Fung M L, St John W M
Department of Physiology, Dartmouth Medical School, Dartmouth-Hitchcock Medical Center, Lebanon, NH 03755.
Respir Physiol. 1994 Nov-Dec;98(3):267-81. doi: 10.1016/0034-5687(94)90076-0.
The purpose was to identify and characterize the discharge patterns of pontile neurons which are responsible for the termination of inspiratory activity. Phrenic discharge is prolonged following destruction of neurons at the junction of mesencephalon and pons by neurotoxins. Neuronal activities were recorded in this region in decerebrate, vagotomized, paralyzed and ventilated cats. At normocapnia, neurons had tonic discharge patterns, most of which were linked to phasic periods of phrenic activity. Peak activities occurred in late neural inspiration or early expiration. In hypercapnia, neuronal discharge frequencies did not increase, rather activity became more concentrated during one portion of the respiratory cycle. In severe hypoxia, neuronal activities diminished in parallel with the prolongation of phrenic discharge and establishment of apneusis. During recovery, some neurons transiently acquired phasic, respiratory-modulated discharge patterns. Neuronal activities from neighboring regions did not exhibit comparable changes in hypercapnia or hypoxia. We conclude that rostral pontile neuronal activities are a primary determinant of the reversible and irreversible terminations of eupneic inspiratory activity.
目的是识别并描述负责吸气活动终止的脑桥神经元的放电模式。在中脑和脑桥交界处的神经元被神经毒素破坏后，膈神经放电会延长。在去大脑、切断迷走神经、麻痹并通气的猫的该区域记录神经元活动。在正常碳酸血症时，神经元具有紧张性放电模式，其中大多数与膈神经活动的相位期相关。峰值活动出现在神经吸气后期或呼气早期。在高碳酸血症时，神经元放电频率并未增加，而是活动在呼吸周期的一部分期间变得更加集中。在严重缺氧时，神经元活动随着膈神经放电的延长和呼吸暂停的建立而减少。在恢复过程中，一些神经元短暂地获得了相位性、呼吸调制的放电模式。来自相邻区域的神经元活动在高碳酸血症或缺氧时未表现出类似变化。我们得出结论，脑桥前部神经元活动是正常呼吸吸气活动可逆和不可逆终止的主要决定因素。
