - Ferreira, Gabriela K
AU  - Ferreira GK
FAU - Rezin, Gislaine T
AU  - Rezin GT
FAU - Moretti, Morgana
AU  - Moretti M
FAU - Valvassori, Samira S
AU  - Valvassori SS
FAU - Quevedo, Joao
AU  - Quevedo J
FAU - Streck, Emilio L
AU  - Streck EL
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Austria
TA  - J Neural Transm (Vienna)
JT  - Journal of neural transmission (Vienna, Austria : 1996)
JID - 9702341
RN  - 5ACL011P69 (Ouabain)
RN  - EC 2.7.3.2 (Creatine Kinase, BB Form)
SB  - IM
MH  - Animals
MH  - Bipolar Disorder/chemically induced/*enzymology/metabolism
MH  - Corpus Striatum/*enzymology/metabolism
MH  - Creatine Kinase, BB Form/antagonists & inhibitors/*metabolism
MH  - Disease Models, Animal
MH  - Hippocampus/*enzymology/metabolism
MH  - Male
MH  - Motor Activity
MH  - Ouabain
MH  - Prefrontal Cortex/*enzymology/metabolism
MH  - Rats
MH  - Rats, Wistar
MH  - Time Factors
EDAT- 2009/11/17 06:00
MHDA- 2010/04/13 06:00
CRDT- 2009/11/14 06:00
PHST- 2009/07/02 00:00 [received]
PHST- 2009/10/25 00:00 [accepted]
PHST- 2009/11/14 06:00 [entrez]
PHST- 2009/11/17 06:00 [pubmed]
PHST- 2010/04/13 06:00 [medline]
AID - 10.1007/s00702-009-0337-3 [doi]
PST - ppublish
SO  - J Neural Transm (Vienna). 2010 Feb;117(2):149-53. doi: 10.1007/s00702-009-0337-3.