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In the crystal structure of the title compound, C 23 H 19 N 5 O 3 ·0.58C 2 H 6 OS·0.42C 2 H 3 N, prepared by the azo coupling of the 4-nitro-phenyl-diazo-nium salt with 3a-( p -tol-yl)-2,3,3a,4-tetra-hydro-1 H -benzo[ d ]pyrrolo-[1,2- a ]imidazol-1-one, the azo mol-ecules are linked by N-H⋯O hydrogen bonds into chains along the a -axis direction, and by the π-π inter-action into [101] chains. The dimethyl sulfoxide and aceto-nitrile solvent mol-ecules occupy the same positions, with populations of 0.585 (3) and 0.415 (3), respectively. These mol-ecules take part in C-H⋯O(N) and C-H⋯π contacts. The energy of the π-π inter-actions was estimated using DFT calculations. The Hirshfeld mol-ecular surface analysis revealed the positions of the most important inter-molecular contacts, such as hydrogen bonds and π-π inter-actions.

The neuronal threshold, which can be determined by the level of depolarization immediately prior to spike generation, is different for responses to conditioned and discriminated stimuli after conditioning. However, it is impossible to determine excitability within a response to stimuli that failed to generate a spike. In the present study we examined the role of the AP threshold of two related Helix defensive neurons in the initiation of an AP during elaboration of the neuronal analog of a classical conditional reflex. These neurons fire in a synchronous manner though spikes sometimes are not generated simultaneously. We compared the change in spike threshold within the responses with other parameters of intracellular activity that also affect the neuronal response, but which can be measured without an analysis of the spike waveform (spike latency, slope of excitatory postsynaptic potentials, etc.). We found that the change in slope is not the reason for the change in the threshold during pairing. The thresholds within conditioned and discriminated responses affected spike generation and their values correlated with the spike presence or absence in related neurons. The excitability changed transiently within the responses, since these alterations were selective for the conditioned and discriminated stimuli and applied primarily to the first spike of the response. The firing threshold seems to be a dynamic property of excitable membrane. Neurons appear to evaluate the significance of the input signal, transiently change their own excitability and only after that compare the magnitude of this signal and threshold.

This work describes the change in an active electrogenesis of the command neurons responsible for defensive closure of a snail's pneumostome during elaborating, extinction and restoration of a classical conditioned defensive reflex to a tactile stimulus. Tactile stimulations applied to different parts of a snail's body served as a differential stimulus. As the biological value of a conditioned stimulus increases due to learning, the excitability of command neurons in response to conditioned stimulus rises. At the same time the neurons demonstrated a reduced excitability in response to a differentiating stimulus.

A change in the active electrogenesis of command neurons of the defensive closing of the spiracle of the edible snail during the development, extinction, and repeat development of a classical conditioned defense reflex in response to tactile stimulation is described in this study; the tactile stimulation of another point of the body served as the differential stimulus. As the biological significance of the conditional stimulus increased as the result of training, the excitability of the command neurons in response to this stimulus increased. At the same time, the neurons manifested reduced excitability in response to the differential stimulus. The possible mechanisms of the rapid reorganization of the excitability of the neurons and the functional significance of the change in the generation threshold of the AP are discussed.

In the paper changes of active electrogenesis of the command neurones of defensive closure of snail pneumostome at elaboration, extinction and repeated elaboration of classic conditioned defensive reflex to tactile stimulus was described; the tactile stimulation of other point of the body served as a differentiating stimulus. During the increase of biological significance of conditioned stimulus as a result of learning the stimulation of the command neurones in response to this stimulus was raised. At the same time the neurones showed decreased excitability in response to differentiating stimulus. Possible mechanisms of quick reconstruction of neurones excitability and functional value of PA generation threshold changes were discussed.

The cholestasis and pancreatitis model was studied experimentally in 144 white rats. The influence of intraperitoneal injections of dalargin on the level of lipid peroxidation and on xanthine oxidase activity of the liver tissues in periods of 1, 3 and 5 hours was investigated. During that period the activity of hepato-specific enzymes in the liver tissues and serum were investigated. The reduction of xanthine oxidase activity in all the periods after injection of dalargin was discovered, the level of malonic dialdehyde was reduced by 43.8% 3 hours later. Simultaneously, the increase of the level of histidase in liver tissues was discovered (on 104.3% and 56.3% after 3 and 5 hours accordingly) and later the tendency to decrease the activity in serum was observed.

Experiments were conducted on 182 rats with acute cholestasis to study the effect of intra-abdominal dalargin injection (10 mcg/kg) with the serotonin antagonist ketanserine (150 mg/kg) on xanthine oxidase (XO) activity and level of lipid peroxidation in the hepatic tissue and on the activity of the hepatospecific enzymes histidase and urokaninase in hepatic tissue and blood serum 1, 3, and 5 hours after the injection. Dalargin reduced XO activity by 32-37% in different periods after the injection, dalargin in combination with ketanserine--by 37-48%. Dalargin reduced the level of lipid peroxidation by 29-35%, and when combined with ketanserine--by 37-49%. The administration of dalargin reveals a distinct tendency towards reduction of the release of the hepatospecific enzymes histidase and urokanase into the blood and increase of their activity in the hepatic tissue. Dalargin with ketanserine produces a similar effect but of a higher degree. These data allow us to speak of the hepatoprotective effect of dalargin, which is potentiated by its injection together with ketanserine. It was found that dalargin (50 mcg/kg, intraperitoneally) increases the leu-enkephalin content in the hepatic tissue more than 3.5 fold one hour after injection.

Results obtained from the study of mechanisms of hepatoprotective effect of transcranial transcutaneous electrostimulation are cited (TTES). In experiments on cholestase and pancreatitis models in rats we studied hepatospecific enzymes i.e. histidase and urokininanse in blood and liver and membrane-linked enzyme 5'-nucleotidase in the liver tissue. We made three series of experiments: 1 - TTES + valium, 2 - synthetis hexapeptide (SH) - leuenkephaline analog; 3 - TTES + valium + SH. Results obtained from experiments showed that mechanisms of TTES hepatoprotective action are in part conditioned by endogenous opiopeptides mobilization which produced membranestabilizing effect on the hepatocyte. We concluded that in patients with hepatic pathology it was reasonable to combine the electroanesthesia with SH.