抄録
The membrane phospholipid phosphatidylinositol phosphates (PIs) are critical signal transducer in eukaryotic cells. Deficient mice in leucin-rich phosphoiositide phosphatase (L-PIPase) showed involuntary movements that were ameliorated by an NMDA-receptor antagonist, MK-801. Enhancement of gliosis and apoptosis were observed in the striatum of the L-PIPase deficient mice. Whole-cell recordings were carried out in the slice preparations obtained from 15-20 day-old PIPase deficient and wild type mice. The resting membrane potential of both medium spiny neurons and cholinergic interneurones in the striatum of L-PIP deficient mice was less hyperpolarized than that of wild type mice. In the cholinergic interneurones of L-PIPase deficient mice, spontaneous firing rate was larger. In addition, NMDA receptor-mediated components of the synaptic currents were enhanced in the medium spiny neurons of L-PIPase deficient mice. These findings suggest that abnormalities in NMDA receptor-mediated synaptic transmission in the striatum could result in the involuntary movements observed in L-PIP deficient mice. [J Physiol Sci. 2007;57 Suppl:S8]
