We investigated the hypothesis that the motor trigeminal nucleus, consisting of expiratory motoneurons, might be influential in termination of inspiration. We addressed the issue by comparing the effects on neural respiration of a reversible, unilateral, pharmacologic blockade of the motor trigeminal nucleus (5M), the medial parabrachial nucleus (PB), and of other nearby structures that are neutral for respiration in anesthetized, vagotomized, paralyzed, and ventilated cats. The blockade was achieved by microinjections of 2% xylocaine, laced with Pontamine Sky Blue to identify sites of injections, from the tip of a penetrating microelectrode. Integrated phrenic neurograms were recorded to quantify the time of neural inspiration (T I), expiration (T E), and the peak phrenic amplitude. We found that blockade of the 5M caused a pattern of apneustic respiration, consisting of a selective prolongation of inspiratory phases that were interrupted by short expiratory pauses. In contrast, blockade of the PB resulted in a prolongation of both T I and T E, which corresponds to a mere slowing of respiration. The results confirmed important functions of the rostral pons in ventilatory control but pointed to the 5M rather than PB as a structure underlying the inspiratory off switch. We conclude that the motor trigeminal nucleus may have a part in the pontine pneumotaxic mechanism.
Ultrastructural examinations of the CB showed that NOS-related NADPH-d activity is present in the chemoreceptor cells (Fig. 1A). The NADPH-d reaction product appeared as small, intense, dark particles scattered in the cytoplasm of the cells. The particles were distributed most densely or tended to aggregate in the perinuclear region, the endoplasmic reticulum channels, and in between the dense-core vesicles but not in the vesicles themselves. These particles were distinguishable from ribosomes from which they were larger and more electron dense. The particles were absent in the control specimens in which B-NADPH was omitted (Fig. 1B). The presence of NOS, which synthesizes a short-lived gaseous NO messenger, may have significant implications for the CB function. NO could not only affect the autonomic and sensory nerve endings but also be a direct participant of the chemoreceptor cell signaling process. The exact role of the nitergic pathway in the CB is unclear at present.
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