Prenatal administration of valproic acid (VA) and its salts is a common approach to modeling impairments to nervous system development; the sequelae of postnatal VA administration have received significantly less study. This study compared the behavioral characteristics of two groups of infant mice exposed to sodium valproate pre- and postnatally; neurocytological methods were also used. Behavioral studies were started from the early postnatal period and ended at age 36 days. Comparison of models showed a delay in early motor development and hyperactivity in both cases, though decreases in interest in new social contacts (interaction with rat pups of the same age) were seen only in animals given postnatal VA injections. In addition, a significant increase in the number of perineuronal satellite oligodendrocytes was seen in the anterior cingulate cortex of animals in both series – pre- and postnatal VA. Studies of the cingulate cortex, a component of the limbic system, are important in considering social interactions and the processes forming and regulating emotional behavior, as well as pathological reactions in different impairments to higher brain functions.
Administration of valproic acid (VPA) and valproate salts prenatally is a common way to model developmental disorders of the nervous system, however, studies of models based on postnatal administration of VPA are much less common. In presented work the behavioral characteristics of two groups of rat pups pre- and postnatally administrated with sodium valproate have been compared; neurocytological methods were also used. Behavioral studies started from infancy and ended on 36th day of life. A comparison of the models showed a delay in early motor development and hyperactivity in both models, however, a decrease in interest in new social contacts was observed only in animals treated with postnatal injections of VPA. Furthermore, a significant increase in the number of perineuronal satellite oligodendrocytes in the cingulate cortex of animals was shown, both in the series with prenatal and in the series with postnatal administration of VPA. Anterior cingulate cortex, as a part of limbic system, is important in social behavioral studies due to its involvement in emotional behavior processing and symptoms in several psychopathological conditions.
Orientation selectivity is an important feature of visual cortical neurons. Optical imaging of the visual cortex allows for the generation of maps of orientation selectivity that reflect the activity of large populations of neurons. To estimate the statistical significance of effects of experimental manipulations, evaluation of the stability of cortical maps over time is required. Here, we performed optical imaging recordings of the visual cortex of anesthetized adult cats. Monocular stimulation with moving clockwise square-wave gratings that continuously changed orientation and direction was used as the mapping stimulus. Recordings were repeated at various time intervals, from 15 min to 16 h. Quantification of map stability was performed on a pixel-by-pixel basis using several techniques. Map reproducibility showed clear dynamics over time. The highest degree of stability was seen in maps recorded 15-45 min apart. Averaging across all time intervals and all stimulus orientations revealed a mean shift of 2.2 +/- 0.1 degrees. There was a significant tendency for larger shifts to occur at longer time intervals. Shifts between 2.8 degrees (mean +/- 2SD) and 5 degrees were observed more frequently at oblique orientations, while shifts greater than 5 degrees appeared more frequently at cardinal orientations. Shifts greater than 5 degrees occurred rarely overall (5.4% of cases) and never exceeded 11 degrees. Shifts of 10-10.6 degrees (0.7%) were seen occasionally at time intervals of more than 4 h. Our findings should be considered when evaluating the potential effect of experimental manipulations on orientation selectivity mapping studies. (C) 2018 IBRO. Published by Elsevier Ltd. All rights reserved.
At present, it remains poorly understood how the olfactory neuron migrates through the thick neuroepithelium during its maturation from a stem cell and how it develops a specific sensitivity to environmental odorants after maturation. We investigated the cytochemical features associated with the development of olfactory cells before and after the incorporation of dendrites into the surface of the olfactory epithelium. Using cytochemical staining for the actin cytoskeleton and other cell components, we found that immature neurons acquire a streamlined shape that resembles a «hot-dog» during their migration: a dense layer of actin microfilaments forms beneath the surface membrane of the growing dendrite, and the bulk of the nuclear material moves inside this layer. We have found that when the cell makes contact with its environment, the dendritic terminal develops a wide actin layer, inside which a pore is formed. It is assumed that the functional receptors of odorants generate across this pore the first intracellular signal from environmental water-soluble odorants. These data illustrate the important role of the cytoskeleton in the differentiation of olfactory cells.
Local cerebrovascular disorders were modeled by reversible photochemical clotting of hemispheric cortical vessels. Mild ischemia led to reversible edema in the surface layers of the cortex: cytotoxic edema of the neuropile, primarily of the distal dendrites. This status led to an increase in the lower delta rhythm frequency band power. After administration of systemic anesthetic, delta rhythm appeared sooner in the ischemic foci than in intact cortical areas. More severe ischemia led to the appearance of dark and pyknotic neurons and reduction of oscillation power in all EEG spectrum bands. Restructuring of primarily dendrites caused by local moderate ischemia of the surface cortical layers at the early stage of neurodegenerative processes stimulated the inhibitory recovery processes.
