Aims:Previous studies have shown that heart rate variability (HRV) measurement is useful in investigating the pathophysiology of various psychiatric disorders. The present study further examined its usefulness in evaluating the mental health of normal subjects with respect to anxiety and depressiveness.

The relationships between depression and gut microbiota, particularly those involving the immune system, have become a major focus of recent research. Here, we analyzed changes in gut microbiota and their sulfur metabolites in the feces of a depression rat model using the modified 14-day social defeat stress (SDS) paradigm. Our results showed that SDS increased fecal Lactobacillus reuteri in correlation with ergothioneine levels at around day 11, which continued for at least 1 month following SDS administration. In vitro study further revealed that L. reuteri is capable of producing ergothioneine. Although the known anti-inflammatory and anti-oxidative actions of ergothioneine suggested that the increased fecal ergothioneine levels may be related to intestinal anti-inflammatory defense mechanisms, no change was observed in the plasma ergothioneine levels during the same observation period, indicating that the defense mechanisms may not be sufficiently reflected in the body. As ergothioneine is a natural ingredient that is absorbed mainly from the upper gastrointestinal tract, we hypothesized that oral ergothioneine may exert antidepressant effects. As expected, oral administration of ergothioneine prior to and during the SDS paradigm had a preventative effect on SDS-induced depressive behaviors, such as social avoidance and depression-like sleep abnormalities, particularly those of rapid eye movement sleep. These findings indicate that ergothioneine, a metabolite of L. reuteri, may be a common substance in the microbiota-gut-brain axis that prevents stress-induced sleep disturbances, especially those associated with depression. Recent research has reported the influence of gut microbiota on cerebral function (i.e., the microbiota-gutbrain axis) 4-9. For example, depressive behaviors develop in germ-free rodents following fecal transplants from human patients with MDD 10,11. On the other hand, decreases in MDD-like behaviors occurred following the administration of prebiotics in mice subjected to mild

Several lines of evidence strongly suggest that accumulation of noradrenaline (NA) in the brain may underlie the hyperarousal symptoms experienced in post-traumatic stress disorder. In animal experiments, however, the effect of stress on NA content appears complex; acute stress reduces the level, while chronic stress tends to increase it. To explain this discrepancy, it is necessary to observe the long-term effects of acute stress on NA metabolism in the brain. In this study, rats were exposed to intermittent intense footshock stress for 1 h, and the brain NA content was measured for 7 days after the stress stimulus. Hypothalamic NA content was immediately reduced and recovered within 24 h. However, a significant NA increase was observed 7 days after the footshock. In the cerebral cortex and hippocampus, an increase in NA content was observed 1 day after the stress and lasted for at least 7 days. The fact that the content of 3-methoxy-4-hydroxyphenylglycol, a major NA metabolite, only transiently increased in all these regions possibly reflects NA release. These results indicate that increase in the brain NA content can be induced by acute stress, though its emergence is delayed. Importantly, this suggests that both acute and chronic stress may lead to NA accumulation under the same mechanism.

Pallido-thalamic transmission was studied by intracellular recording from neurons in the ventrolateral (VL) and ventroanterior (VA) nuclei of the thalamus in cats anesthetized with pentobarbital. Stimulation of the entopeduncular nucleus (ENT) produced short latency, inhibitory postsynaptic potentials in the VL-VA neurons (1.60 ms on average). When stimuli were applied closer to the VL-VA region along the pallido-thalamic pathway, i.e., to the rostral Forel's field, the IPSP latency was significantly reduced. Linear regression analysis of the IPSP latency against conduction distance between different stimulating the recording positions indicated that the IPSP was produced through a monosynaptic pathway at a conduction velocity of 5 to 11 m/s. The neurons which received IPSPs from the ENT distributed in the rostromedial VL and in the rostral VA, whereas relay cells responding only to the contralateral brachium conjunctivum were found in the caudal VL and in the dorsolateral portion of the rostral VL-VA complex. Reciprocal convergence of pallidal and cerebellar impulses were observed in only a small number of cells, which were located in the border between the two neuron groups. Recording of extracellular field potentials and focal stimulation within and around the rostral VL also indicated that the fiber potentials arose from the ENT nucleus and propagated along a bundle of fibers which terminated within the rostromedial VL-VA complex. These results are all explicable by assuming that the entopeduncular neurons are inhibitory in nature and so inhibit thalamic neurons monosynaptically.

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