Abstract
Neurons within the parabrachial complex appear to play a key role in controlling breathing frequency since local application of opioid receptor agonists produces bradypnea and apnea. To characterize the excitatory neurotransmission underlying the discharge of these PRG neurons, we antagonized glutamatergic inputs to AMPA and NMDA receptors with microejections of 2,3‐dihydroxy‐6‐nitro‐7‐sulfamoylbenzo‐(f)quinoxaline (NBQX) and 2‐amino‐5‐phosphonovalerate (AP5) in a decerebrate, vagotomized, ventilated and paralyzed canine model. Histograms (CTHs) triggered from the phrenic neurogram were used to quantify the activity of simultaneously recorded PRG neurons. NBQX reduced the discharge frequency (Fn) of all subtypes of PRG neurons by 25‐30% while AP5 decreased Fn by an additional 35‐45%, with the greatest depression occurring in non‐respiratory modulated (NRM) and expiratory (E) neurons after AP5. These data suggest that most (~70%) of the excitation of PRG neurons is mediated via AMPA and NMDA receptors with the latter contributing ~33% more drive than the former.Grant Funding Source: Supported by VA Medical Research Funds I01 BX000721‐01
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