title: Effects of creatine and β-guanidinopropionic acid and alterations in creatine transporter and creatine kinases expression in acute seizure and chronic epilepsy models.
abstract: BACKGROUND
  In order to confirm the roles of creatine (Cr) in epilepsy, we investigated the anti-convulsive effects of Cr, creatine transporter (CRT) and creatine kinases (CKs) against chemical-induced acute seizure activity and chronic epileptic seizure activity.
  
  
  RESULTS
  Two hr after pilocarpine (PILO)-seizure induction, ubiquitous mitochondrial CK (uMtCK) immunoreactivity was unaltered as compared to control level. However, brain-type cytoplasm CK (BCK) immunoreactivity was decreased to 70% of control level. CRT immunoreactivity was decreased to 60% of control level. Following Cr or Tat-CK treatment, uMtCK or CRT immunoreactivity was unaffected, while BCK immunoreactivity in Cr treated group was increased to 3.6-fold of control levels. β-Guanidinopropionic acid (GPA, a competitive CRT inhibitor) reduced BCK and CRT expression. In addition, Cr and tat-BCK treatment delayed the beginning of seizure activity after PILO injection. However, GPA treatment induced spontaneous seizure activity without PILO treatment. In chronic epilepsy rats, both uMtCK and CRT immunoreactivities were reduced in the hippocampus. In contrast, BCK immunoreactivity was similar to that observed in control animals. Cr-, GPA and tat-BCK treatment could not change EEG.
  
  
  CONCLUSIONS
  Cr/CK circuit may play an important role in sustaining or exacerbating acute seizure activity, but not chronic epileptic discharge.
authors.affiliation: Department of Biomedical Sciences, College of Life Science, Hallym University, Chunchon Kangwon-Do 200-702, Republic of Korea.
authors.forename: Dae Won
authors.initials: DW
authors.lastname: Kim
authors.forename: Seong-Il
authors.initials: SI
authors.lastname: Yeo
authors.forename: Hea Jin
authors.initials: HJ
authors.lastname: Ryu
authors.forename: Ji-Eun
authors.initials: JE
authors.lastname: Kim
authors.forename: Hong-Ki
authors.initials: HK
authors.lastname: Song
authors.forename: Oh-Shin
authors.initials: OS
authors.lastname: Kwon
authors.forename: Soo Young
authors.initials: SY
authors.lastname: Choi
authors.forename: Tae-Cheon
authors.initials: TC
authors.lastname: Kang
mesh_terms: D000208:Acute Disease; D000818:Animals; D056547:CA1 Region, Hippocampal / Q000187:drug effects / Q000201:enzymology / Q000378:metabolism; D002908:Chronic Disease; D003401:Creatine / Q000502:physiology*; D003402:Creatine Kinase / Q000037:antagonists & inhibitors / Q000096:biosynthesis*; D004195:Disease Models, Animal; D004827:Epilepsy / Q000188:drug therapy / Q000201:enzymology / Q000378:metabolism*; D006146:Guanidines / Q000494:pharmacology*; D007150:Immunohistochemistry; D008297:Male; D026901:Membrane Transport Proteins / Q000096:biosynthesis / Q000378:metabolism*; D011422:Propionates / Q000494:pharmacology*; D051381:Rats; D017207:Rats, Sprague-Dawley
chemical_list: D006146:Guanidines; D026901:Membrane Transport Proteins; D011422:Propionates; C080679:creatine transporter; D003402:Creatine Kinase; D003401:Creatine; C005775:guanidinopropionic acid