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Aim: To study an effect of corticosterone (100 nM) on spontaneous inhibitory postsynaptic currents (sIPSC) in pyramidal neurons of CA1 area and a role of inhibitory CB1-expressing synapses in the development of corticosterone-induced effects., Material and Methods: The experiments were performed on acute slices of the rat ventral hippocampus using whole-cell configuration of the patch-clamp technique., Results and Conclusion: The addition of corticosterone resulted in a small, but significant, increase in the frequency of sIPSCs during the first 10 minutes and then this parameter returned to the basal level. Corticosterone treatment resulted in a considerable decrease in the sIPSC amplitude 40 minutes after the beginning of treatment. The activation of CB1 receptors weakly affected sIPSC characteristics, however, the addition of corticosterone did not induce the rapid elevation in the sIPSC frequency, which occurred on the 10th minute in the control, as well as a decrease in the sIPSC amplitude, which was observed in the control on the 40th min after the beginning of corticosterone treatment. The data obtained suggest that both rapid and slow effects of corticosterone are associated with the activity of CB1-expressing inhibitory synapses of the hippocampus.

The aim of the work was the analysis of the changes in a number of labile synaptopodin-positi- ve dendritic spines in parietal cortex and the CA1 field of the hippocampus, which characterize plasticity of intracellular interaction, and of the memorization after short-term repeated immobili- zation stress (daily for 5 minutes, 10 days), both in control rats and in rats subjected to prenatal hypoxia (E14, 7% of O2, 3 hours). There were observed deterioration of short-term and long-term memory, decrease in number labile spines in the CA1 field of the hippocampus (for 17.3 ± 10.4%; p ≤ 0.05) and their increase in a molecular layer of brain parietal cortex (for 36.9 ± 9.2%) at the adult rats with normal embryogenesis after immobilization stress in comparison with control intact animals. At the rats subjected to a prenatal hypoxia, regardless of that, they were ex- posed to an immobilized stress at an adult stage or not, was noted both violation of short-term and long-term memory, and decrease in number labile spines in the CA1 field of the hippocampus (for 22.9 ± 10.5%) and parietal cortex (for 28.1 ± 9.3%). The obtained data allow to conclude that the increase of plasticity providing adaptive behavior of animals, takes place in neocortical neuronal networks as a reply to a short-term repeating stress only at normal brain formation during embryo- genesis, while, violation of embryogenesis leads to decrease in plasticity and adaptive opportuni- ties of the nervous system during further ontogenesis.

Gluco- and mineralocorticoid receptors are believed to play important roles in mechanisms of the hypothalamic-pituitary-adrenal axis (HPA) regulation, neuronal death/survival, as well as learning and memory processes. Imbalanced levels of MR and GR result in impairment of HPA activity and can promote neuronal injury and loss following exposures to extreme factors. In the present study, using quantitative immunohistochemistry, the comparative analysis of the effects of hypobaric hypoxia in several modes on expression profiles of GR and MR in dorsal (CA1) and ventral (dentate gyrus) hippocampus was performed. According to the data obtained, severe injurious hypoxia induced prominent disturbances of GR and MR expression in the cells of CA1 and dentate gyrus that correlated to the remarkable neuronal injury/loss in CA1 and dysregulated HPA activity. Sets of three- or six-trial (but not one-trial) preconditioning using mild hypoxia prior to severe hypoxia prevented these abnormalities.

The aim of the study was to evaluate, by using immunohistochemistry (demonstration of Iba-1 protein), the morphological features of the rat hippocampal microglia and to describe its cellular types during the response to a single total brain ischemia of 12 min duration. The results obtained suggest the existence of several morphologic types of microgliocytes in the intact hippocampus, while some more types appear in response to ischemic lesion of neurons. These changes in general population of the hippocampal microgliocytes is related to their functional activation. During the post-ischemic period (3, 7 and 14 days following the challenge), there appeared multiple micro-outgrowths of the microglial cell processes, which suggests the enhancement of their interaction with surrounding cellular elements and may be the manifestation of the process of the elimination of neuropil lesioned synaptic structures.

