RESUMEN
The anterior piriform cortex (APC) is essential for the anorectic reactions to an amino acid-imbalanced diet, and it also responds to repletion of the limiting amino acid. In the present study, we examine the dynamic changes of the interstitial dopamine metabolites in the APC following feeding of either an amino acid-corrected or -imbalanced diet. Microdialysates, collected from the APC, were analyzed using HPLC with electrochemical detection. The concentrations were 19.7 +/- 4.8 microg/L for 3, 4-dyhydroxyphenylacetic acid and 25.1 +/- 4.4 microg/L for homovanillic acid, respectively, in the baseline dialysates. After diet treatments, no significant changes occurred in 3, 4-dyhydroxyphenylacetic acid in the corrected (n = 7) or imbalanced (n = 9) groups vs. the basal group (n = 7). However, after feeding the threonine-corrected diet, the concentration of homovanillic acid was significantly less (P < 0.01) than after the basal and imbalanced diets. The homovanillic acid level in the corrected group was already significantly lower than in the basal group by 20 min (P < 0.05), and reached its lowest level at 70 min (P < 0.05). The concentrations of homovanillic acid in the corrected group remained at this low level until the end of the experiment. The present results introduce the idea that the dopaminergic system is involved in the feeding responses to essential amino acid repletion.
Asunto(s)
Aminoácidos Esenciales/farmacología , Corteza Cerebral/efectos de los fármacos , Dopamina/metabolismo , Treonina/farmacología , Ácido 3,4-Dihidroxifenilacético/análisis , Animales , Corteza Cerebral/metabolismo , Cromatografía Líquida de Alta Presión , Dieta , Ácido Homovanílico/análisis , Masculino , Microdiálisis , Ratas , Ratas Sprague-Dawley , Treonina/administración & dosificación , Treonina/deficienciaRESUMEN
Amino acid-imbalanced (IMB) diets induce an acute amino acid deficiency and hypophagic responses in most animals. The neural circuits underlying these responses are unknown. To ascertain potential neural circuits involved in the recognition of IMB, we measured the concentrations of norepinephrine, dopamine, serotonin, their metabolites and 20 amino acids in 14 rat brain areas in three studies. Rats were prefed a basal diet with L-amino acids as the protein source for at least 1 wk. For the experiments, either threonine or isoleucine IMB diet was offered for 2.5 or 3.5 h. Brains were taken before (using a mildly IMB diet) or after (using moderately or severely IMB diet) food intake was significantly (P < 0.05) depressed. Brain areas were dissected and analyzed for monoamines, metabolites and amino acids. Only in the anterior piriform cortex (APC), a brain area that may contain the amino acid chemosensor, was the limiting amino acid lower in IMB groups than in controls across all of the experiments. Before the onset of the anorectic response to the IMB diets, monoaminergic activity was affected in areas that have recognized monosynaptic connections with the APC. We propose a circuit for the neural responses in the initial recognition of acute amino acid deprivation that begins with activation of the APC and includes areas in the hindbrain and hypothalamus. After a significant hypophagic response, serotonergic indicators were altered in areas of the taste pathway and the limbic system. These results suggest that different circuits mediate the initial recognition and secondary conditioned responses to IMB diets.
Asunto(s)
Aminoácidos/deficiencia , Anorexia/fisiopatología , Encéfalo/fisiopatología , Dieta/efectos adversos , Aminoácidos/sangre , Aminoácidos/metabolismo , Animales , Monoaminas Biogénicas/metabolismo , Encéfalo/metabolismo , Masculino , Vías Nerviosas/fisiopatología , Neurotransmisores/metabolismo , Ratas , Ratas Sprague-DawleyRESUMEN
Rats offered an amino acid-imbalanced diet (IMB) respond to the ensuing amino acid deficiency rapidly with a decrease in food intake of at least 50%. Pretreatment with tropisetron (TROP), an antagonist at serotonin3 (5-HT3) and 5-HT4 receptors, increases intake of IMB to approximately 85% of control. Vagotomy has two effects: it increases intake of an IMB to about 65%, and also blocks the increased response to tropisetron. This indicates that the greater IMB intake after tropisetron, approximately 20% more than in vagotomized rats, is dependent on an intact vagus. Rats were either 1) vagotomized or sham-operated, or 2) given tropisetron or saline injections. We then examined free-feeding meal patterns in rats fed an IMB to determine whether the microstructure of the feeding behavior differed, either between treatments, or by comparison with the meal patterns in rats fed the control diet. Vagotomy did not alter meal patterns in rats consuming the basal control diet. During the first 6 h after introduction of the IMB, the control rats showed significantly longer intermeal intervals (over twice the length of intervals recorded in those fed the basal diet), with corresponding effects on meal numbers, which were restored to basal values in tropisetron and vagotomized rats. Meal size was increased after vagotomy also. After 6 h, in intact tropisetron-treated rats only, a fourfold faster rate of eating throughout the late dark period accounted for the significantly greater intake of the IMB than in controls. The results demonstrated differential effects of the two treatments on the anorectic responses to amino acid deficiency.