Are ATP and glutamate released from slowly adapting pulmonary stretch receptor afferents in the NTS?

摘要

The slowly adapting pulmonary stretch receptors (SARs) are an important mechanosensory component of the respiratory system involved in the lung inflation control, regulating the inspiratory and expiratory phase timing through connections with neurones within the brainstem involved with the control of respiratory activity. The activation of these receptors evokes responses of inspiratory shortening and expiratory lengthening, collectively termed as the Breuer-Hering reflex, and is characterized by the mono-synaptic activation of the pump cells located in a discrete region of the nucleus tractus solitarius (NTS), whose pattern of discharge is determined by the lung inflation. In a very elegant series of experiments, Bonham et al, (1993) demonstrated that glutamate, acting on its non-NMDA receptors, is the neurotransmitter released by the SARs afferents in the NTS, once the broad-spectrum glutamatergic receptor antagonist kynurenic acid. (KYN) or the non-NMDA receptor antagonists CNQX and DNQX, but not the NMDA receptor antagonist AP-5;, microinjected in a delineated area of the NTS containing the major population of pump cells, were able to attenuate/prevent the apnoea evoked by the Breuer-Hering activation. Thus, the concept that glutamate is the neurotransmitter released by SARs terminal in the NTS has been well accepted for the last 15 years or so#