Intracerebroventricular alloxan reduces 2-deoxy-D-glucose analgesia.
2-Deoxy-D-glucose (2DG) analgesia, mediated in part by endogenous opiate and hypothalamo-hypophysial systems is presumably activated by its stress-related properties. Recently 2DG hyperphagia, but not 2DG hyperglycemia was reduced by central pretreatment with the pancreatic beta-cell toxin, alloxan; this deficit was eliminated by co-administration of 3M D-glucose. The present experiment examined whether intracerebroventricular pretreatment with alloxan (40 or 200 micrograms) altered 2DG analgesia (400 or 700 mg/kg, IP) on the tail-flick and jump tests, and whether 3M D-glucose co-administration ameliorated any deficits. Both alloxan doses significantly reduced 2DG analgesia (400 mg/kg) on both tests. 2DG analgesia (700 mg/kg) was significantly reduced by both alloxan doses on the jump test, but only by the higher alloxan pretreatment on the tail-flick test. 3M D-glucose co-administration ameliorated alloxan-induced analgesic deficits more effectively at the lower 2DG dose. Neither alloxan nor alloxan/3M D-glucose treatments altered basal thresholds. These data pertain both to alloxan's effects upon coding of 2DG effects as stressful, and to the role of diabetes and/or central glucoreceptors in analgesic processes.
Lubin
E
E
Department of Psychology, Queens College, City University of New York, Flushing 11367.
Bodnar
R J
RJ
D000496:Alloxan / Q000008:administration & dosage*; D000818:Animals; D001522:Behavior, Animal / Q000187:drug effects; D007276:Injections, Intraventricular; D008297:Male; D010146:Pain / Q000188:drug therapy*; D051381:Rats; D011919:Rats, Inbred Strains
D000496:Alloxan