title: Role of glutamate receptors in the development and maintenance of bladder overactivity after cerebral infarction in the rat.
abstract: OBJECTIVE
  To investigate the role of glutamate receptors in overactive bladder (OAB) caused by cerebral infarction (CI) we examined the effects of 2 different types of receptors antagonists on OAB induced by left middle cerebral artery (MCA) occlusion.
  
  
  METHODS
  Female rats were intravenously injected with dizocilpine, an NMDA (N-methyl-D-aspartate) receptor antagonist, or NBQX (2,3-dioxo-6-nitro-1,2,3,4-tetrahydrobenzo(f)quinoxaline-7-sulfonamide), an AMPA (alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid) receptor antagonist, before or after MCA occlusion. Awake rats were cystometrically examined for 8 hours. Detrusor strips were evaluated for force development in response to dizocilpine and NBQX.
  
  
  RESULTS
  In CI rats without pretreatment bladder capacity (BC) was significantly decreased after MCA occlusion and remained consistently below half that of pre-occlusion capacity. Dizocilpine (0.5 mg/kg intravenously) administered before MCA occlusion blocked the decrease in BC in awake rats 5 to 8 hours after MCA occlusion. In CI rats pretreated with NBQX (10 or 30 mg/kg intravenously) BC was not different from that in rats without pretreatment. Increasing doses of dizocilpine (0.01 to 10 mg/kg) or NBQX (0.1 to 30 mg/kg) increased rat BC 2 hours after MCA occlusion. NBQX did not change the BC of sham operated rats. No differences in the contractile response to dizocilpine or NBQX of detrusor strips from sham operated and CI rats were observed.
  
  
  CONCLUSIONS
  These results indicate that NMDA receptor has an essential role in the development of OAB after CI. AMPA receptor antagonist cannot block the development of OAB. However, AMPA receptor antagonist temporally inhibits OAB after it is established by CI.
authors.affiliation: Department of Urology, Faculty of Medical Science, University of Fukui, Matsuoka, Fukui, Japan. oyoko@fmsrsa.fukui-med.ac.jp
authors.forename: Osamu
authors.initials: O
authors.lastname: Yokoyama
authors.forename: Hiroaki
authors.initials: H
authors.lastname: Mizuno
authors.forename: Kazuto
authors.initials: K
authors.lastname: Komatsu
authors.forename: Hironobu
authors.initials: H
authors.lastname: Akino
authors.forename: Kazuya
authors.initials: K
authors.lastname: Tanase
authors.forename: Mikio
authors.initials: M
authors.lastname: Namiki
mesh_terms: D000818:Animals; D002544:Cerebral Infarction / Q000150:complications*; D016291:Dizocilpine Maleate / Q000494:pharmacology; D004305:Dose-Response Relationship, Drug; D018691:Excitatory Amino Acid Antagonists / Q000494:pharmacology; D005260:Female; D011810:Quinoxalines / Q000494:pharmacology; D051381:Rats; D017207:Rats, Sprague-Dawley; D018091:Receptors, AMPA / Q000037:antagonists & inhibitors; D017470:Receptors, Glutamate / Q000187:drug effects / Q000502:physiology*; D001745:Urinary Bladder Diseases / Q000209:etiology* / Q000503:physiopathology*
chemical_list: D018691:Excitatory Amino Acid Antagonists; D011810:Quinoxalines; D018091:Receptors, AMPA; D017470:Receptors, Glutamate; C062865:2,3-dioxo-6-nitro-7-sulfamoylbenzo(f)quinoxaline; D016291:Dizocilpine Maleate