Intracerebroventricular alloxan reduces 2-deoxy-D-glucose analgesia

Edward Lubin, Richard J. Bodnar

Research output: Contribution to journalArticlepeer-review

6 Scopus citations

Abstract

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 μg) 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.

Original languageEnglish
Pages (from-to)465-470
Number of pages6
JournalPhysiology and Behavior
Volume42
Issue number5
DOIs
StatePublished - 1988
Externally publishedYes

Keywords

  • 2-Deoxy-D-glucose analgesia
  • 3M D-Glucose
  • Alloxan
  • Diabetes
  • Pain
  • Rats
  • Stress

Fingerprint

Dive into the research topics of 'Intracerebroventricular alloxan reduces 2-deoxy-D-glucose analgesia'. Together they form a unique fingerprint.

Cite this