The aim of this study was to determine the effect of ischemic postconditioning on hippocampal CA1 neuronal survival and cytoplasmic activity of lactate dehydrogenase (LDH) in the gerbil model of cerebral ischemia-reperfusion injury. Ischemia was induced by bilateral common carotid artery occlusion (for 7 min) in male Mongolian gerbils (Meriones unguiculatus). Ischemic postconditioning protocol comprised 3 cycles of 15 s reperfusion/15 s ischemia. After 48 h of reperfusion, CA1 neuronal death was detected by Nissl staining and the cytoplasmic LDH was demonstrated histochemically in CA1 area of the hippocampus with a quantitative cytophotometric assessment of the enzyme activity. The results have shown that 7 min ischemia resulted in a significant decrease in the number of viable neurons (up to 24%) in the CA1 area of hippocampus; in addition, it reduced the activity of LDH in these neurons (from 0.260 +/- 0.009 to 0.190 +/- 0.006 relative units). The application of ischemic postconditioning significantly increased the number of viable neurons (up to 52.9%, P < 0.01) in the CA1 area of hippocampus, and it was accompanied by an increase in the activity of LDH (0.240 +/- 0.008 relative units, P < 0.001).

Application of choline (5 and 10 mM) to electrically stimulated (1 Hz) rat hippocampal slices evoked epileptoid activity manifested by generation of extra population spikes. Application of methyllycaconitine (10 nM), a specific agonist for α7-subunit of nicotinic acetylcholine receptors, did not prevent generation of extra population spikes. In contrast, pretreatment of slices with Mg(2+) (5 mM) or blockade of NMDA-type glutamate receptors with MK-801 (100 μM) prevented generation of the extra population spikes. It was hypothesized that elevation of choline concentration during cerebral pathology can promote activation of NMDA-receptors and provoke epileptoid activity not related to activation of α7-subunit of nicotinic acetylcholine receptor.

The study has shown that influence of acute hypoxia in perinatal period leads to structural changes in motor and visual of the neocortex for 20 postnatal days in the form of disturbance of the structural organisation of the neocortex layers. Different fields of hippocampus in perinatal period differently react to hypoxia, and evidence of existence of a long-term perinatal hypoxia was obtained. It is established that after action of acute hypoxia in all the fields there is a cellular destruction, and thinning of pyramidal neurones layers. The most expressed cellular destruction takes place in fields CA4 and CA3. In process of augmentation, the destruction of cells remains appreciable in the field CA4, reduced in the field CA3 and not found in the field CA1; however, in fascia dentate, the destruction of granular neurones with age augmentation increases. Along with in reduction of the dimensions of cellular bodies pyramidal neurones in all fields of hippocampus takes place. Also in all fields of hippocampus, activation of astrocytic reaction occurs, more expressed in the field CA4. The hypoxia influence in the early postnatal period can affect synaptogenes, particularly the formation of giant synapses in a dentate fascia. Study of functional features of the excitatory system of such animals has shown that hypoxia can induce appreciable disturbances of behavioural responses. In rats, disturbances of inhibiting functions of the cerebral cortex, raised anxiety, and spatial learning and working memory disturbances have been noted.

A comparative study of the nervous tissue and distribution of the spine apparatus protein synaptopodin was performed in all layers of the brain sensorymotor cortex and hippocampal CA1 area in control rats and in the rats submitted to hypoxia at E14 and E18. It was found that beginning from the 20th day of postnatal development, in rats submitted to hypoxia both at E14 and E18 there was observed a statistically significant decrease of the mean number of labile synaptopodin-positive spines in the stratum radiatum molecular of the hippocampus area CA1. The decrease of the number of labile spines in the sensorymotor brain cortex was revealed only in the I layer beginning from the 20th day after birth in the rats submitted to hypoxia at E14. Maximal differences in the studied brain areas were observed in adult rats (exposed to hypoxia at E14: in the neocortex--a decrease by 23 +/- 10%, in hippocampus--by 24 +/- 8%, respectively). In adult animals, the increased degeneration of neuzons was not detected. It is suggested that disturbances in cognitive functions and in the capability for learning observed in rats after prenatal hypoxia can be due to a decrease of the amount of the labile synaptopodin-positive spines, which leads to a change of the structural-functional properties of neuronal networks and to a decrease of their plasticity.