Abstract
Facial motoneurons of the rat respond to arginine vasopressin by generating a voltage-dependent inward current which is sodium-dependent and is resistant to tetrodotoxin. In the present study, we have investigated the action of N- methyl- d-aspartate (NMDA) on these same neurones. We have obtained single-electrode voltage-clamp recordings from brainstem slices of newborn rats. In a majority of vasopressin-sensitive facial motoneurones, NMDA induced an inward current. This action was direct, was concentration-related and could be suppressed by the specific competitive antagonist d-2-amino-5-phosphopentanoic acid ( d-AP5). The NMDA-evoked current increased in amplitude as the neuronal membrane was depolarized. It could be blocked by the noncompetitive antagonist MK-801. It was potentiated following removal of extracellular magnesium, and was attenuated or suppressed when the external magnesium concentration was increased from 1 to 10 mM. By contrast, none of these treatments affected the vasopressin-induced current. These results show that facial motoneurones in the rat possess functional NMDA receptors and indicate that NMDA and vasopressin affect the bioelectrical properties of these neurones by turning on distinct voltage-dependent inward currents.
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