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Electrocorticograms of vibration induced effects were studied in intact and labyrinthectomized rabbits under midbrain reticular formation and renoreactive structures blockade. There was involvement of the specific (vestibular) and non-specific brain structures in the mechanisms underlying the cortex' electric activity. The article contains a review of the vibration-related shifts in the cortex, both specific and nonspecific--and in other afferent modalities (proprioceptive, somatic, visceral).

The influence of arecoline, amphethamine and aethimizol upon the nature of frequency distribution on the electrogram of the midbrain reticular formation, dorsal hippocampus and the large hemispheres cortex was studied on rabbits undergoing chronic experiments with a unipolar lead of biopotentials. It is shown that, when observed visually, intravenous administration of arecoline (0.025-0.05 mg/kg), amphethamine (1 mg/kg) and aethimizol 3 mg/kg) causes similar changes on the electroencephalogram, i.e. the reaction of activation. However, the frequency analysis of the EEG within the range of 1.5 to 100 Hz showed the influence of each one of the above drugs on the nature of frequency distribution of these structures on the EG to be dissimilar. The unidirectional character distinguishing the effects of arecoline, amphethamine and aethimizol is conditioned by their common system stimulating action on the central nervous system, this manifesting itself in the reactions of activation. On the other hand, the differences in the re-distribution of the EEG frequency characteristics occurring under the influence of each of these drugs are due to the engagement of dissimilar mechanisms of the intracentral regulation in each individual case.

In freely mobile rabbits with electrodes preliminarily implanted in the brain structures ketamine (5 mg/kg intravenously or 20 mg/kg intramuscularly) exhibited properties of GABA receptor agonist decreasing the direct excitability of the mesencephalic reticular formation and periaqueductal gray matter and reducing their activating effect on the frontal cortex (FC) and dorsal region of the hippocamp (DH). GABA-mimetics (muscimol, baclofen, aminooxyacetic acid) as well as GABA system antagonists (bicuculline, thiosemicarbazide) attenuated ketamine action at the level of DH and especially FC.

The effect of systemic administration of agonists and antagonists of GABA system on excitability and intracentral relationships of the brain structures was found during chronic experiments on rabbits with bipolar electrodes implanted in the region of the frontal cortex, dorsal hippocampus, midbrain reticular formation and central gray matter. The changes of the functional state of the cerebral formations were suggested to be related to a different degree of the involvement of GABA receptors of types A and B.

It has been established in experiments on conscious cats that variation in spontaneous activity of the midbrain reticular formation neurones in response to microiontophoretic application of morphine largely coincides with the pattern of changes in impulsation in response to administration of leu-enkephalin rather than to met-enkephalin. Concurrent application of the subthreshold dose of enkephalins and morphine has revealed a possibility of the effects summation, the highest pharmacological activity being exhibited by leu-enkephalin combined with morphine. Selective blocking by enkephalins and morphine has been observed of evoked neuronal responses to peripheral exposures (ECS, stimulation of the sciatic nerve). Meanwhile the responses of cortical origin have been found to remain unchanged.

Under conditions of free behaviour of rabbits with electrodes implanted into the brain structures it was found that ketamine and sodium thiopental decrease the excitability in the dorsal hippocamp, reticular formation and periaqueductal gray matter of the midbrain. Excitability of the frontal neocortex increases during general anesthesia with ketamine and decreases during thiopental narcosis. Changes in excitability of the studied cerebral structures during general anesthesia can be determined by common N-cholinoblocking and alpha-adrenomimetic properties of ketamine and thiopental at the level of the dorsal hippocamp, cholinoblocking and adrenoblocking properties at the level of the reticular formation and central gray matter. In the frontal cortex ketamine presented properties of an M-cholinomimetic and adrenomimetic agent, sodium thiopental--those of a M-cholinoblocker and beta-adrenoblocker.

In a dose of 100 mg/kg and with intravenous administration to rabbits lithium chloride produces a depressing influence on the spontaneous bioelectric activity of the cerebral cortex and its subcortical formations, which extends from the cortex to subcortical structures. The compound brings down the electric excitability of the hippocampus, caudate nucleus, tonsils, reticular formation of the mesensephalic segment and of the thalamus, while in a dose of 300 mg/kg it increases the excitability of the motor cortex. No correlation between the lithium chloride induced electroencephalographic changes in the cerebral structures, on the one hand, and the content therein of biogenic amines and accumulation of lithium ions, on the other, was revealed.

