Abstract
Neonatal maternal separation (NMS) affects respiratory control development. Adult rats previously subjected to NMS show a hypoxic ventilatory response (HVR) ~25% greater than controls. NMS augments the capacity for GABAergic neurotransmission within key structures regulating the HVR. Despite enhancement of inhibitory modulation, NMS rats still produce a HVR larger than controls, suggesting that NMS disrupts the balance between excitatory and inhibitory modulation. To address this issue, we tested the hypothesis that, in awake rats, altered glutamatergic modulation contributes to the enhancement of the HVR observed in NMS rats. Rats were instrumented for intracerebroventricular (ICV) injection of pharmacological agents while monitoring ventilatory activity using whole body plethysmography at rest and during hypoxia (12% O2, 20 min). Following vehicle injection, the HVR of NMS rats was greater than controls. ICV injection of the selective non‐NMDA receptor antagonist CNQX (500 μg) attenuated the HVR of NMS but not control rats. These results indicate that NMS rats are more sensitive to CNQX and suggest that early life stress exposure augments non‐NMDA receptor expression in CNS regions regulating the HVR. We propose that early life exposure to stress can compromise the development of key neurotransmitter systems in a way that may predispose to respiratory disorders. Supported by the CIHR.
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