Parabrachial nucleus lesions impair feeding response elicited by 2,5- anhydro-D-mannitol

H. J. Grill, M. I. Friedman, R. Norgren, G. Scalera, R. Seeley

Research output: Contribution to journalArticle

24 Citations (Scopus)

Abstract

Systemic injection of the fructose analogue 2,5-anhydro-D-mannitol (2,5- AM) elicits a feeding response and induces c-fos activity in the parabrachial nuclei (PBN). We used bilateral ibotenic acid lesions of PBN to determine whether the activation inferred from c-fos activity was causally related to the feeding response. The relationship between the PBN lesion and feeding behavior was also examined with the glucose analogue 2-deoxy-D-glucose (2- DG). The PBN lesions interfered with the feeding response to 2,5-AM but spared the feeding response to 2-DG. Rats were also tested in a conditioned taste-aversion paradigm. Differences were observed in the relationship between lesion extent and behavioral deficit for feeding responses to 2,5-AM and taste-guided intake after taste-aversion conditioning. These data provide the first demonstration that central lesions can disrupt feeding responses to peripherally acting 2,5-AM. The results suggest that the neural substrate for this response differs from that mediating taste-aversion conditioning and from that involved in the feeding response to 2-DG.

Original languageEnglish (US)
Pages (from-to)R676-R682
JournalAmerican Journal of Physiology - Regulatory Integrative and Comparative Physiology
Volume268
Issue number3 37-3
StatePublished - Jan 1 1995

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mannitol
conditioned behavior
Ibotenic Acid
glucose
Deoxyglucose
Feeding Behavior
Fructose
feeding behavior
fructose
injection
Glucose
Injections
Parabrachial Nucleus
2,5-anhydromannitol
acids
rats
Conditioning (Psychology)

All Science Journal Classification (ASJC) codes

  • Physiology
  • Physiology (medical)

Cite this

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abstract = "Systemic injection of the fructose analogue 2,5-anhydro-D-mannitol (2,5- AM) elicits a feeding response and induces c-fos activity in the parabrachial nuclei (PBN). We used bilateral ibotenic acid lesions of PBN to determine whether the activation inferred from c-fos activity was causally related to the feeding response. The relationship between the PBN lesion and feeding behavior was also examined with the glucose analogue 2-deoxy-D-glucose (2- DG). The PBN lesions interfered with the feeding response to 2,5-AM but spared the feeding response to 2-DG. Rats were also tested in a conditioned taste-aversion paradigm. Differences were observed in the relationship between lesion extent and behavioral deficit for feeding responses to 2,5-AM and taste-guided intake after taste-aversion conditioning. These data provide the first demonstration that central lesions can disrupt feeding responses to peripherally acting 2,5-AM. The results suggest that the neural substrate for this response differs from that mediating taste-aversion conditioning and from that involved in the feeding response to 2-DG.",
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Parabrachial nucleus lesions impair feeding response elicited by 2,5- anhydro-D-mannitol. / Grill, H. J.; Friedman, M. I.; Norgren, R.; Scalera, G.; Seeley, R.

In: American Journal of Physiology - Regulatory Integrative and Comparative Physiology, Vol. 268, No. 3 37-3, 01.01.1995, p. R676-R682.

Research output: Contribution to journalArticle

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AU - Grill, H. J.

AU - Friedman, M. I.

AU - Norgren, R.

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AU - Seeley, R.

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AB - Systemic injection of the fructose analogue 2,5-anhydro-D-mannitol (2,5- AM) elicits a feeding response and induces c-fos activity in the parabrachial nuclei (PBN). We used bilateral ibotenic acid lesions of PBN to determine whether the activation inferred from c-fos activity was causally related to the feeding response. The relationship between the PBN lesion and feeding behavior was also examined with the glucose analogue 2-deoxy-D-glucose (2- DG). The PBN lesions interfered with the feeding response to 2,5-AM but spared the feeding response to 2-DG. Rats were also tested in a conditioned taste-aversion paradigm. Differences were observed in the relationship between lesion extent and behavioral deficit for feeding responses to 2,5-AM and taste-guided intake after taste-aversion conditioning. These data provide the first demonstration that central lesions can disrupt feeding responses to peripherally acting 2,5-AM. The results suggest that the neural substrate for this response differs from that mediating taste-aversion conditioning and from that involved in the feeding response to 2-DG.

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