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Main conclusion: Specific sound patterns can affect plant development. Plants are responsive to environmental stimuli such as sound. However, little is known about their sensory apparatus, mechanisms, and signaling pathways triggered by these stimuli. Thus, it is important to understand the effect of sounds on plants and their technological potential. This review addresses the effects of sounds on plants, the sensory elements inherent to sound detection by the cell, as well as the triggering of signaling pathways that culminate in plant responses. The importance of sound standardization for the study of phytoacoustics is demonstrated. Studies on the sounds emitted or reflected by plants, acoustic stress in plants, and recognition of some sound patterns by plants are also explored. [ABSTRACT FROM AUTHOR]

In this study, our hypothesis was that workplace noise can alter brain element levels like immobilization and light-dark cycle shift, and we aimed to investigate the effects of workplace noise on element levels of brain areas as well as changes in blood of chronically noise-exposed rats. Twenty-four rats were randomly divided into three groups. The first group was the control. The second group (noise exposed) was subjected to daily 8 h 85 dB workplace noise for 15 days, and the third group (noise exposed plus normal condition) was also subjected to the same noise exposure and then returned to normal condition for 15 days. In noise-exposed group, Na, K, Ca, Mg , Fe, Cu, and Zn levels in plasma significantly increased when compared with controls ( p = 0.03 for Na; p = 0.005 for K and Mg; p = 0.002 for Ca and Fe; p = 0.01 for Cu and Zn). In this group, Fe level of temporal lobe significantly increased ( p = 0.021) while Mg level significantly increased in frontal ( p = 0.021) and temporal ( p = 0.001) lobes when compared with controls. In the noise-exposed plus normal condition group, plasma Na, K, Fe, Cu, and Zn levels were greatly similar to controls. But, plasma Ca and Mg levels significantly decreased when compared with controls ( p = 0.002 and p = 0.007) and noise-exposed group ( p = 0.002 and p = 0.001). Fe level of temporal lobe significantly increased when compared with controls ( p = 0.001) and noise exposed group ( p = 0.001). These alterations may be attributed to impaired intake of water and micronutrients or their excretions, emerging by acoustic stress. [ABSTRACT FROM AUTHOR]

Strong acoustic stimulation (105 dB SPL white noise) elicited c-fos expression in neurons in several acoustic system nuclei and in stress-sensitive hypothalamic nuclei and limbic areas in rats. In the present study, using this type of loud noise for 30 min, Fos-like immunoreactivity (Fos-ir) was investigated in neurons that synthesize tuberoinfundibular peptide of 39 residues (TIP39) in the rat brain: in the subparafascicular area of the thalamus, the posterior intralaminar complex of the thalamus and the medial paralemniscal nucleus in the lateral part of the pons. By double labeling, Fos-ir was shown in nearly 80% of TIP39-positive cells in the medial paralemniscal nucleus, 43% in the posterior intralaminar complex and 18.5% in the subparafascicular area 30 min after the end of a 30-min loud noise period. In control rats, only few neurons, including 0–4% of TIP39-positive neurons showed Fos-ir. While the majority of the Fos-ir neurons were TIP39-positive in the subparafascicular area and medial paralemniscal nucleus, a fairly high number of TIP39-immunonegative, chemically uncharacterized neurons expressed c-fos in the subparafascicular area and the posterior intralaminar complex of the thalamus. These observations clearly show that some TIP39 neurons in the so-called “acoustic thalamus” and the majority of TIP39 neurons in the medial paralemniscal nucleus are sensitive to loud noise and they may participate in the central organization of responses to acoustic stress. Furthermore, the present data suggest that non-TIP39-expressing neurons may play a prevalent role in the activity of the “acoustic thalamus”. [ABSTRACT FROM AUTHOR]

The effect of circulation arrest on the development of stress-induced injuries was studied in Krushinsky—Molodkina rats genetically predisposed to audiogenic seizure. Resuscitated rats were subjected to acoustic stress 1.5 month after circulation arrest. The severity of neurological disorders and the frequency and severity of intracranial hemorrhages increased, while excitability of the central nervous system remained unchanged during stress. Thus, the resistance to stress considerably decreased in rats survived a short-term circulatory arrest due to dysfunction of the autonomic nervous regulation of hemodynamics rather than enhanced excitability of the central nervous system. [ABSTRACT FROM AUTHOR]