Influence de la formation reticulaire et du cortex cerebral sur l'excitabilite motrice au cours de l'hypoxie

Abstract

In curarised cats, acute progressive hypoxia (6.5% O 2 in N 2 induces reticular facilitation of motoneurons excitability. The delay of the onset and the manner of development of this phenomenon depend on three factors: early chemoreflex reticular excitation, direct excitation of reticular cells, and release of a corticofugal inhibitory influence. In the unanesthetised animal with a functional cortex, the onset and the manner of development of motor facilitation of reticular origin depend entirely on the last of these factors. 1. 1. In é preparations where telencephalic influence had been eliminated by a diencephalic transection of the brain stem ( tronc cérébral isolé preparation), acute progressive hypoxia (APH) produces progressive facilitation of the monosynaptic masseter reflex (cranial homologue of a monosynaptic extension reflex). 2. 2. After elimination of the aortic and carotid chemoreceptors, APH still produces motor facilitation, although it is less intense and more delayed than previously. At relatively high partial pressures of oxygen, the progressive facilitation of the motoneurons therefore arises from the increased discharge of the carotid and aortic chemoreceptors. At very low partial pressures of oxygen, however, the facilitatory reticular formation can be excited by another mechanism. Unit recording in an islet of é shows that this action consists of a direct humoral activation of reticular cells. 3. 3. In ordinary é preparations, the development of motor facilitation due to hypoxia is entirely different owing to the presence of a cortical control system. ( a) At a time corresponding to that when motor facilitation appears in diencephalic animals, a cortical arousal of chemoceptor origin is observed in the intact preparation. However, no appreciable motor facilitation can be observed at this time. ( b) When electrocortical activity ceases, reticular facilitation appears suddenly and immediately reaches its maximum value; its coincidence with the cessation of electrocortical activity can be regarded as statistically significant. ( c) When the arterial chemoreceptors are eliminated by transecting the IXth and Xth cranial nerves, the phase of cortical arousal does not appear; the sudden facilitation of reticular origin, however, still appears at the very moment when cortical electrical activity ceases. These results indicate that: ( a) in the é preparation with functional cortex, reticular activity is subject to tonic inhibitory control which ceases at the moment when cortical activity stops; ( b) reticular excitation provoked by intensification of chemoreceptor discharge is controlled in a phasic manner by the same cortical system; ( c) these conclusions are similar to those derived from a series of earlier investigations which demonstrated the existence of a feed-back system, comprising the ascending activating system, a diffuse cortical system and a cortico-reticular descending system; the static and dynamic properties of this system can account for both the motor and the cortical manifestations obtained during hypoxia. 4. 4. In the non-curarised é preparation or in a preparation with a transection at the level of D 2, acute progressive hypoxia gives rise to a series of movements beginning at the same time as cortical arousal and ceasing at the same time as the convulsions. Since the descending facilitatory reticular activity is not increased simultaneously, it appears that the latter is not necessary for the development even of intense motor activity. The functional consequences of this fact are considered in relation to homeostatic regulation.