A. A. Mokrushin

Heat Shock Protein HSP70 Increases the Resistance of Cortical Cells to Glutamate Excitotoxicity

Preincubation of cultured slices of the olfactory cortex of rat brain with heat shock protein in a concentration of 1 µg/ml protected the pre- and postsynaptic mechanisms of glutamatergic synaptic transmission from glutamate excitotoxicity (50 mM) inducing blockade of excitatory postsynaptic function and reducing presynaptic processes. It was hypothesized that heat shock protein protects AMPA and NMDA receptor-mediated processes.

Analysis of Perfusates Collected from Surviving Rat Brain Olfactory Cortex Slices

Tetanization of the lateral olfactory tract fibres results in development of the long-term potentiation (LTP) in piriform cortex in vitro (1,2,3). Mechanisms of the transformation of short-term processes of excitability in the nervous system (e.g., generation of action potential, synaptic events) into long-lasting ones like LTP are unclear. Release of some endogenous substances and their retrograde actions may be a possible mechanism of this transformation.

Effects of long-term exposure of nerve cells to autoblood in in vitro model of hemorrhagic stroke

Changes in bioelectrical activity of nerve cells after their long-term exposure to autoblood were studied in vitro on cultured brain slices. This model simulated the events characteristic of a hemorrhagic stroke. Brain slice was placed into a glass vial with autoblood for 60–420 min, after which the slice was transferred into a perfusion chamber and after washing from autoblood their focal potentials were recorded. The level and reversibility of disorders in nerve cell activity were detected by comparing the parameters of focal potentials with the control values. Delayed effects of autoblood were detected, manifesting in the progress in disorders of nerve cell activity with prolongation of exposure in the blood, and the period after which they could be restored was determined.

Electrophysiological characteristics of depressive states in rats with passive strategies of adaptive behavior

The behavior of rats in a T-maze was used to select individuals with a passive strategy of adaptive behavior from a population of Wistar rats. These animals were subjected to water immersion and olfactory cortex slices were prepared from the brain 10 days later and used for recording of evoked focal potentials and the effects of tetanic stimulation. Postsynaptic potentials, of both the AMPA and NMDA types, were initially of decreased amplitude in passive rats. After unavoidable stress, the suppression of excitatory potentials increased and there was a simultaneous increase in the amplitude of inhibitory GABAB-ergic mechanisms. Addition of corticoliberin (10−10 M) to the incubation medium led to reversible blockade of synaptic transmission. Tetanic stimulation of slices from stressed rats led to the development of posttetanic depression in 84% of cases and to post-tetanic potentiation in 12%; this is evidence for profound changes in synaptic transmission. Thus, activation of corticoliberinergic mechanisms in cortical structures does not promote recovery from depressive states in rats with the passive behavioral strategy induced by unavoidable stress.

Neurotropic effect of exogenous L-carnosine in cultured slices of the olfactory cortex from rat brain

Incubation of cultured slices of the olfactory cortex from rat brain with L-carnosine in concentrations of 50, 250, and 500 µM induced activation of glutamatergic and GABAB-ergic mechanisms and facilitated long-term posttetanic potentiation. The effect of L-carnosine is mediated by its effect on AMPA-and NMDA-related glutamatergic receptors and on inhibitory GABAB receptors.

Effects of Deep Cooling and Re-Warming on Ionotropic Glutamatergic Receptors In Vitro

We studied the effects of cooling to -10°C and re-warming to 37°C on slices of rat olfactory cortex. The amplitudes of action potential in the lateral olfactory tract and excitatory postsynaptic potential activated by AMPA recovered during slow cooling/re-warming (0.1°C/min), while during rapid cooling/re-warming (9°C/min), they surpassed the control values. NMDA receptor-dependent mechanism was blocked in both cooling/re-warming modes. Swelling of the brain slices was observed during re-warming, especially during rapid cooling/re-warming. Nerve fibers of the lateral olfactory tract and AMPA-related processes survived deep cooling/re-warming, while NMDA-related processes were irreversibly blocked.

Effects of Corticoliberin on Synaptic Transmission in Rat Olfactory Cortex Slices in a Water Immersion Model of Depression

Corticoliberin (corticotrophin-releasing factor, CRF, CRH) is an active regulator of endocrine, autonomic, and immune functions in stress, as well as a mediator of anxiety, determining the behavioral stress response. The present report describes studies of its action on neuron activity evoked by microstimulation of olfactory cortex slices. Behavioral testing in a T maze was used to select individuals with a passive behavioral strategy from a population of Wistar rats, and the animals were subjected to water immersion. Olfactory cortex slices were prepared 10 days later and evoked focal potentials were recorded on perfusion with medium containing corticoliberin (0.1 μM). Among active rats, 60% of slices retained high excitability after stress, and corticoliberin produced only insignificant reductions in the amplitudes of excitatory potentials in these slices, simultaneously increasing the amplitudes of inhibitory potentials. Low excitability was found in 40% of slices from active stressed rats, and corticoliberin had a significant inhibitory effect in these slices. Addition of corticoliberin to the incubation medium used for slices from passive rats with initially low excitability led to complete blockade of synaptic transmission. These data support the involvement of corticoliberin in the development of depression.

Effects of Exogenous Application of Corticotropin- Releasing Hormone to Slices of the Olfactory Cortex from Rats with an Active Strategy of Adaptive Behavior on the Water-Immersion Model of Depression

Experiments were performed on male Wistar rats. The specimens with an active strategy of behavior were exposed to unavoidable water-immersion stress. Surviving slices of the olfactory cortex were obtained 10 days after stress. The neurohormone had a strong inhibitory effect in 40% slices from active rats. The activity of glutamate receptors decreased, while the function of GABA receptors increased in 60% slices. Our results indicate that the depressive state of behaviorally active animals due to exposure to unavoidable stress is not necessarily mediated by the corticoliberinergic mechanisms in cortical structures.