Does a schizophrenia-linked mutation in PIP5K2A fail to activate neuronal M channels?
Our results suggest that the schizophrenia-linked mutation of the kinase results in reduced KCNQ channel function and thereby might explain the loss of dopaminergic control in schizophrenic patients. Moreover, the addictive potential of dopaminergic drugs often observed in schizophrenic patients might be explained by this mechanism. At least, the insufficiency of (N251S)-PIP5K2A to stimulate neuronal M channels may contribute to the clinical phenotype of schizophrenia.
Prolonged holding of whole blood at 22 degrees C prior to component preparation does not increase the level of platelet activation.