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EN
A distribution of dendrites was studied in mouse barrel field after a neonatal partial lession of vibrissal follicles using anti-MAP-2 immunohistochemistry.The effect of a neonatal vibrissal follicles removal was studied in adult mice: barrels correspodning to intact follicles were enlarged whereas those representing removed follicles had not developed.MAP-2 immunopositive profiles were considered to be dendritic clusters and their packing density (a number per unit area) was calculated in an enlarged barrel and compared to a control barrel in a contralatral hamisphere.A decrease in the packing density of large dendritic clusters, presumably arising from layer V, was observed in an enlarged barrel in comparison to its control counterpart.This result may indicate a selective neonatal lesion of vibrissal follicles.
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Glutamate is the predominant excitatory neurotransmitter in the central nervous system (CNS) and glutamatergic transmission is critical for controlling neuronal activity. Glutamate is stored in synaptic vesicles and released upon stimulation. The homeostasis of glutamatergic system is maintained by a set of transporters present in plasma membrane and in the membrane of synaptic vesicles. The family of vesicular glutamate transporters in mammals is comprised of three highly homologous proteins: VGLUT1-3. The expression of particular VGLUTs is largely complementary with limited overlap and so far they are most specific markers for neurons that use glutamate as neurotransmitter. VGLUTs are regulated developmentally and determine functionally distinct populations of glutamatergic neurons. Controlling the activity of these proteins could potentially modulate the efficiency of excitatory neurotransmission. This review summarizes the recent knowledge concerning molecular and functional characteristic of vesicular glutamate transporters, their development, contribution to synaptic plasticity and their involvement in pathology of the nervous system.
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The effect of focal photothrombotic stroke on the distribution of D1 dopamine receptor (D1R) sites was examined in different cortical areas of rat brain with quantitative receptor autoradiography using [3H]SCH23390 as a ligand. Unilateral cortical stroke was located in the primary somatosensory cortex. After different survival times (1, 7 and 28 days) D1R binding levels were determined in the lesion core, penumbra, frontoparietal motor (FrPaM) and somatosensory (FrPaSS) areas as well as in homotopic regions in the contralateral hemisphere. One day after stroke, D1R density decreased by 36% (P<0.01) in the lesion core relative to sham-operated controls. At 7th day binding density was further reduced by 56% (P<0.002). Twenty-eight days after infarction, D1R binding returned to control level. No alterations in D1R binding levels were found in penumbra and other investigated regions. We suggest that the return of D1R binding to control level in the area initially corresponding to the infarct results from the shrinkage of the lesion volume.
EN
Synapsins are a family of proteins associated with synaptic vesicles that are widely used as markers of synaptic terminals. We decided to investigate synapsin I expression in the mouse primary somatosensory cortex (SI). Immunostaining experiments using a polyclonal antibody against C-terminal domain of synapsin Ia/b (anti-SynI-C) showed an unusual pattern in the SI cortex compared to other regions of the neocortex. The staining delineated the cells located in barrel hollows. The immunoreactive product was located on the perikarya and proximal dendrites of gabaergic neurons found in layer IV and VI of the SI cortex. Other anti-synapsin antibodies did not reveal this pattern within the SI cortex, although in the hippocampus all antibodies examined produced a similar pattern of immunostaining. Deglycosylation of sections resulted in complete loss of immunodecoration on the cell perikarya. We suggest that the anti-SynI-C recognizes a saccharide surface epitope, possibly an element of perineuronal nets that is specific for the primary somatosensory cortex.
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A form of activity dependent, functional plasticity can be induced in the barrel cortex by sensory deprivation without damage to the sensory receptors. Changes of cortical representation of a spared C3 vibrissa, when all other whiskers were plucked out, were mapped with 2-deoxyglucose autoradiography in mice and rats after a short-lasting deprivation. An increase in the volume of cortical column activated by the spared vibrissa was found previously that if deprivation is commenced immediately after birth, yhe changes in cortical representation of the spared whisker appeared in the third week of life. In search of a possible reason for the delayed expression of functional plasticity in neonatal animals we examined the developmental curves of neurotransmitter receptor binding for several transmitters thought to be involved in plstic processes of the cerebral cortex. We found that the beta noradrenergic and miscarinic cholinergic receptor binding increased rapidly at the end of the second postnatal week and subsequently remained high. By contrast, the metabotropic glutamate receptor binding decreased during the first month of postnatal development. The AMPA receptors binding values rose during the first two weeks of life, and then decreased. Together with our previous data on the development of NMDA and GABA receptor and voltage dependent calcium channel binding, the results suggest that slow development of functional plasticity in neonatal animals may be due to low levels of receptors of several neurotransmitters implicated in brain plasticity.
EN
The effects of photothrombotic stroke in primary somatosensory cortex on astroglial and microglial activation in various regions of lesioned brain were examined at different time points, using immunohistochemistry and lectin binding. The increase in GFAP expression was observed exclusively in the ipsilateral hemisphere, both in the perilesional area and cortical regions distant from the infarct. This remote increase was detectable up to sixty days after the infarct. Transient GFAP elevation was also found in the hippocampus one day after photothrombosis, whereas it was more prolonged in amygdala, as demonstrated at four days after lesion. In contrast to a widespread astrocytic activation, the microglial response was shortlasting and local, confined to lesion and perilesional area. Widespread and prolonged activation of astrocytes after stroke may provide factors promoting slowly developing recovery processes in the whole brain, while microglial response seems to be involved in local repair and removal of cellular debris.
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