N-methyl-d-aspartate lesions of the lateral hypothalamus do not reduce amphetamine or fenfluramine anorexia but enhance the acquisition of eating in response to tail pinch in the rat

Judith M. Clark, Andrew J M Clark, Philip Winn

Research output: Contribution to journalArticle

9 Citations (Scopus)

Abstract

These experiments examine the acquisition of tail pinch-induced eating and responses to the anorectic agents d-amphetamine and d,l-fenfluramine by rats bearing N-methyl-d-aspartate (NMDA) lesions of the lateral hypothalamus. Lesioned rats lost weight following surgery but had no significant eating or drinking difficulties in the home cage (Clark et al. 1990). The acquisition of eating in response to tail pinch was enhanced in lateral hypothalamic-lesioned rats: they ate on earlier test sessions than controls and less pressure was required to elicit eating. Home cage food intake over the period when tail pinch was being examined was not affected by the lateral hypothalamic lesions. There were no significant differences between lateral hypothalamic-lesioned and control rats in terms of their anorectic responses to either d-amphetamine or d,l-fenfluramine, though the lesioned rats had a lower baseline intake. These data suggest that the lateral hypothalamus is not an important site for the mediation of amphetamine or fenfluramine anorexia but is involved in the acquisition of tail pinch-induced eating. The disinhibition of responding to tail pinch by lateral hypothalamic lesions is discussed in terms of the possible role the lateral hypothalamus plays in regulating cortical activity. The role of the medial hypothalamus and nonhypothalamic systems in the response to anorectic drugs and tail pinch is discussed.

Original languageEnglish
Pages (from-to)331-337
Number of pages7
JournalPsychopharmacology
Volume109
Issue number3
DOIs
Publication statusPublished - 1 Nov 1992

Fingerprint

Lateral Hypothalamic Area
Fenfluramine
Anorexia
Amphetamine
Aspartic Acid
Tail
Eating
Appetite Depressants
Dextroamphetamine
Middle Hypothalamus
Drinking
Pressure
Weights and Measures
Pharmaceutical Preparations

Keywords

  • amphetamine
  • anorexia
  • eating
  • excitotoxic lesion
  • fenfluramine
  • lateral hypothalamus
  • tail pinch
  • dexamphetamine
  • n methyl dextro aspartic acid
  • animal experiment
  • brain injury
  • controlled study
  • intraperitoneal drug administration

Cite this

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title = "N-methyl-d-aspartate lesions of the lateral hypothalamus do not reduce amphetamine or fenfluramine anorexia but enhance the acquisition of eating in response to tail pinch in the rat",
abstract = "These experiments examine the acquisition of tail pinch-induced eating and responses to the anorectic agents d-amphetamine and d,l-fenfluramine by rats bearing N-methyl-d-aspartate (NMDA) lesions of the lateral hypothalamus. Lesioned rats lost weight following surgery but had no significant eating or drinking difficulties in the home cage (Clark et al. 1990). The acquisition of eating in response to tail pinch was enhanced in lateral hypothalamic-lesioned rats: they ate on earlier test sessions than controls and less pressure was required to elicit eating. Home cage food intake over the period when tail pinch was being examined was not affected by the lateral hypothalamic lesions. There were no significant differences between lateral hypothalamic-lesioned and control rats in terms of their anorectic responses to either d-amphetamine or d,l-fenfluramine, though the lesioned rats had a lower baseline intake. These data suggest that the lateral hypothalamus is not an important site for the mediation of amphetamine or fenfluramine anorexia but is involved in the acquisition of tail pinch-induced eating. The disinhibition of responding to tail pinch by lateral hypothalamic lesions is discussed in terms of the possible role the lateral hypothalamus plays in regulating cortical activity. The role of the medial hypothalamus and nonhypothalamic systems in the response to anorectic drugs and tail pinch is discussed.",
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AU - Winn, Philip

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N2 - These experiments examine the acquisition of tail pinch-induced eating and responses to the anorectic agents d-amphetamine and d,l-fenfluramine by rats bearing N-methyl-d-aspartate (NMDA) lesions of the lateral hypothalamus. Lesioned rats lost weight following surgery but had no significant eating or drinking difficulties in the home cage (Clark et al. 1990). The acquisition of eating in response to tail pinch was enhanced in lateral hypothalamic-lesioned rats: they ate on earlier test sessions than controls and less pressure was required to elicit eating. Home cage food intake over the period when tail pinch was being examined was not affected by the lateral hypothalamic lesions. There were no significant differences between lateral hypothalamic-lesioned and control rats in terms of their anorectic responses to either d-amphetamine or d,l-fenfluramine, though the lesioned rats had a lower baseline intake. These data suggest that the lateral hypothalamus is not an important site for the mediation of amphetamine or fenfluramine anorexia but is involved in the acquisition of tail pinch-induced eating. The disinhibition of responding to tail pinch by lateral hypothalamic lesions is discussed in terms of the possible role the lateral hypothalamus plays in regulating cortical activity. The role of the medial hypothalamus and nonhypothalamic systems in the response to anorectic drugs and tail pinch is discussed.

AB - These experiments examine the acquisition of tail pinch-induced eating and responses to the anorectic agents d-amphetamine and d,l-fenfluramine by rats bearing N-methyl-d-aspartate (NMDA) lesions of the lateral hypothalamus. Lesioned rats lost weight following surgery but had no significant eating or drinking difficulties in the home cage (Clark et al. 1990). The acquisition of eating in response to tail pinch was enhanced in lateral hypothalamic-lesioned rats: they ate on earlier test sessions than controls and less pressure was required to elicit eating. Home cage food intake over the period when tail pinch was being examined was not affected by the lateral hypothalamic lesions. There were no significant differences between lateral hypothalamic-lesioned and control rats in terms of their anorectic responses to either d-amphetamine or d,l-fenfluramine, though the lesioned rats had a lower baseline intake. These data suggest that the lateral hypothalamus is not an important site for the mediation of amphetamine or fenfluramine anorexia but is involved in the acquisition of tail pinch-induced eating. The disinhibition of responding to tail pinch by lateral hypothalamic lesions is discussed in terms of the possible role the lateral hypothalamus plays in regulating cortical activity. The role of the medial hypothalamus and nonhypothalamic systems in the response to anorectic drugs and tail pinch is discussed.

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