The nature of the suppression of food intake by lateral hypothalamic lesions in rats

Baillie, P; Morrison, S. D.

doi:10.1113/jphysiol.1963.sp007054

Cited by 67 publications

(22 citation statements)

References 16 publications

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“…Older studies of the LH have demonstrated that lesions of the LH suppress food intake(Anand and Brobeck, 1951; Baillie and Morrison, 1963). With the discovery that LH nuclei(see Figs 1l; 2k; 4D: LH) contain the peptide transmitters orexins(Sakurai et al, 1998) came further evidence for glucose-sensing properties in these neurons of the hypothalamus.…”

Section: Discussionmentioning

confidence: 99%

Review of the neuroanatomic landscape implicated in glucose sensing and regulation of nutrient signaling: Immunophenotypic localization of diabetes gene Tcf7l2 in the developing murine brain

Weaver

Turner

Hall

2012

Journal of Chemical Neuroanatomy

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Genetic variants in the transcription factor 7-like 2(Tcf7l2) gene have been found to confer a significant risk of type 2 diabetes and attenuated insulin secretion. Based on its genomic wide association Tcf7l2 is considered the single most important predictor of diabetes to date. Previous studies of Tcf7l2 mRNA localization in the adult brain suggest a putative role of Tcf7l2 in the CNS regulation of energy homeostasis. The present study further characterizes the immunophenotypic distribution of peptide expression in the brains of Tcf7l2 progeny during developmental time periods between E12.5 and P1. Tcf7l2 −/− is lethal beyond P1. Results show that while negligible TCF7L2 expression is found in the developing brains of Tcf7l2−/−mice, TCF7L2 protein is relatively widespread and robustly expressed in the brain by E18.5 and exhibits specific expression within neuronal populations and regions of the brain in Tcf7l2+/- and Tcf7l2+/+ progeny. Strong immunophenotypic labeling was found in the diencephalic structure of the thalamus that suggests a role of Tcf7l2 in the development and maintenance of thalamic activity. Strongly expressed TCF7L2 was localized in select hypothalamic and preoptic nuclei indicative of Tcf7l2 function within neurons controlling energy balance. Definitive neuronal staining for TCF7L2 within nuclei of the brain stem and circumventricular organs extends TCF7L2 localization within autonomic neurons and its potential integration with autonomic function. In addition robust TCF7L2 expression was found in the tectal and tegmental structures of the superior and inferior colliculi as well as transient expression in neuroepithelium of the cerebral and hippocampal cortices of E16 and E18.5. Patterns of TCF7L2 peptide localization when compared to the adult protein synthetic chemical/anatomical landscape of glucose sensing exhibit a good correlational fit between its expression and regions, nuclei, and pathways regulating energy homeostasis via integration and response to peripheral endocrine, metabolic and neuronal signaling. TCF was also found co-localized with peptides that regulate energy homeostasis including AgRP, POMC and NPY. TCF7l2, some variants of which have been shown to impair GLP-1-induced insulin secretion, was also found co-localize with GLP-1 in adult TCF wild type progeny. Impaired Tcf7l2-mediated neural regulation may contribute to the risk and/or underlying pathophysiology of type 2 diabetes that has found high expression in genomic studies of Tcf7l2 variants.

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Section: Discussionmentioning

confidence: 99%

Review of the neuroanatomic landscape implicated in glucose sensing and regulation of nutrient signaling: Immunophenotypic localization of diabetes gene Tcf7l2 in the developing murine brain

Weaver

Turner

Hall

2012

Journal of Chemical Neuroanatomy

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“…This is indicated by the greater facility of aphagic rats in intragastric feeding where exteroceptive stimulation is also present (Baillie & Morrison, 1963) 342 S. D. MORRISON than where exteroceptive stimulation is prevented (Rodgers et al 1965). It is also indicated by the recovery of lever pressing for food although the delivered food is not ingested (this work and Baillie & Morrison, 1963) and, at a later stage of recovery, by the drinking of a liquid diet or sweetened water and the rejection of plain water, or the acceptance of plain water and the rejection of water containing quinine (Teitelbaum & Epstein, 1962).…”

Section: Discussionmentioning

confidence: 99%

“…If the presence or absence of motor abnormality could be established the weighing of various possible causes of the aphagia could be given a firmer base. Rats with lesions in the lateral hypothalamus show abnormal posture and movement (Baillie & Morrison, 1963;Teitelbaum & Epstein, 1962) and decrease in spontaneous locomotor activity (Gladfelter & Brobeck, 1962), but these changes were not firmly associated with feeding effects.…”

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confidence: 99%

The relationship of energy expenditure and spontaneous activity to the aphagia of rats with lesions in the lateral hypothalamus

Morrison¹

1968

The Journal of Physiology

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SUMMARY1. Lesions in the lateral hypothalamus of rats always produced an immediate increase in total energy expenditure. The increase was maintained for 24 hr or longer only in rats that became and remained aphagic. Rats that showed no recovery from the aphagia and were maintained by tube feeding showed a second, larger increase in metabolic rate after about 7 days.2. The increase in total energy expenditure was associated, initially, with almost continuous motor activity. With continued aphagia an abnormally differentiated pattern of activity appeared at the same time as the second increase in metabolic rate, and the compartment of energy attributable to activity remained high (34 % as compared with 23 % in normal rats). These changes were accompanied by a recovery of an instrumental response for food (lever pressing), of interest in offered foods and of grooming activity.3. Metabolic abnormality not attributable to activity was indicated by increased creatinine excretion of aphagic but not of hypophagic rats.4. Rats that recovered spontaneous feeding after aphagia returned towards a normal differentiated pattern of activity, with bursts of activity separated by periods of rest, but showed residual abnormality in creatinine excretion.5. The intimate association between increase of energy expenditure, abnormality of motor activity and the aphagia produced by lateral hypothalamic lesions is consistent with the hypothesis that motor incoordination or disorganization is a cause of the aphagia.

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“…The only two papers known to the authors which bear on the subject have been quoted above. Baillie and Morrison (1963) conditioned rats to feed themselves intragastrically by pressing a lever. Animals so conditioned continued to feed themselves in this way after destruction of the "appetite" centre, though they no longer took food by the mouth.…”

Section: Disoussionmentioning

confidence: 99%

“…Anand and Brobeck (1952) published diagrams showing the areas in the rat hypothalamus in which destructive lesions produce hyperphagia and aphagia respectively. Recently, Baillie and Morrison (1963) have shown that lesions in the ventrolateral hypothalamus produce a "true aphagia", since rats, conditioned to obtain food intragastrically by lever pressing, continued to do so after the establishment of such lesions, although they no longer took food or fluid by mouth.…”

Section: Introductionmentioning

confidence: 99%

An Attempt to Produce Hyperphagia in Sheep by Electrical Damage to the Hypothalamus

Holmes¹,

Fraser²

1965

Aust. Jnl. Of Bio. Sci.

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The nature of the suppression of food intake by lateral hypothalamic lesions in rats

Cited by 67 publications

References 16 publications

Review of the neuroanatomic landscape implicated in glucose sensing and regulation of nutrient signaling: Immunophenotypic localization of diabetes gene Tcf7l2 in the developing murine brain

Review of the neuroanatomic landscape implicated in glucose sensing and regulation of nutrient signaling: Immunophenotypic localization of diabetes gene Tcf7l2 in the developing murine brain

The relationship of energy expenditure and spontaneous activity to the aphagia of rats with lesions in the lateral hypothalamus

An Attempt to Produce Hyperphagia in Sheep by Electrical Damage to the Hypothalamus

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