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International audience; Residing at high altitude may lead to reduced blood oxygen saturation in the brain and altered metabolism in frontal cortical brain areas, probably due to chronic hypobaric hypoxia. These changes may underlie the increased rates of depression and suicidal behavior that have been associated with life at higher altitudes. To test the hypothesis that hypobaric hypoxia is responsible for development of mood disorders due to alterations in neurochemistry, we assessed depression-like behavior in parallel to levels of brain metabolites in rats housed at simulated altitude. 32 female Sprague Dawley rats were housed either in a hypobaric hypoxia chamber at 10,000 ft of simulated altitude for 1 week or at local conditions (4500 ft of elevation in Salt Lake City, Utah). Depression-like behavior was assessed using the forced swim test (FST) and levels of neurometabolites were estimated by in vivo proton magnetic resonance spectroscopy in the frontal cortex, the striatum and the hippocampus at baseline and after a week of exposure to hypobaric hypoxia. After hypoxia exposure the animals demonstrated increased immobility behavior and shortened latency to immobility in the FST. Elevated ratios of myo-inositol, glutamate, and the sum of myo-inositol and glycine to total creatine were observed in the frontal cortex of hypoxia treated rats. A decrease in the ratio of alanine to total creatine was also noted. This study shows that hypoxia induced alterations in frontal lobe brain metabolites, aggravated depression-like behavior and might be a factor in increased rates of psychiatric disorders observed in populations living at high altitudes.

Anxiety disorders are known to be comorbid with migraine, and cortical spreading depression (CSD) is the most likely cause of the migraine aura. To search for possible correlations between susceptibility to CSD and anxiety we used the open field test in male Sprague-Dawley rats chronically treated with the preventive anti-migraine drugs valproate or riboflavin. Animals avoiding the central area of the open field chamber and those with less exploratory activity (i.e. rearing) were considered more anxious. After 4 weeks of treatment CSDs were elicited by application of 1 M KCl over the occipital cortex and the number of CSDs occurring over a 2 hour period was compared to the previously assessed open field behaviour. Higher anxiety-like behaviour was significantly correlated with a higher frequency of KCl-induced CSDs. In saline-treated animals, fewer rearings were found in animals with more frequent CSDs (R= −1.00). The duration of ambulatory episodes in the open field center correlated negatively with number of CSDs in the valproate group (R= −0.83; p

Atmospheric pressure fluctuations (APF) might induce mechanical effects in the pars flaccida (PF) of the eardrum. To clarify these effects, different kinds of pressure oscillations (PO), chosen within the range of naturally occurring APF, were applied to the middle ears (ME) of gerbils. The linear displacement of the PF during a PO in the ME was measured by laser interferometry. The compliance of the PF to PO was calculated as the ratio of the amplitude of a PF oscillation to the amplitude of a PO. The displacement of the PF traced the PO in the entire range of frequencies (from 10 mHz to 200 mHz) and amplitudes (from 10 Pa to 110 Pa) applied to the ME. Moreover, the PF is found to be displaced by pressure pulses of a few pascals only using a PO with a complex shape. The differences found in the compliance of the PF due to PO with low (less than 20 Pa) and high (more than 90 Pa) amplitude point out that the mechanism of pressure regulation in the ME through the mechanical reaction of the PF in gerbil ears is better adapted to ordinary levels of natural APF than to extraordinary levels. The implications of these findings for the physiology of the human ME with respect to adaptation to natural APF are discussed.