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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.

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In the present electron microscopic study the effect of continuous white noise on the morphology of synapses and neuronal porosome complex (the neurotransmitter-release or secretory machinery) in two subcortical auditory brain regions - colliculus inferior and medial geniculate body in cat, were investigated. Several morphological alterations in some synapses were detected in both subcortical areas. These alterations mainly indicate to the decrease of functional activity of synapses. Rarely important pathological modifications in pre- and post-synaptic regions were detected. In addition to descriptive studies, the morphometric analysis of porosome diameter and depth was performed in colliculus inferior and medial geniculate body. The results revealed that while white noise has no effect on the porosome diameter and depth in colliculus inferior, it provokes significant alterations in the morphology of porosome complex in medial geniculate body. In particular, the significant increase of porosome depth in this nucleus may reflect the alteration in neurotransmission.

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Dendrites and spines undergo dynamic changes in physiological conditions, such as learning and memory, and in pathological conditions, such as epilepsy. Abnormalities in dendritic spines have commonly been observed in brain specimens from epilepsy patients and animal models of epilepsy. However, the functional implications and clinical consequences of this dendritic pathology for epilepsy are uncertain. Motility of dendritic spines and axonal filopodia has been recently discovered by the advanced imaging techniques, and remains to a large degree an exciting phenomenology in search of function. Here we demonstrate the effect of kainic acid (KA), which is a structural analog of glutamate, on dendritic spine motility in hippocampal CA1 area at the different stages of brain development. In order to reveal the changes that take place in spine and filopodial motility in the epileptic model of brain, time-lapse imaging of acute hippocampal slices treated with various concentrations of KA after different incubation time points was performed. The effects of KA exposure were tested on the slices from young (postnatal day (P)7-P10) and adolescent (P28-P30) Thy1-YFPH transgenic mice. Slices were treated with either 50 µM or 100 µM of KA, for either 30 or 100 min. The results obtained in our experiments show diverse effects of KA in 2 different age groups. According to our results, 100 µM/100 min KA treatment increases spine motility at early stage of brain development (P10) by 41.5%, while in P30 mice spine motility is increased only by 3%. Our findings also indicate that effect of KA on hippocampal dendritic spine motility is predominantly time- rather than concentration-dependent.

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It is known that myo-inositol pretreatment attenuates the seizure severity and several biochemical changes provoked by experimentally induced status epilepticus. However, it remains unidentified whether such properties of myo-inositol influence the structure of epileptic brain. In the present light and electron microscopic research we elucidate if pretreatment with myo-inositol has positive effect on hippocampal cell loss, and cell and synapses damage provoked by kainic acid-induced status epilepticus. Adult male Wistar rats were treated with (i) saline, (ii) saline + kainic acid, (iii) myo-inositol + kainic acid. Assessment of cell loss at 2, 14, and 30 days after treatment demonstrate cytoprotective effect of myo-inositol in CA1 and CA3 areas. It was strongly expressed in pyramidal layer of CA1, radial and oriental layers of CA3 and in less degree-in other layers of both fields. Ultrastructural alterations were described in CA1, 14 days after treatment. The structure of neurons, synapses, and porosomes are well preserved in the rats pretreated with myo-inositol in comparing with rats treated with only kainic acid.

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