Activities of the somatomotor (MA), cardiovascular and respiratory systems were investigated in conditions of activation and blockade of ryanodine receptors (RyR) impaired cholinergic regulation in rat pups aged 3, 16 and 30 days. It was found that blockage of RyR by dantrolene has a negative chronotropic effect, the severity of which decreases with age, reduces the respiratory rate in rats on P3 and practically does not change in older animals. The amplitude of EMG and the power of motor bursts decreases in rats on P3-P16 and increases on P30. The duration of MA in the activity- rest cycle remains unchanged at P3 and decreases at P16-P30, which indicates a different change in the pattern of MA in rats of different ages after the blockade of RyR. Caffeine-induced activation of RyR is accompanied by an increase in heart rate and respiratory rate in rats on P30 and does not cause significant changes in these parameters on P3-P16. There has been an increase in all MA indices, especially in P3. Certain age-related regularities were revealed in the conditions of acetylcholinesterase inhibition by physostigmine, carried out against the background of RyR inhibition or activation. Maximum sensitivity to such effects was found in rats on P3. It was shown that in early postnatal ontogenesis of rats the sensitivity of RyR, including RyR2, to dantrolene is higher than in adult animals. Changes in RyR activity level do not prevent the development of pathological forms of heart rhythm that developing in rats after the physostigmine injection.

The effects of calcium-channel blockers (CCBs) (verapamil, nifedipine) on heart rate, respiration rate and motor activity were studied in 3-30-day-old rats. The role of calcium channels in development of disturbances of a heart and respiratory rhythms after introduction to newborn rats of acetylcholinesterase (AChE) inhibitor of physostigmine was revealed. Parameters of functional activity of heart, respiratory and somatomotor systems in case of blockade of calcium channels were studied also under conditions of the activation of cholinoceptive structures caused by an injection to infant rats of AChE inhibitor after premedication by CCBs. It is shown that use of calcium channels blockers leads to development of bradycardia, and verapamil causes more expressed disturbance of a heart rhythm in rats of younger age, while blockade of dihydropyridinic receptors by nifedipine has no ontogenetic specifics. Similar ontogenetic dynamics concerns also reaction of respiratory system. Verapamil have a detrimental effect on respiration, up to a stop, in 3-7-day-old and to a lesser extent in 16-30-day-old infant rats. Nifedipine slightly reduces a respiration rate at younger infant rats, but raises it at the mature rats. The nifedipine injection more in comparison with verapamil changes the level and a pattern of motor activity. Preliminary blockade of calcium channels does not render significant change of reaction at the subsequent introduction of physostigmin.

Interaction of slow-wave rhythmic components of cardiac, respiratory and motor activities was analyzed in non-narcotized of newborn 1-day-old (P1) and 16-day-old (P16) Wistar rat pups under normal and impaired cholinergic regulation. Functional activity of these three systems is rhythmic, and coordination of their functioning is an important element of the mechanism of adaptive rearrangements under changing factors of the external and internal environment. The acetylcholinesterase inhibitor physostigmine (eserine) was used to increase the level of endogenous acetylcholine and enhance cholinergic effects. To reveal the role of N-cholinoreceptors in intersystemic somatovisceral interactions (ISI), we performed blockade of this receptor type with benzohexonium. Administration of physostigmine leads to the development of a number of pathological reactions and a decrease in the level of ISI in all ranges of modulating rhythms in rats of both ages. ISI in younger rats appear to be more resistant to changes in the level of cholinergic activation. Blockade of N-cholinoreceptors causes inhibition of ISI at P1 and partially to their potentialization at P16. The activation of cholinoreactive structures, which occurred against the background of cholinoreceptors blockade, reduces the pathological effects of physostigmine in animals of both ages, but at the same time leads to an attenuation of ISI. This weakening is more pronounced in 16-day old rats, which may indicate the formation of the definitive level of cholinergic regulation in the first weeks of postnatal ontogenesis.