[Cortical and thalamic regulating mechanisms of the pulse neuron activity of oblongata medulla respiration center of the rats in normal condition and during hypoxia].

In normoxia, the orbitofrontal cortex and thalamic mediodorsal nucleus (MDN) basically inhibit the pulse activity of bulbar respiratory neurons and respiration in general. During initial hypoxia (4,000-5,000 m) a slight reduction of PO2 in the inspired air increases excitability of all the brain structures including those under study. However, strengthening of the orbitofrontal cortex and MDN inhibitory effect was leveled down by activizing brain structures, and the direct exciting effect of reduced PO2 on peripheral and central chemoreceptors. As a result, respiration became hurried in that period. Still, this inhibitory effect appears to play a positive role too. Unobstructed enhancement of activizing neural and humoral regulators of respiration might have led to intense hyperventilation fraught with an opposite action, i.e., inhibition, if not arrest of respiration consequent to reduced PO2 blood level, etc. Under acute hypoxia (7.5,000-8,000 m), oxygen deficit brings about inhibition, of all the brain structures including the orbitofrontal cortex and MDN. Moderation of their inhibitory effect in this period also plays an important role as it stimulates liberation of activizing systems and a relative increase in the ventilatory function of respiration.