Dissociation of analgesic and hyperphagic responses following 2-deoxy-D-glucose.
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| 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 pretreatment. 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.
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| Authors | R J Bodnar, E Kramer, D A Simone, A L Kirchgessner, J Scalisi |
| Journal | The International journal of neuroscience (Int J Neurosci) Vol. 21 Issue 3-4 Pg. 225-36 (Nov 1983) ISSN: 0020-7454 [Print] England |
| PMID | 6584411 (Publication Type: Journal Article, Research Support, U.S. Gov't, P.H.S.) |
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