Nasopharyngeal reflexes: role of brain monoamines in central integration. a review

Abstract

The nasopharyngeal reflex in the rabbit (respiratory suppression, activation of vagal and sympathetic nerves, and reduction in oxygen usage) is initiated by trigeminal nerves and is enhanced by the arterial baroreceptor and by loss of lung inflation afferent activity. A review of (i) the functional anatomy of central nervous catecholamine and 5-hydroxytryptamine pathways participating in cardiorespiratory regulation, (ii) studies of the reflex in pontine, thalamic, and intact-brain rabbits in which the arterial baroreceptor and lung inflation inputs were manipulated, and (iii) studies of the reflex in rabbits in which central nervous catecholamine and 5-hydroxytryptamine were depleted indicates that the trigeminal nerve can initiate the reflex pattern during maintained ventilation at the ponto-medullo-spinal level through interactions that may include convergence with glossopharyngeal and vagal nerves in the nucleus of the solitary tract. By contrast, loss of lung inflation activity in itself activates vagal and sympathetic pathways through interactions with arterial baroreceptor activity and diencephalic influences. The vagal output component of the reflex is relatively independent of either central nervous monoamine, but the sympathetic vasoconstrictor component appears clearly dependent on central nervous catecholamine and, to a much lesser extent, on 5-hydroxytryptamine. Both monoamines play a role in respiratory suppression. Pentobarbitone blocks centrally the vagal output component of the nasopharyngeal reflex by a monoamine-independent mechanism. The findings provide a framework for testing postulates concerning central nervous catecholamine integration and neurotransmitter control of submergence reflexes in diving species.