Activation of ionotropic excitatory amino acid (EAA) receptors modulates both eupnea and gasping in the arterially‐perfused adult rat preparation

Abstract

Previous work from our laboratory in an arterially‐perfused adult rat preparation has shown that blockade of ionotropic EAA receptors reduces or abolishes basal phrenic nerve discharge and markedly enhances inspiratory neural network complexity. Further, we have demonstrated that during EAA receptor blockade, gasping can still be elicited. The effect of activation of ionotropic glutamate receptors on phrenic motor discharge requires clarification. We examined the effects of perfusion with the glutamate analog DLH on phrenic burst timing and inspiratory neural network complexity in the arterially‐perfused adult rat preparation. DLH (500 μM, n=8) transiently increased phrenic burst frequency by 41% (P=0.005) mediated by decreasing the duration between bursts by 55% (p<0.001), followed by a 36% increased stabilization of burst frequency (P=0.074). Post‐inspiratory activity was also increased. DLH decreased the duration of the peripheral chemoreflex from 23.8±1.7 to 13.2±1.4 s (P<0.001), the duration of ischemia‐induced gasping from 58.6±5.3 to 33.4±2.3 s (P<0.001), and the onset latency to gasping by 79% (P<0.001). These findings support a role for ionotropic EAA neurotransmission in establishing the temporal dynamics of basal phrenic nerve discharge and suggest that it also has a role in determining the onset and duration of the peripheral chemoreflex and gasping. Supported by NS045321 and NS049310