In experiments on rabbits with electrodes chronically implanted in the brain structures thiopental exhibited properties of a pronounced GABA receptor agonist. Muscimol potentiated the suppressive effect of the general anesthetic agent on electrographic and behavioral correlates of excitability of the periaqueductal gray matter, mesencephalic reticular formation and especially dorsal hippocampus and frontal neocortex. On the contrary, bicuculline reduced the anesthetic effect of thiopental but potentiated the inhibitory action of the cortex and hippocampus on the midbrain formations as compared with the effects of the barbiturate proper.

Experiments set upon 32 cats demonstrated that d, l-amphetamine (1-3 mg/kg, intravenously) augmented the number of responding units, modified the structure of the response and the intensity of the reaction from the sensorimotor (somatosensory) cortex neurones following stimulation of the mesencephalic reticular formation. Weakening of phasical and significant intensification of tonic reactions from the lateral hypothalamus was noted, this being attended by a rise of areactive neurones. A single stimulation of the antero-medial hypothalamus evoked inhibitory responses more often than it did in controls. Its rhythmical stimulation was less frequently accompanied by activation which stressed the inhibitory nature of the cortical response. It is suggested that the action of d, l-amphetamine on the cortex depends not only upon mobilization of brain stem reticular formation, but also on the greater reticulo-hypothalamic interaction, as well as on the direct excitation (stimulation) of the hypothalamic centres.

In tests with cats and rabbits sydnocarb in doses of 3,4-8.5-17 mg/kg (per os or intraperitoneally) produces a more lasting reticulo-cortical activation than does amphetamine used in respectively equimolecular amounts. According to the EEG finding there is also observed a substantial difference in the nature of interaction of these stimulants with chlorpromazine, reserpine and imipramine.

Pyrasidol (1,10-trimethylene-8-methyl-1,2,3,4-tetrahydropyrasino/1,2-q/indol hydrochloride) produces an activating influence on the EEG of the brain cortex, the reticular formation of the mesencephalon and hippocampus. It potentiates the electroencephalographic effects of amphetamine, 1-DOPA and 5-oxytryptophan, displays no central cholinolytic activity and has no influence on the electrophysiological effects of anticholinesterase and cholinomimetic agents.

Spontaneous activity of reticular formation neurons responding to the stimulation of pyramidal tract axons and different peripheral conductors is liable to changes during microiontophoretic exposures to acetylcholine, L-glutamate, serotonin and mesaton. The test neurons showed the highest sensitivity to L-glutamate and acetylcholine. 80% of the neurons responded to exposures to several substances. The time course of evoked reactions in the presence of microiontophoresis of biologically active substances is uncertain in character. Different components of evoked responses might react dissimilarly to microiontophoretic application of the substances. 20% of the neurons manifested significant differences as regards the time course of evoked efferent and afferent responses.

Through local stimulation of various structures of medulla oblongata a centrogenic bronchial spasm was simulated in acute tests on cats. A peripheral bronchial spasm was reporduced by stimulating the peripheral length of the vagus. An experimental bronchial spasm caused by activation of reticular nuclei and of a single fascicular nucleus halidor suppressed with doses half as large as the ones needed to inhibit the peripheral spasm. An application of halidor to the ground of the fourth ventricle tended to immediately lessen the intensity of the bronchial spasm, this suggesting a central component in the action of the drug.

It has been established in chronic experiments on rabbits that accumulation of endogenous acetylcholine (galanthamine--1 mg/kg) prevents the development of sodium hydroxybutyrate (500 mg/kg) ability to increase the excitability of the mesencephalic reticular formation and to reduce the level of frontal cortex excitability. Inhibition of the central muscarinic (metamizyl--2 mg/kg) or nicotinic (eterofen--10 mg/kg) cholinoreceptors prevents the stimulant action or sodium hydroxybutyrate on the excitability of the dorsal hippocamp and mesencephalic reticular formation. Blockade of the central N-cholinoreceptors changes the marked effect of sodium hydroxybutyrate on the blood content of the test brain structures. This may attest to the participation of N-cholinoreceptors in the effects of sodium hydroxybutyrate.