Age-dependent supersensitivity to the glycogenolytic effect of K⁺ in the cerebral cortex of the spontaneously epileptic quaking mouse mutant

K⁺, at concentrations reached in the extracellular space during neuronal activity (5-10 mM), promotes a time- and concentration-dependent hydrolysis of [³H]glycogen newly synthesized by mouse cerebral cortical slices. In the present study, the glycogenolytic action of K⁺ was examined in the neocortex of the quaking mouse, a spontaneously epileptic mutant characterized by deficient myelination of the CNS. The potency and efficacy of K⁺ in eliciting glycogen hydrolysis was greatly enhanced in cerebral cortical slices prepared from homozygous quaking mice (qk/qk) older than 7 weeks of age, indicating a supersensitive response to a metabolic action of the ion. A detailed ontogenic analysis showed an evolution of the supersensitive response to K⁺ which is reminiscent of the previously described increase in the number of α₂-adrenoreceptors in the brainstem of this mutant. In contrast to the altered response to K⁺, the glycogenolytic action of noradrenaline and vasoactive intestinal peptide reported earlier was equally expressed in qk/qk and in their unaffected littermates.