Human beings are exposed to compressed air or a nitrogen-oxygen mixture, they will produce signs and symptoms of nitrogen narcosis such as amnesia or even loss of memory, which may be disappeared once back to the normobaric environment. This study was designed to investigate the effect of nitrogen narcosis induced by repetitive hyperbaric nitrogen-oxygen mixture exposure on long-term cognitive function in newborn mice and the underlying mechanisms. The electroencephalogram frequency was decreased while the amplitude was increased in a pressure-dependent manner during 0.6, 1.2, 1.8 MPa (million pascal) nitrogen-oxygen mixture exposures in adult mice. Nitrogen narcosis in postnatal days 7–9 mice but not in adult mice induced by repetitive hyperbaric exposure prolonged the latency to find the platform and decreased the number of platform-site crossovers during Morris water maze tests, and reduced the time in the center during the open field tests. An increase in the expression of cleaved caspase-3 in the hippocampus and cortex were observed immediately on the first day after hyperbaric exposure, and this lasted for seven days. Additionally, nitrogen narcosis induced loss of the dendritic spines but not of the neurons, which may mainly account for the cognitive dysfunction. Nitrogen narcosis induced long-term cognitive and emotional dysfunction in the postnatal mice but not in the adult mice, which may result from neuronal apoptosis and especially reduction of dendritic spines of neurons.

This study was aimed to observe the effects of skull defects on the brain in rats and further to investigate its underlying pathophysiological. Three different sizes of skull were removed in rats to produce models of skull defect, and then the behavioral changes were detected using a grip strength meter and neurobehavioral severity scale scores. The authors further examined the levels of cell apoptosis and autophagy, the cerebral blood flow with immunoblotting, and immunofluorescence micro-ultrasound system, respectively. The authors found that the sensory function but not the grip was impaired on the 6th day after a 5 × 10 mm defect while the motor function was on the 2nd day. In addition, the authors found an increment in B-cell lymphoma-2/BCL2-Associated X (Bcl2/Bax) and LC3 II/ I expression, a maker of apoptosis and autophagy, respectively, in the defective hemisphere especially at the edge of the defective area. Importantly, the blood flow of internal carotid artery began to decline at 2 hours, and reached minimum on the 4th day, but began to recover on the 6th day in the hemi-defect group. In conclusion, a larger skull defect could impair the cognitive function but not the motor function and its underlying pathophysiology were mainly related to a decrease in cerebral flow.