No abstract

The present study investigated the operational features of whisker-evoked EPSPs in barreloid cells and the ability of the whisker-to-barreloid pathway to relay high rates of whisker deflection in lightly anesthetized rats. Results show that lemniscal EPSPs are single-fiber events with fast rise times (<500 microsec) that strongly depress at short inter-EPSP intervals. They occur at short latencies (3.84 +/- 0.96 msec) with little jitters (<300 microsec) after electrical stimulation of the whisker follicle. Waveform analysis indicates that one to three lemniscal axons converge on individual barreloid cells to produce EPSPs of similar rise times but different amplitudes. When challenged by high rates of whisker deflection, cells in the whisker-to-barreloid pathway demonstrate a remarkable frequency-following ability. Primary vibrissa afferents could follow in a phase-locked manner trains of sinusoidal deflections at up to 1 kHz. Although trigeminothalamic cells could still faithfully follow deflection rates of 200-300 Hz, the actual frequency-following ability of individual cells depends on the amplitude, velocity, and direction of displacements. The discharges of trigeminothalamic cells induce corresponding phase-locked EPSPs in barreloid cells, which trigger burst discharges at stimulus onset. During the following cycles of the stimulus train, few action potentials ensue because of the strong synaptic depression at lemniscal synapses. It is concluded that the whisker-to-barreloid pathway can relay vibratory inputs with a high degree of temporal precision, but that the relay of this information to the cerebral cortex requires the action of modulators, and possibly phase-locked discharges among an ensemble of relay cells.

This study investigated sex-specific effects of repeated stress and food restriction on food intake, body weight, corticosterone plasma levels and expression of corticotropin-releasing factor (CRF) in the hypothalamus and relaxin-3 in the nucleus incertus (NI). The CRF and relaxin-3 expression is affected by stress, and these neuropeptides produce opposite effects on feeding (anorexigenic and orexigenic, respectively), but sexspecific regulation of CRF and relaxin-3 by chronic stress is not fully understood. Male and female rats were fed ad libitum chow (AC) or ad libitum chow and intermittent palatable liquid Ensure without food restriction (ACE), or combined with repeated food restriction (60% chow, 2 days per week; RCE). Half of the rats were submitted to 1-h restraint stress once a week. In total, seven weekly cycles were applied. The body weight of the RCE stressed male rats significantly decreased, whereas the body weight of the RCE stressed female rats significantly increased compared with the respective control groups. The stressed female RCE rats considerably overate chow during recovery from stress and food restriction. The RCE female rats showed elevated plasma corticosterone levels and low expression of CRF mRNA in the paraventricular hypothalamic nucleus but not in the medial preoptic area. The NI expression of relaxin-3 mRNA was significantly higher in the stressed RCE female rats compared with other groups. An increase in the expression of orexigenic relaxin-3 and misbalanced hypothalamic-pituitary-adrenal axis activity may contribute to the overeating and increased body weight seen in chronically stressed and repeatedly food-restricted female rats.

The time course of the action of food deprivation on the functional activation of corticotropin-releasing hormone (CRH) neurons and on the expression of the genes encoding CRH and its receptors of type 1 (CRH_rR) and 2α (CRH₂-R) in the brain were assessed in lean (Fa/?) and obese (fa/fa) Zucker rats. Fa/? and fa/fa rats were assigned to food deprivation periods of 0, 3, 6, 12, and 24 h. Measurements of Fos immunoreactivity and CRH mRNA were carried out on the same brain sections to assess the state of activation of CRH neurons. In situ hybridization histochemistry was employed to measure the mRNAs encoding CRH and its receptors. In fa/fa rats, food deprivation induced a rapid expression of Fos in CRH cells of several brain regions that include the paraventricular hypothalamic nucleus (PVN), the bed nucleus of the stria terminalis (BNST), the anterodorsal preoptic nucleus, the medial preoptic nucleus, the substantia innominata and Barrington’s nucleus. The colocalization of Fos immunoreactivity and CRH mRNA was particularly noticeable in the PVN of fa/fa rats, where the majority of the CRH cells of the parvocellular division of the nucleus displayed Fos-positive nuclei, 12 h after the onset of fasting. In obese rats, food deprivation also produced an increase in the CRH mRNA levels in the BNST as well as high and low expressions of the CRH₁-R in, respectively, the PVN and the anterior lobe of the pituitary. The expression of CRH]-R in the PVN of obese rats occurred 12 h after the onset of the deprivation. In Fa/? rats, food deprivation induced no marked activation of the CRH cells, a slow decrease in the CRH mRNA levels in the BNST and the central nucleus of the amygdala, and a gradual decrease in the expression of CRH₂-R gene in the ventromedial hypothalamic nucleus. These results demonstrate that food deprivation is capable of generating in obese Zucker rats a stress-like response that translates into a particularly striking activation of the hypothalamic-pituitary-adrenal axis. This response contrasts with that observed in Fa/? rats, in which the action of food deprivation on the CRH system seems more compatible with the known effects of CRH in the regulation of energy balance.