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% N2-5% CO2) 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 Mg2+ in the physiological medium was lowered from 1.25 X 10(-3) M to zero. The absence of Mg2+ 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 X 10(-3) M Mg2+ decreased the amplitude of the MSR to 23 +/- 6% of control, whilst in zero Mg2+ a decrease to only 50 +/- 5% of control was observed. These data provide further evidence that the response to adenosine, at the A1-receptor, is sensitive to Mg2+ ion concentration and suggest that there is an absolute requirement for Mg2+ 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 Mg2+ during or after exposure to hypoxia in altering the actions of adenosine on neuronal activity or synaptic events.