Our objective was to study the relationship between the satiety induced by high-protein meals and the activation of brain areas involved in the onset of satiety. In rats, we used immunohistochemistry to monitor brain centers activated by a meal by receiving information from the gastrointestinal tract or via humoral pathways. In the nucleus of the solitary tract (NTS), the acute or chronic intake of high-protein meals led to increased activation of the noradrenergic/adrenergic neurons involved in cholecystokinin-induced satiety. In the arcuate nucleus of the hypothalamus, the melanocortin pathway was also more strongly activated after the acute or chronic intake of high-protein meals. Moreover, the glucagon-like peptide 1 pathway arising from the NTS, which is triggered, among other behaviors, during nonphysiological anorexia, was not activated by high-protein meals, supporting the lack of aversive behavior associated with this diet. Taken together, these results show that the ability of high-protein meals to inhibit food intake occurs alongside the activation, in nutrient-sensitive brain areas, of several specific neuronal populations involved in satiety.
Penile afferents present in the dorsal nerve of the penis (DNP) convey sensory information from the penis to the spinal cord and represent the afferent limb of reflexive erections. Immunocytochemical staining of Fos was used to identify spinal neurons that receive excitatory inputs from the DNP in anesthetized rats. Intracavernous pressure (ICP) was recorded as an index of erection. Dissection as well as stimulation of the DNP elicited a comparable increase in Fos staining. Labeling was present in the dorsal horn, the dorsal gray commissure, and the sacral parasympathetic nucleus, supporting the hypothesis of direct or indirect afferent projection from the penis and penile sheath in these areas. No change in ICP was observed in these rats. Stimulation of the DNP elicited both increased Fos labeling and ICP after spinalization, demonstrating the presence of a supraspinal inhibitory control exerted on the polysynaptic intraspinal circuitry responsible for reflexive penile erection.
Transition from a normal- (NP) to a high-protein (HP) diet induces a rapid depression in food intake and a progressive but incomplete return to the initial intake during the succeeding days. The aim of this study was to determine which CNS regions are involved in the HP diet-induced satiety in rats. Brains were collected from 3 groups of adult rats after habituation to an NP diet (21 d), during the transition phase to a HP diet (2 d), or after habituation to the HP diet (21 d). Fos expression was measured in several brain areas that are involved in the control of food intake (solitary tract nucleus, anterior piriform cortex, lateral hypothalamus, arcuate nucleus, posterior para ventricular nucleus, medio ventral hypothalamus, dorso medial hypothalamus, amygdala, and accumbens nucleus). Changes occurred in the majority of these regions during the transition period from the NP diet to the HP diet. After habituation to the HP diet, significant changes in Fos expression were restricted to an increase in the nucleus of the solitary tract and a decrease in the ventromedial hypothalamus and the cortex of the amygdala. Considering the functional characteristics of these areas, the present results suggest that the vagus nerve conveys the information relative to the quantity of protein ingested, that hypothalamic sites regulate food intake and may alter sympathetic nervous system activity, and that higher brain functions such as memory processing by the limbic system or food reward system are involved in the HP diet-induced satiety in rats.
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