Zink verstärkt die Glyzinrezeptorantwort. Ist Zink an den Rezeptor gebunden, strömen Chlorid-Ionen vermehrt ein (linkes Bild, rechter Ionenkanal). Dies verstärkt die Wirkung von Glyzin innerhalb neuronaler Schaltkreise. Die Mutation der Zinkbindungsstelle am Glyzinrezeptor verhindert, dass Zink den Chlorideinstrom verstärkt (rechtes Bild), und verursacht Symptome ähnlich der menschlichen Schreckerkrankung Hyperekplexie.
Max-Planck-Institut für Hirnforschung
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