Dissociation of analgesic and hyperphagic responses following 2-deoxy-d-glucose

Richard J. Bodnar, Elisse Kramer, Donald A. Simone, Annette L. Kirchgessner, Jennie Scalisi

Research output: Contribution to journalArticlepeer-review

8 Scopus citations

Abstract

Injection of 2-deoxy-D-glucose (2DG) elicits both analgesic and hyperphagic responses in rats. While pituitary dysfunction, decreased dopamine availability, or neonatal monosodium glutamate treatment decreases 2DG hyperphagia, they increase 2DG analgesia. In contrast, 2-DG analgesia alone is decreased by repeated 2-DG injections, while 2-DG hyperphagia alone is decreased following naloxone prretreatment. The present four experiments examined further mechanisms subserving these two induced responses. In the first experiment, rats were deprived of food for 6 h following 2-DG (600 mg/kg). While 2-DG hyperphagia persisted in the absence of glucoprivation, 2-DG analgesia failed to occur after this delay. In the second experiment, acute exposure to inescapable foot shock (4 mA, 0.5 s/5 s for 1 h) preceded administration of 2-DG (600 mg/kg). While 2-DG hyperphagia was eliminated by this procedure, 2-DG analgesia was significantly potentiated. In the third experiment, repeated morphine (10 mg/kg) injections over 14 days eliminated 2-DG analgesia on the fifteenth day, but failed to affect 2-DG hyperphagia. In the fourth experiment, lesions placed in either the lateral hypothalamus or zona incerta decreased 2-DG hyperphagia, but failed to affect 2-DG analgesia. These results are discussed in terms of common and dissociative mechanisms mediating both responses.

Original languageEnglish (US)
Pages (from-to)225-236
Number of pages12
JournalInternational Journal of Neuroscience
Volume21
Issue number3-4
DOIs
StatePublished - 1983

Bibliographical note

Funding Information:
Address all correspondence to : Dr. R. Bodnar, Department of Psychology, Queens College, CUNY, 65-30 Kissena Blvd., Flushing, NY 11367. This research was supported in part by NIH 5 SO5 RR07064.

Copyright:
Copyright 2014 Elsevier B.V., All rights reserved.

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