RESUMO
The intergeniculate leaflet (IGL) is classically known as the area of the Thalamic Lateral Geniculate Complex providing the suprachiasmatic nucleus (SCN) non-photic information. In the present study we investigated whether this information might be related to the metabolic state of the animal. The following groups of male Wistar rats were used for analysis of neuropeptide Y (NPY) and c-Fos in the IGL and SCN. (1) Fed ad libitum. (2) Fasted for 48 h. (3) Fasted for 48 h followed by refeeding for 3 h. (4) Monosodium glutamate-lesioned and 48 h fasted. (5) Electrolytic lesion in the IGL and 48 h fasted. The results were quantified by optical densitometry. Neuronal tracers were injected in two brain areas that receive metabolic information from the periphery, the arcuate nucleus (ARC) and Nucleus of the Tractus Solitarius to investigate whether there is an anatomical relationship with the IGL. Lesion studies showed the IGL, and not the ARC, as origin of most NPY projections to the SCN. Fasting induced important changes in the NPY expression in the IGL, coinciding with similar changes of NPY/glutamate decarboxylase projections of the IGL to the SCN. These changes revealed that the IGL is involved in the transmission of metabolic information to the SCN. In fasted animals IGL lesion resulted in a significant increase of c-Fos in the SCN as compared to intact fasted animals demonstrating the inhibitory influence of the IGL to the SCN in fasting conditions. When the animal after fasting was refed, an increase of c-Fos in the SCN indicated a removal of this inhibitory input. Together these observations show that in addition to increased inhibitory IGL input during fasting, the negative metabolic condition also results in increased excitatory input to the SCN via other pathways. Consequently the present observations show that at least part of the non-photic input to the SCN, arising from the IGL contains information about metabolic conditions.
Assuntos
Corpos Geniculados/metabolismo , Neuropeptídeo Y/metabolismo , Núcleo Supraquiasmático/metabolismo , Animais , Jejum/metabolismo , Masculino , Vias Neurais/metabolismo , Distribuição Aleatória , Ratos , Ratos WistarRESUMO
The clock gene protein Per 1 (PER1) is expressed in several brain structures and oscillates associated with the suprachiasmatic nucleus (SCN). Restricted feeding schedules (RFS) induce anticipatory activity and impose daily oscillations of c-Fos and clock proteins in brain structures. Daily access to a palatable treat (chocolate) also elicits anticipatory activity and induces c-Fos expression mainly in corticolimbic structures. Here the influence of daily access to food or chocolate was explored by the analysis of the oscillatory patterns of PER1 in hypothalamic and corticolimbic structures. Wistar rats were exposed to RFS or to daily access to chocolate for 3 weeks. Persistence of food or chocolate entrained rhythms was determined 8 days after cessation of the feeding protocols. RFS and chocolate induced a phase shift in PER1 rhythmicity in corticolimbic structures with peak values at zeitgeber time 12 and a higher amplitude in the chocolate group. Both RFS and chocolate groups showed an upregulation of PER1 in the SCN. Food and chocolate entrained rhythms persisted for 8 days in behavior and in PER1 expression in the dorsomedial hypothalamic nucleus, accumbens, prefrontal cortex and central amygdala. The present data demonstrate the existence of different oscillatory systems in the brain that can be activated by entrainment to metabolic stimuli or to reward and suggest the participation of PER1 in both entraining pathways. Persistence and amplification of PER1 oscillations in structures associated with reward suggest that this oscillatory process is fundamental to food addictive behavior.
Assuntos
Encéfalo/metabolismo , Proteínas de Ciclo Celular/metabolismo , Ritmo Circadiano/fisiologia , Comportamento Alimentar/fisiologia , Motivação , Recompensa , Análise de Variância , Animais , Comportamento Animal , Encéfalo/anatomia & histologia , Cacau , Contagem de Células , Alimentos , Masculino , Atividade Motora/fisiologia , Proteínas Circadianas Period , Ratos , Ratos WistarRESUMO
Individuals engaged in shift- or night-work show disturbed diurnal rhythms, out of phase with temporal signals associated to the light/dark (LD) cycle, resulting in internal desynchronization. The mechanisms underlying internal desynchrony have been mainly investigated in experimental animals with protocols that induce phase shifts of the LD cycle and thus modify the activity of the suprachiasmatic nucleus (SCN). In this study we developed an animal model of night-work in which the light-day cycle remained stable and rats were required to be active in a rotating wheel for 8 h daily during their sleeping phase (W-SP). This group was compared with rats that were working in the wheel during their activity phase (W-AP) and with undisturbed rats (C). We provide evidence that forced activity during the sleeping phase (W-SP group) alters not only activity, but also the temporal pattern of food intake. In consequence W-SP rats showed a loss of glucose rhythmicity and a reversed rhythm of triacylglycerols. In contrast W-AP rats did not show such changes and exhibited metabolic rhythms similar to those of the controls. The three groups exhibited the nocturnal corticosterone increase, in addition the W-SP and W-AP groups showed increase of plasma corticosterone associated with the start of the working session. Forced activity during the sleep phase did not modify SCN activity characterized by the temporal patterns of PER1 and PER2 proteins, which remained in phase with the LD cycle. These observations indicate that a working regimen during the sleeping period elicits internal desynchronization in which activity combined with feeding uncouples metabolic functions from the biological clock which remains fixed to the LD cycle. The present data suggest that in the night worker the combination of work and eating during working hours may be the cause of internal desynchronization.