PARTICULARITIES ASSOCIATED WITH THE EXPRESSION OF GLIAL ACIDIC FIBRILLARY PROTEIN ON THE STRUCTURAL COMPONENTS OF CEREBELLUM OF THE RATS INFLUENCED BY THE FOOD ADDITIVES COMPLEX

The aim: To define the degree for glial acidic fibrillary protein expression on the structural components of cerebellum of the rats in health and when rats influenced by the food additives complex. Materials and methods: In order to determine the degree of expression of the immunohistochemical marker GFAP on the structural components of the cerebellum of rats we applied immunohistochemical, morphometric and statistical methods in our study. Results: In histological specimens at the end of 1st week of observation in the gray matter of the cerebellum there occurred a gradual increase in 1.16 times of the average number of GFAP-positive cells. At the end of 4th week of the experimental study, the average number of GFAP-positive cells increased accurately (at p<0.05 compared to the control group) in 1.27 times, at the end of 8th week it has increased in 1.99 times, at the end of 12th week in 2.25, and at the end of 16th week in 2.39 times. Conclusions: The outcomes of our study are as follows the increase in the average number of GFAP-positive cells is directly related to the decrease in the average number of major neurons of the gray matter of the brain, while the fluctuations in the average number of astrocytic glia cells represent a compensatory mechanism in the recovery of gray matter neurons of the brain from neural stem cells with the subsequent development of reactive astrogliosis and, thereafter the possible development of neuropathology.

Cerebral microangiopathy (disease of small blood vessels) and age-related hypogonadism in men

The review discusses the contribution of age-related male hypogonadism to the formation of cerebral microangiopathy (disease of small brain vessels) (CMA/SVD). The current explanation of the nature of CMA by an ischemic-hypoxic process, which is based on hypo- or hyperperfusion of the white matter of brain due to a complex of various causes, does not explain the etiopathogenesis of CMA. The article considers a violation of the neuroglyovascular connection, represented by a vessel, astrocytic glia, and a neuron, as the cause of SVD development. The main role in the CMA formation is assigned to endothelial dysfunction, all variants of which (vasomotor, thrombophilic, adhesive, angiogenic) can be traced in SVD. The role of disorders of the main functions of arterial vessels — conducting and damping, as well as liquorodynamics disorders in the CMA pathogenesis is discussed. The data indicating the involvement of testosterone and its derivatives in the formation of cerebral vascular pathology are presented. It is emphasized that this participation can be of one kind in men with early physiological uncomplicated hypogonadism, when the hypothalamic-pituitary system is involved in the process, and of another kind in complicated or late climax. At that, an increase in the production of gonadotropin — releasing hormone (GnRH), the content of FSH and LH in peripheral blood is considered as a reaction to an age-related decrease in androgen function, and the vegetative dysfunction, metabolic and other disorders inherent in this period of life – as a result of changes in the functioning of the entire hypothalamus-pituitary-testicular axis. In complicated age-related hypogonadism, the resulting endocrine or somatic pathology is included in the process of small vessel disease formation. In late hypogonadism, the androgen function fades, and the hypothalamic-pituitary system begins to function in a different mode. Often, the clinic and mechanism of CMA formation are determined by diseases inherent in old age. The differences in the pathogenetic mechanisms of CMA development at various periods of IgG determine the need for a differentiated approach to the preventive means and methods of CMA therapy in men of the involutional period. The presented information may be useful for better understanding of CMA development in individuals with age-related hypogonadism.

Cellular correlates of proneural and notch-delta gene expression in the regenerating zebrafish retina

Fish can regenerate retinal neurons following ocular injury. Evidence is mounting that astrocytic glia function as inducible, regenerative stem cells in this process, but the underlying molecular events that enable neuronal regeneration are comparatively unclear. In the current study gene array, quantitative real-time PCR, in situ hybridization, and immunohistochemical approaches were used to identify, in the damaged retina of adult zebrafish, correlations between transcriptional events and entry into the cell cycle by Müller cells, a type of astrocytic cell present in all vertebrate retinas that is a candidate ‘stem cell’ of regenerated neurons. A proneural gene (achaete-scute homolog 1a, ash1a) and neurogenic components of the Notch signaling pathway, including notch3 and deltaA, were implicated. An injury-induced, enhanced expression of ash1a was observed in Müller cells, which is hypothesized to contribute to the transition of these cells, or their cellular progeny, into a notch3-expressing, regenerative progenitor. A model of vertebrate retinal repair is suggested in which damage-induced expression of proneural genes, plus canonical Notch-Delta signaling, could contribute to retinal stem cell promotion and subsequent regenerative neurogenesis.

D-Serine as a putative glial neurotransmitter

Abundant recent evidence favors a neurotransmitter/neuromodulator role for D-serine. D-serine is synthesized from L-serine by serine racemase in astrocytic glia that ensheath synapses, especially in regions of the brain that are enriched in NMDA-glutamate receptors. D-serine is more potent than glycine at activating the ‘glycine’ site of these receptors. Moreover, selective degradation of D-serine but not glycine by D-amino acid oxidase markedly reduces NMDA neurotransmission. D-serine appears to be released physiologically in response to activation by glutamate of AMPA-glutamate receptors on D-serine-containing glia. This causes glutamate-receptor-interacting protein, which binds serine racemase, to stimulate enzyme activity and D-serine release. Thus, glutamate triggers the release of D-serine so that the two amino acids can act together on postsynaptic NMDA receptors. D-serine also plays a role in neural development, being released from Bergmann glia to chemokinetically enhance the migration of granule cell cerebellar neurons from the external to the internal granular layer.

Differences in attachment between herpes simplex type 1 and type 2 viruses to neurons and glial cells

Fractions of nerve cell perikarya, synaptosomes, and astrocytic glia were prepared from human, monkey , rabbit, rat, and mouse brain tissue. The herpes simplex virus type 1 (HSV-1) and type 2 (HSV-2) binding capacity of these fractions was studied. Pretreatment of fractions with one type of HSV and the subsequent testing of adsorption of homotypic and heterotypic virus ws employed to reveal type selectivity of virus binding receptors. A higher density of HSV-1 than of HSV-2 selective receptors was found on synaptosomes and glial cells, except with mouse-derived preparations. Synaptosomal and glial cell preparations of mouse brains adsorbed both types of HSV well. Little or no adsorption was observed with HSV-1 and HSV-2 to neuronal perikarya. The type selectivity of HSV binding receptors on brain cells ws demonstrated on preparations of human synaptosomes and mouse glial cells. Some possible implications of the observations on the HSV infection of the nervous system are discussed.