Figure 1
Abnormal short-term synaptic plasticity in Df(16)5+/− mice is caused by Mrpl40 haploinsufficiency. (a) Diagram depicting genes in the 22.q11.2 genomic region of the human chromosome 22 and the syntenic region of mouse chromosome 16. Red horizontal bar represents genomic regions hemizygously deleted in Df(16)5+/− mice, and gray horizontal bar represents genomic regions hemizygously deleted in Df(16)1+/− mice. Note that 2510002D24Rik, Mrpl40 and Hira genes are mapped outside the Df(16)1 microdeletion. (b) Input–output relations in Df(16)5+/− and wild-type (WT) littermates. (c) Short-term potentiation (STP, comprising facilitation, depression and augmentation) induced by the high-frequency (80 Hz) train. The first time point represents an average of five baseline excitatory postsynaptic currents (EPSCs) delivered at low frequency. The top inset shows the protocol for measuring STP, recovery from depression and augmentation in the same experiment. (d–f) Average facilitation tested by paired-pulse ratio in separate experiments (d), recovery from depression tested 5 s after the 80-Hz train (e) and augmentation tested 5–120 s after the 80-Hz train in Df(16)5+/− and WT mice (f). Insets show representative EPSC traces. (g, h) Mean STP of EPSCs induced by the 80-Hz train of synaptic stimulation of Schaffer collaterals (g) and augmentation (h) in Mrpl40+/− mice and their WT littermates. Numbers of neurons are shown in parentheses. N.D., not significantly different. Data are represented as mean±s.e.m. *P<0.05.
