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Behavioral and neurochemical reactions of small laboratory animals (mice and rats of different age) under exposure to ultralow-intensity electromagnetic fields (EMF, frequency of 4200 and 970 MHz, modulated by a quasistochastic signal in the range of 20-20,000 Hz, power density 15 microW/cm2, specific body absorption rate up to 4.5 mJ/kg) were studied. The EMF basically inhibited the locomotor and exploratory activity in the "open-field" test. The species- and age-specific features rather than radiation conditions dominated. However, decrease in the EMF frequency considerably intensified the observed effect. Change in animal behavior was accompanied by shifts in neurochemical processes, i.e., sharp activation of serotoninergic and inhibition of morepinephrinergic system.

Rats were divided in two groups by the reaction of emotional resonance (RER): with emotionally positive reactions (I, with fast RER acquisition, up to 100 s) and with emotionally negative reactions (II, with slow RER acquisition, more than 200 s). After the RER acquisition, the activity of 5-hydroxitryptophan (5-HT) system of the I group of animals was lower than in the II group. The activity of noradrenaline (NA) and dopamine (DA) systems of the I group of animals was higher than in the II group. The between-group differences were enhanced by subcutaneous injection of dalargin. In some brain structures dalargin reversed these relations. These findings point to a complicated interpenetrating character of emotionally positive and emotionally negative states. Emotionally positive states include components of emotionally positive states, and emotionally negative states include components of emotionally positive states. Increase in 5-HT activity and decrease in activity of NA, DA, and opioid (OP) systems induce formation of emotionally negative states. Decrease in 5-HT activity and increase in activity of NA, DA, and OP systems induce formation of the emotionally positive state. It is suggested that 5-HT, NA, and DA systems play the central role in the processes of reinforcement, acquire the evaluative function, and are included in realization of all types of behaviors. OP is a primary modulator system which accompanies the unconditioned pain stimulus and connects it with systems of evaluative function.

In rat brain cortex, haloperidol initiates the long-term potentiation of K(+)-induced Ca(2+)-dependent noradrenaline (NA) and dopamine (DA) secretion in vitro and in vivo. In both cases, the long-term potentiation is caused by the long-term increase in catecholamine content in the NA and DA terminals, as it has been shown in cortical tangential slices. Acute intraperitoneal haloperidol injection (2.5 mg/kg) evokes catalepsy and increases the content of NA and DA in the brain structures with localization of catecholamine receptors on terminals. This increase appears to be caused, predominantly, by modification of the terminal DA receptors, since only a trend to catecholamine increase is observed in the brain structures with a mixed type of NA and DA receptor localization (on somata and terminals). It is suggested that the long-term and diffuse action of haloperidol after its acute administration consists in the anxiogenic reaction and consolidation of catalepsy without an additional procedure of training and in the absence of unconditioned stimulus.

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.

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 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 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.

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.

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.