Context: White noise is known to have detrimental effects on different brain regions, especially auditory regions, including inferior colliculus. Although the basis for such alterations has been hypothesized to result from abnormalities in neurotransmitter release, the mechanism is unclear. The final step in neurotransmission is the docking and transient fusion of synaptic vesicles at the base of cup-shaped lipoprotein structures called porosomes at the presynaptic membrane and the consequent release of neurotransmitters. Earlier studies in cat brain document altered morphology of the secretory portal the porosome at nerve terminals in the inferior colliculus following white noise exposure. The current study was performed to test the hypothesis of possible changes to synaptic vesicle size in the colliculus, following white noise exposure. Material and Methods: Electron microscopic morphometry of synaptic vesicles size in axo-dendritic synapses at the colliculus region of the cat brain was performed. Results: We report, for first time, decreased size of both docked and undocked vesicles in high-intensity white noise-exposed animals. In both control and experimental animals, docked vesicles are demonstrated to be smaller than undocked vesicles, suggesting fractional discharge of vesicular contents via porosome-mediated kiss-and-run mechanism. Conclusion: These studies advance our understanding of neurotransmitter release and the impact of white noise on brain function.

Background: Human exposure to infrasound is increasing due to man-made factors, such as occupational conditions, wind farms and transportation. The concern among the public regarding the safety of infrasound exposure is growing. Aims: To evaluate whether exposure to infrasound interferes directly with human cardiac function and contributes to pathological processes. Setting: The University Hospital of Mainz, Germany. Methods: Human myocardial tissues, obtained from patients undergoing cardiac surgery, were prepared in small muscle samples and stimulated electrically in-vitro for a period of almost two hours under physiological conditions to induce continuous pulsatile contractions and simulating a working human heart. Two samples were obtained from each donor: one was subjected to infrasound for 60 min and the other served as a control. Their contraction forces (CF) and durations (CD) were measured before and after each testing period and their relative changes (CF_% and CD_%) were calculated and introduced in a multilinear regression model. The following three infrasound levels of exposure were used in this study: 100, 110 and 120 dBz. Results: The measured CF_% corresponded negatively with the infrasound level measured in dBz (R₂ = 0.631; P = 0.018). The decrease measured almost −11% at 110 dBz and −18% at 120 dBz, after correction for control. The CD on the other hand remained unchanged. Conclusions: Exposure to high levels of infrasound (more than 100 dBz) interferes with cardiac muscle contractile ability, as early as one hour after exposure. There are numerous additional studies which support this conclusion. These results should be taken into account when considering environmental regulations.