title: Inhibition of pre-ischeamic conditioning in the mouse caudate brain slice by NMDA- or adenosine A1 receptor antagonists.
abstract: Evidence suggests that pre-ischeamic conditioning (PIC) offers protection against a subsequent ischeamic event. Although some brain areas such as the hippocampus have received much attention, the receptor mechanisms of PIC in other brain regions are unknown. We have previously shown that 10 min oxygen and glucose deprivation (OGD) evokes tolerance to a second OGD event in the caudate. Here we further examine the effect of length of conditioning event on the second OGD event. Caudate mouse brain slices were superfused with artificial cerebro-spinal fluid (aCSF) bubbled with 95%O(2)/5%CO(2). OGD was achieved by reducing the aCSF glucose concentration and by bubbling with 95%N(2)/5%CO(2). After approximately 5 min OGD a large dopamine efflux was observed, presumably caused by anoxic depolarisation. On applying a second OGD event, 60 min later, dopamine efflux was delayed and reduced. We first examined the effect of varying the length of the conditioning event from 5 to 40 min and found tolerance to PIC increased with increasing duration of conditioning. We then examined the receptor mechanism(s) underlying PIC. We found that pre-incubation with either MK-801 or 8-cyclopentyl-1,3-dipropylxanthine (DPCPX) reduced tolerance to the second OGD event. These data suggest that either N-methyl-D-aspartate (NMDA) or adenosine A(1) receptor activation evokes PIC in the mouse caudate.
authors.affiliation: School of Psychology, University of Leicester, Lancaster Road, Leicester LE1 9HN, UK.
authors.forename: Nikky K
authors.initials: NK
authors.lastname: Chauhan
authors.forename: Andrew M J
authors.initials: AM
authors.lastname: Young
authors.forename: Claire L
authors.initials: CL
authors.lastname: Gibson
authors.forename: Colin
authors.initials: C
authors.lastname: Davidson
mesh_terms: D058916:Adenosine A1 Receptor Antagonists / Q000494:pharmacology*; D000818:Animals; D002545:Brain Ischemia / Q000150:complications / Q000378:metabolism / Q000473:pathology / Q000628:therapy*; D002421:Caudate Nucleus / Q000098:blood supply* / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D016291:Dizocilpine Maleate / Q000494:pharmacology; D004298:Dopamine / Q000378:metabolism; D005947:Glucose / Q000172:deficiency; D006323:Heart Arrest / Q000150:complications; D019194:Ischemic Preconditioning / Q000379:methods*; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D010100:Oxygen / Q000378:metabolism; D043682:Receptor, Adenosine A1 / Q000378:metabolism*; D016194:Receptors, N-Methyl-D-Aspartate / Q000037:antagonists & inhibitors*; D015398:Signal Transduction / Q000187:drug effects; D013778:Tetrazolium Salts / Q000378:metabolism; D014970:Xanthines / Q000494:pharmacology
chemical_list: D058916:Adenosine A1 Receptor Antagonists; D043682:Receptor, Adenosine A1; D016194:Receptors, N-Methyl-D-Aspartate; D013778:Tetrazolium Salts; D014970:Xanthines; D016291:Dizocilpine Maleate; C009591:triphenyltetrazolium; C051360:1,3-dipropyl-8-cyclopentylxanthine; D005947:Glucose; D010100:Oxygen; D004298:Dopamine