Trigeminal reflex regulation of the glottis depends on central glycinergic inhibition in the rat

Abstract

Dutschmann, Mathias, and Julian F. R. Paton. Trigeminal reflex regulation of the glottis depends on central glycinergic inhibition in the rat. Am J Physiol Regulatory Integrative Comp Physiol 282: R999-R1005, 2002; 10.1152/ ajpregu.00502.2001.-In an unanesthetized decerebrate in situ arterially perfused brain stem preparation of mature rat, strychnine (0.05-0.2 M) blockade of glycine receptors caused postinspiratory glottal constriction to occur earlier, shifting from early expiration to inspiration. This resulted in a paradoxical inspiratory-related narrowing of the upper airway. Stimulation of the trigeminal ethmoidal nerve (EN5; 20 Hz, 100 s, 0.5-2 V) evoked a diving response, which included a reflex apnea, glottal constriction, and bradycardia. After strychnine administration, this pattern was converted to a maintained phrenic nerve discharge and a reduced glottal constriction that was interrupted intermittently by transient abductions. The onset of firing of postinspiratory neurons shifted from early expiration into neural inspiration in the presence of strychnine, but neurons maintained their tonic activation during EN5 stimulation, as observed during control. Inspiratory neurons that were hyperpolarized by EN5 stimulation in control conditions were powerfully excited after loss of glycinergic inhibition. Thus the integrity of glycinergic inhibition within the pontomedullary respiratory network is critical for the coordination of cranial and spinal motor outflows during eupnea but also for protective reflex regulation of the upper airway.ventral respiratory group; upper airway patency; synaptic inhibition; diving response THE NETWORK MODEL for respiratory rhythm generation comprises three phases of respiration: inspiration, postinspiration, and expiration. During eupnea, there is a respiratory modulation of the upper airway such that the vocal fold is dilated (abducted) to decrease airway resistance during inspiration and constricted (adducted) during early expiration or postinspiration. This postinspiratory glottal constriction is particularly important for slowing expiratory airflow out of the lungs to allow time for efficient gas exchange and to maintain functional residual capacity, thereby preventing lung collapse (for review, see Ref. In the mammal one of the most potent upper airway protective reflexes occurs during diving. Activation of nasotrigeminal afferents evokes a diving response (7, 17) that includes a profound constriction of the glottis (15) to ensure that water cannot enter the bronchi. In the present study, we assessed the role of central glycinergic neurotransmission for the functional integrity of upper airway adduction during the diving response. We show that both the ongoing eupneic modulation of the upper airway and the reflexly evoked glottic closure during a diving response are massively disrupted after blockade of glycinergic neurotransmission. MATERIALS AND METHODS Preparation of animals.Experiments were performed on mature rats (Wistar, 70-100 g) of either sex. We employed the...

Dynamic Changes in Glottal Resistance during Exposure to Severe Hypoxia in Neonatal Rats In Situ

“…pump muscles) targets. Pharmacologic blockade of glycine receptors in the neonatal or adult respiratory network caused a paradoxic inspiratory glottal constriction, although rhythmic network activity persisted (16,17). This result parallels the upper airway response to severe hypoxia demonstrated in the present study.…”

“…In one study, gasping during severe hypoxia was reported to be accompanied by a massive reduction or total abolishment of postinspiratory motor activity destined for the upper airway (11,14). Recent studies showed that an obvious absence of postinspiratory motor activity does not necessarily mean a cessation of the activity of postinspiratory motor neurones (15)(16)(17). We found that postinspiratory neurones (including adductor motor neurones) discharged earlier in the respiratory cycle during the inspiratory phase.…”

“…This transformation is likely to include disturbances of ion homeostasis within the brain (e.g. increased extracellular potassium ion concentration), membrane depolarization, and failure of chloride ion-mediated synaptic inhibition provided by glycinergic and GABAergic neurones of the respiratory network (15)(16)(17)23,25,28). In particular, glycinergic inhibition was demonstrated to be essential for the coordination of respiratory motor output to cranial (e.g.…”

“…We found that postinspiratory neurones (including adductor motor neurones) discharged earlier in the respiratory cycle during the inspiratory phase. This was demonstrated by pharmacologic blockade of inhibitory glycinergic neurotransmission, which abolished synaptic inhibition of postinspiratory neurones during the inspiratory phase and revealed an inspiratory depolarization (15)(16)(17). Functionally, this had significant effects on respiratory modulation of upper airway resistance.…”

“…Functionally, this had significant effects on respiratory modulation of upper airway resistance. The phase shift of postinspiratory adductor motor discharge into neural inspiration manifested a paradoxic inspiratory glottal constriction (16,17).…”