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Injection of haloperidol (2.5 mg/kg) immediately after elaboration of the passive avoidance conditioned reflex stabilized retrieval of the conditioned reflex on the 2nd, 7th, and 14th days. Catalepsy induced by haloperidol injection was increased after the completion of passive avoidance conditioning. Conditioned reflex retrieval decreased catalepsy which was retrieved without repeated haloperidol injection. In contrast to the control animals, in the animals after conditioning the most pronounced catalepsy was observed immediately after the conditioned reflex retrieval with the following stabilization at the lower level. The auto enhancement of catalepsy retrieval was more expressed on the 14th day (as compared with the 7th day) both in the control and learned animals, but in the latter it did not depend on the testing time (in contrast to the control animals.

Catalepsy induced by a single intraperitoneal injection of haloperidol (2.5 mg/kg) was consolidated and without additional influences and retained within 2 week (being tested on the 2nd, 7th, and 14th days after injection). Enhancement of catalepsy retrieval was observed during testing of the same animals on the 14th day as compared with the 7th day. Maximal catalepsy expression was reached after 2 hours of testing procedure which points to the existence of the mechanism of autoenhancement of retrieval which is probably underlain by the automodulation of the long-lasting modulatory DA receptors. The retrieval of catalepsy is suggested to be induced by a situational conditioned stimulus, since on the 2nd, 7th and 14th days it may be reproduced without repeated haloperidol injection only in the testing box.

It was shown that active noradrenaline-14C (NA) uptake by the rat brain synaptosomes is inhibited by ouabain (0.1 M) and K-depolarization. Acquisition of the defensive conditioned reflex leads to inhibition of active NA uptake by the synaptosomes. This effect may be connected both with changes in the presynaptic membrane state and possible enhancement of the postsynaptic adrenoreceptor function.

A mathematical model quantitatively describing the value of secreted mediator per each successive impulse in the series of presynaptic impulses is presented. The model is plotted with the account taken of the role of presynaptic adrenoreceptors regulating noradrenaline secretion. It has been shown that a decrease observed in neurophysiological experiments and further stabilization of postsynaptic responses in the series of presynaptic impulses of given frequency are not connected with a decreased content of noradrenaline in nerve endings, but may be connected with the work of presynaptic alpha and beta adrenoreceptors.

The process of noradrenaline secretion regulation by autoreceptors is described in the terms of the stationary-kinetic reaction. Constants of this reaction are determined using the authors' own data. Analysis of the model has permitted explaining some data from literature which were used to refute the principle of noradrenaline secretion self-regulation by autoreceptors.

A mathematical model is presented which quantitatively describes the value of secreted mediator and its dependence on the activity of autoadrenoreceptors in the series of presynaptic impulses. Suggestion that the first impulse in the series is the smallest and comes into the zone of sensitivity of presynaptic beta-adrenoreceptor in the model used facilitates the adrenergic synaptic transmission in the series of presynaptic impulsation experimentally described in synapses of vas deference. Conditions determining the synaptic depression and reduction in adrenergic transmission are analysed.

Purified tetanus toxin (TT) (80-800 Dlm/mg protein) releases both endogenous and exogenous (14)C-norepinephrine from the isolated nerve endings (synaptosomes) of the rat brain. Within the investigated range of concentrations TT does not suppress norepinephrine release induced by different ways of depolarizing the synaptosomes in vitro.

The influence of learning local protein synthesis was studied in the rat hippocampal synaptosomes. It is found that elaboration of two-way avoidance conditioned reflex causes a decrease in ability of hippocampal synaptosomes to include H3-leucin into proteins in experiments in vitro. It is suggested that cyclic adenosin 3'5'-monophosphate plays a definite role in controlling protein synthesis in the nerve endings during different influences including learning because its addition to the incubation medium activates sharply this process.

A procedure has been suggested for simultaneous recording of 14C-noradrenaline active uptake and induced secretion by rat brain synaptosomes. Active noradrenaline uptake was shown to depend on the presence in the incubation medium of Ca2+. Removal of Ca2+ from the incubation medium considerably reduces the intensity of noradrenaline uptake by the synaptosomes. Unlike the induced secretion in potassium depolarization of synaptosomal membranes, spontaneous release of noradrenaline does not depend on the presence of Ca2+ in the incubation medium.

A hypothesis of the role of autoadrenoreceptors in the processes of synaptic depression, facilitation, PSP amplitude stabilization and amplitude increase with the stimulation frequency growth is described by means of a mathematical model. Synaptic depression is realized by activation of alpha-autoadrenoreceptors, synaptic facilitation--by beta-autoadrenoreceptors activation. A "stable secretion zone" is formed between the autoadrenoreceptor activation curves at which noradrenaline secretion is stabilized. Experimental studies of H3-NA secretion from rats cerebral cortex slices showed that autoadrenoreceptors really form a stable secretion zone. The presence of stable secretion zone provides for self-facilitation and stabilization of H3-NA secretion elicited by 5-fold consecutive K+-depolarizations of slices with time interval 30 min. The absence of the stable secretion zone leads to destabilization of H3-NA secretion. With an increase of the stimulation intensity the curves of autoadrenoreceptors activity and stable secretion zone shift toward high noradrenaline concentrations.

A mathematical model is presented which quantitatively describes the value of secreted mediator to each subsequent impulse in the series of presynaptic impulses. The model is constructed with the account taken of the role of presynaptic adrenoreceptors regulating noradrenaline secretion. An analysis of the model shows that the observed decrease and further stabilization of presynaptic responses in the series of presynaptic impulses observed in neurophysiological experiments can be connected with the work of alpha- and beta-autoadrenoreceptors. The increase of impulsation frequency affects the sensitivity of these receptors, which brings about an increase of concentration of secreted to each subsequent impulse mediator in the synaptic slit in the series of presynaptic impulses and stabilization of secretion at a higher level.

Prenatal influence of ethanol doesn't induce the changes of 3H-NA secretion intensity from rat cerebral cortex slices, but induces an increase of coefficient of variation of 3H-NA secretion intensity. The self-facilitation and stabilization of secretion are described during study of 3H-NA secretion intensity in the series of successive depolarization of control animals slices. Prenatal influence of ethanol induces self-facilitation but destabilize 3H-NA secretion. The results show that prenatal influence of ethanol breaks of autoreceptors function which are a cause of 3H-NA secretion destabilization. The break of the higher nervous activity is followed by the break of regulation mechanisms of adrenergic transmission effectiveness which is induced by prenatal influence of ethanol.