Role of inhibitory neurotransmission in the control of XXXX hypoglossal motoneuron activity in vivo.

@entity1026 @entity8959 @entity1246 @entity2944 @entity235 @entity1027 @entity5094 @entity528
Hypoglossal motoneurons (HMNs) innervate all tongue muscles and are vital for maintenance of upper airway patency during inspiration. The relative contributions of the various synaptic inputs to the spontaneous discharge of HMNs in vivo are incompletely understood, especially at the cellular level. The purpose of this study was to determine the role of endogenously activated @entity1246 (A) and @entity8959 receptors in the control of the inspiratory HMN (IHMN) activity in a decerebrate @entity235 model. Multibarrel micropipettes were used to record extracellular unit activity of individual IHMNs during local antagonism of @entity1246 (A) receptors with @entity1027 and @entity5094 or @entity8959 receptors with @entity1026 . Only @entity1027 had a significant effect on peak and average discharge frequency and on the slope of the augmenting neuronal discharge pattern. These parameters were increased by 30 +/- 7% (P < 0.001), 30 +/- 8% (P < 0.001), and 25 +/- 7% (P < 0.001), respectively. The effects of @entity5094 and @entity1026 on the spontaneous neuronal discharge and its pattern were negligible. Our data suggest that @entity1027 -sensitive GABAergic, but not @entity5094 -sensitive GABAergic or glycinergic, inhibitory mechanisms actively attenuate the activity of IHMNs in vagotomized decerebrate @entity235 during hyperoxic @entity2944 . The pattern of GABAergic attenuation of IHMN discharge is characteristic of gain modulation similar to that in @entity528 , but the degree of attenuation ( approximately 25%) is less than that seen in bulbospinal premotor neurons ( approximately 60%). The current studies only assess effects on active neuron discharge and do not resolve whether the lack of effect of @entity5094 and @entity1026 on IHMNs also extends to the inactive expiratory phase.
