The nature of the chick's magnesium‐sensitive retinal spreading depression

Abstract

Spreading depression (SD) in the chick retina is completely suppressed by 10 mM MgCl₂ in the bathing solution (Mg-sensitive SD). However, after increasing the KCl concentration in the Mg solution to values between 10 and 20 mM the retina can again exhibit SDs (Mg-insensitive SD). It has been postulated that the Mg-sensitive SD is a glutamatergic phenomenon. This is supported by the effect of four gl(utamate)-antagonists—L-proline, glutamic acid diethyl ester (GDEE), D-α-aminoadipate (D-AA), and 2-amino-4-phosphonobutyrate (APB)—which all suppressed this type of SD. It was suggested that this effect is due to competitive binding of glutamate involved in the Mg-sensitive SD and the gl-antagonist to glutamate receptors. The suppression of SD could be reversed by washing the preparation in a physiologic salt solution. The gl-antagonists in relatively high concentrations had a cytotoxic effect which, when severe, suppressed SD and prevented the recovery of this phenomenon by washing the compound out of the tissue. The compounds examined had, in addition to their gl-antagonistic properties, a gl-agonistic effect, which was postulated to enhance the Na⁺ permeability of neural membranes resulting in a release of K⁺ into the extracellular space. In preparations bathed in 10 mM MgCl₂ (which suppresses Mg-sensitive SDs) the four compounds investigated promoted Mg-insensitive SDs supposedly when the extracellular K⁺ concentration reached values between 10 and 20 mequiv.