Effect of magnesium on depression of the monosynaptic reflex induced by 2-chloroadenosine or hypoxia in the isolated spinal cord of neonatal rats

Superfusion of the isolated spinal cord of neonatal rats (4–9 days postpartum) with physiological medium containing 2-chloroadenosine (2-CA) or anoxic medium (equilibrated with 95% N 2-5% CO 2) depressed the evoked monosynaptic reflex (MSR) recorded extracellularly from a ventral spinal root. The effectiveness of 2-CA or anoxic medium in depressing the MSR was significantly reduced when the concentration of Mg 2+ in the physiological medium was lowered from 1.25 × 10 −3 M to zero. The absence of Mg 2+ resulted in a 7-fold shift to the right of the concentration-response curve to 2-CA and a reduction in the maximal depression of the MSR from 100% to 65 ± 4% (mean ± S.E.M.) of control. A 10 min exposure to anoxic medium containing 1.25 × 10 −3 M Mg 2+ decreased the amplitude of the MSR to 23 ± 6% of control, whilst in zero Mg 2+ a decrease to only 50 ± 5% of control was observed. These data provide further evidence that the response to adenosine, at the A 1-receptor, is sensitive to Mg 2+ ion concentration and suggest that there is an absolute requirement for Mg 2+ in order to obtain full expression of the adenosine effect. Furthermore, the data are consistent with the hypothesis that adenosine is an important mediator of hypoxia-induced depression of the evoked MSR in the spinal cord, and suggest a potential role for Mg 2+ during or after exposure to hypoxia in altering the actions of adenosine on neuronal activity or synaptic events.