The responses of A5 region neurons, the phrenic nerve, and systemic blood pressure to short-term hypoxia were examined in rats under conditions of spontaneous respiration. Tonic and respiration-modulated neurons increasing their discharge activity during hypoxia were identified. This hypoxia-induced response was more pronounced in the neurons with baseline discharge rate of 0.1-4.5 Hz (electrical activity of neurons increased by 4-5 times) compared to neurons with the baseline activity of 5.4-49.6 Hz (discharge rate increased by 1.4-2.0 times). The latency and duration of activation of all types A5 neurons correlated with the parameters of activation of the phrenic nerve. During hypoxia, activation of A5 neurons corresponded to the period of blood pressure drop (one-third of the reaction time), but not to the period of plateau or recovery phase. Low-, middle, and high-frequency A5 neurons participated in the modulation of hypoxia-provoked respiratory and hypotensive responses. Modulation of the respiratory response by A5 neurons was observed during the entire period of phrenic nerve activation, while modulation of the hypotensive response occurred only during blood pressure decrease.

Acute experiments were performed on urethane-anesthetized adult laboratory rats to investigate the effects of microinjections of 10(-13)-10(-4) M bombesin into the solitary tract nucleus on measures of respiration. Bombesin microinjections were found to stimulate respiration, inducing significant increases in the level of pulmonary ventilation, increases in respiratory volume, and increases in the bioelectrical activity of the inspiratory muscles. The most marked respiratory reactions were seen after intermediate peptide doses (10(-10)-10(-7) M). These respiratory effects of bombesin were found to result from its ability to suppress the inspiration-inhibiting Hering-Breuer reflex at the level of the solitary tract nucleus. The fact that ultralow doses of bombesin were active, along with the distribution of endogenous bombesin and its specific receptors in the solitary tract nucleus, and the ability of this peptide to modulate the Hering-Breuer reflex all provide evidence that bombesin is involved in controlling respiration at the level of the dorsal structures of the respiratory center.

We recorded spike activity of noradrenergic neurons of zone A5 (n = 89) in the brain of anesthetized rats under conditions of hypoxic stimulation (breathing with pure N 2 , 10 sec), thermonociceptive stimulation (tail-flick test), and reversible hypothermal blocking of the central respiratory activity. Hypoxic stimulation of peripheral О 2 -sensitive chemoreceptors considerably increased the discharge frequency in all the examined neurons and induced tachypnea and a hypotensive reaction. Sixty-nine (77.5%) neurons of the studied group were tested using nociceptive stimulation (thermal stimulation of the tail); such stimulation resulted in a multifold increase in their discharge frequency. This was accompanied by tachypnea and a hypertensive response. Thus, we first demonstrated the role of nociception in the control of activity of noradrenergic neurons in zone A5 and the role of nociceptive afferent signals in the modulation of functions of the respiratory and cardiovascular systems mediated by neurons of the above zone. Under conditions of blocking of the central respiratory activity, we examined 36 (40.4%) neurons of zone A5 and first observed the effect of strong activation of a significant proportion of these cells upon switching off of respiration. This fact shows that there is an activating "respiratory" drive on neurons of zone A5 (probably, from the side of an expiratory neuronal population of the respiratory center) and allows us to hypothesize on the genesis of "respiratory" modulation of these cells. The activity of 16 (18.0%) cells was recorded under conditions of consecutive applications of the above stimuli; all the neurons were activated by the respective afferent influences. The simultaneously induced effects of hypoxic and nociceptive stimulations on the activity of neurons of zone A5 were additive. Thus, we first obtained proofs in favor of the multimodality of noradrenergic neurons of the above zone. This feature is a significant factor providing integrative interaction between the respiratory and cardiovascular systems and the system of nociception.

In narcotized albino rats, thermal nociceptive stimulation elevated systemic blood pressure and increased the frequency of respiratory rhythm generation. Unilateral microinjection of ketamine hydrochloride, a selective blocker for NMDA receptors, into A5 region did not change the baseline parameters of multineuronal activity in the phrenic nerve and systemic blood pressure. Under conditions of NMDA-receptor blockade, thermal nociceptive stimulation evoked more pronounced respiratory response (in comparison to that observed before ketamine treatment), but induced smaller blood pressure rise. Unilateral microinjection of GAMS, a selective blocker for non-NMDA receptors, into A5 region did not modify the examined baseline parameters and the nociceptive response. It is concluded that during thermal nociceptive stimulation, activity of the respiratory center and blood pressure in rats are controlled by neuronal structures in A5 region via NMDA subtype of glutamate receptors.

Aim - to find out the neurophysiological correlatives of motor imagery after the simulation of the motor pattern. Materials and methods. Monopolar EEG was recorded using EEG recording system Neuron - Spectrum - 4 / VPM at 7 right-handed volunteers aged 18-19 years. EEG was recorded according to the system 10-5 in the projection of the sensorimotor cortex of the left hemisphere during the imagination of two movements in the right hand (flexing the fingers, elbow flexion) before and after 30 seconds of simulation of movement patterns using the rehabilitation device Power Plate. Results. After the simulation of the motor pattern, the imagination of the two types of movement correlated with desynchronization of alpha-, beta- EEG rhythms, increasing the number of leads with the reaction of desynchronization (p