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Adult rats previously exposed to early postnatal overnutrition by raising them in small litters become persistently predisposed to overweight, hyperphagia and hyperleptinaemia. The hypothesis was raised that feeding\u2010related peptides could be involved through altered effects on neuronal activity of the regulatory systems of such rats. This was studied on brain slices of small\u2010litter rats and normal\u2010weight controls between days\u200360 and 120 of life. Neurons of the medial parvocellular part of the paraventricular nucleus were significantly activated by the adiposity signals leptin, insulin and amylin in controls. This is a kind of negative feedback, because activation of these neurons is known to be followed <jats:italic>in vivo<\/jats:italic> by increased energy expenditure. GABAergic mechanisms seem to affect these neuronal responses because the activating effects of insulin and amylin were reduced in the presence of a GABA<jats:sub>A<\/jats:sub> receptor antagonist. In overweight small\u2010litter rats, however, the neuronal responses to the adiposity signals were significantly changed; activating effects were reduced and inhibitory effects increased. By means of blockade of GABA<jats:sub>A<\/jats:sub> receptors, significant alterations in the neuronal responses to leptin, insulin and amylin in small\u2010litter rats were prevented. Responses to the peptides were reversed and now resembled those of controls. In conclusion, changes in neuronal wiring with GABAergic interneurons seem to contribute to a persistently reduced negative feedback of adiposity signals in early postnatally overfed rats.<\/jats:p>","DOI":"10.1111\/j.1460-9568.2006.04636.x","type":"journal-article","created":{"date-parts":[[2006,3,8]],"date-time":"2006-03-08T15:58:44Z","timestamp":1141833524000},"page":"1248-1254","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":17,"title":["GABA<sub>A<\/sub> receptor antagonists prevent abnormalities in leptin, insulin and amylin actions on paraventricular hypothalamic neurons of overweight 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