Structural changes in the sensorimotor cortex of the cerebral hemispheres were studied in rats with experimental hemorrhagic stroke in the internal capsule. Changes in the shape and decrease in the density distribution of spines on apical dendrites of layer V pyramidal neurons of the sensorimotor cortex were revealed. Some fractions isolated from the complex of neurotrophic factors of the cerebral cortex of animals with a favorable outcome of hemorrhagic stroke were shown to affect the distal and proximal dendritic loci. As differentiated from the “nonactive” fraction, the “active” fraction improved the behavior of rats surviving hemorrhagic stroke. The density distribution of spines (particularly in the distal region of apical dendrites of pyramidal neurons in layer V of the cerebral cortex) was stabilized after treatment with the “active” fraction. The “nonactive” fraction had a selective effect on the proximal loci.
It has been shown that 4% carbon dioxide (CO2) in the air above reaction mixture inhibits the initiation of the formation of silver nanoparticles from complexes with biogenic amines (noradrenaline and serotonin). At the same concentration of CO2 in the air above solution of AgNO3, which is used for staining nerve tissues by the method of Golgi, neurons are preferentially stained, whereas at a concentration of 0.06%, vessels are stained. It is suggested that the entry of free silver ions to neurons is due to the inhibition of sites of initiation of silver nanoparticles in vessels at high CO2 concentrations, while the lack of inhibition leads to silver precipitation in vessels at low CO2 concentrations. It can be assumed that, for stable silver impregnation, the concentration of CO2 must be controlled.
We studied the role of cholinergic systems of the rat brain in the mechanisms of acute response of the neocortex and hippocampus to acute hypobaric hypoxia. The activity of choline acetyltransferase and Na/K-ATPase and the protein content were measured in subfractions of synaptic membranes and the synaptoplasm of “light” and “heavy” synaptosomes. The same biochemical indices were measured in fractions of light and heavy synaptosomes from the nucleus of the solitary tract of the medulla oblongata. In the neocortex, we analyzed the ultrastructure of the synaptic pool. We found active involvement of cholinergic systems in the response to acute hypoxia in all brain structures studied. The synapses of cholinergic projection neurons from the basal nuclei of the frontal cortex (light fractions of synaptosomes), neocortical interneurons (heavy fractions of synaptosomes), and, presumably, GABAergic interneurons of the hippocampus (heavy fraction) were the most sensitive to hypoxia. At the limit of resistance to hypoxia, increased metabolic activity predominated in the synapses of rats that had poorly resistance to hypoxia, while in highly resistant rats this activity was diminished. This difference is related to the different duration of their exposure to critical altitude. We found a reduction in the number of synapses and staging in the development of the functional response of synapses to acute hypoxia. We propose a mechanism for the structural and functional reorganization of synaptic links during acute hypoxia, which is general for both poorly and highly resistant rats. We also hypothesize that a reduction of synapses is one of early triggers that switches neurons to levels of interaction that are adequate for hypoxia.
A standardized experimental model of intracerebral hemorrhagic stroke in small laboratory animals is developed and advanced for chronic neurobiological studies of normal and pathological higher nervous activity as well as disorders developed after acute hemorrhages. A device is advanced which allows a researcher to destroy appropriate brain structures (tissues and local blood vessels) with necessary precision by four-six rotations of curved stereotaxically inserted mandrel-wire knife and, subsequently, to inject autoblood into the area of the lesion. The advanced model is convenient for the reproduction of lesions in different brain regions (for the purpose of experimental knockouts) in neurophysiological, neuropharmacological, and clinical investigations.
Quantitative analysis of synapses in layer I of the sensorimotor cortex in rats with low resistance to hypoxia revealed pronounced changes in the number of synaptic vesicles docked at the presynaptic membrane in active synaptic zones under conditions of acute hypobaric hypoxia. In high-resistant animals the number of, docked synaptic vesicles under these conditions remained unchanged. In was hypothesized that high sensitivity to hypoxia in low-resistant rats is determined by high reactivity of the synaptic transmission system.
The method of stopped flow was used to follow the changes in light scattering by the vesicles of plasmalemma and tonoplast isolated from maize (Zea maysL.) roots and treated by osmotic pressure. In both membrane preparations, the rate of the process depended on the osmotic gradient and was described with the simple exponential function. The rate constants derived from these functions were the following: the coefficient of water permeability in the tonoplast (P= 165 ± 7 μm/s) exceeded by an order of magnitude the corresponding index for plasmalemma (11 ± 2 μm/s). The presence of HgCl2(1.6 nmol/μg membrane protein) decreased the tonoplast water permeability by 80%. Microviscosity studies of the hydrocarbon zone in the isolated membranes by using a fluorescent diphenylhexatriene probe demonstrated that the two membranes do not differ in the phase state of their lipid bilayer. The authors conclude that the observed difference in water permeability does not depend on the state of the lipid phase and probably reflects the dissimilar functional activity of plasmalemma and tonoplast aquaporins.
Local reversible changes in neuronal dendrites and astroglial cells of layers I and II of the cerebral cortex were observed 1 day after short-term photochemical thrombosis of blood vessels in superficial cortical layers. These changes manifested themselves in swelling of perivascular glia and accumulation of glycogen in the bodies and processes of astroglial cells. Neurons reacted to ischemia by swelling of distal dendrites in the upper third of layer 1 (plexiform layer). The content of astroglial glycogen in the region of neuropil containing varicose dendrite enlargements was several times lower than in regions with intact dendrites, which suggests that varicose locuses had a higher demand for energy substrates.