Osteopetrosis and thalamic hypomyelinosis with synaptic degeneration in DAP12-deficient mice
J. Clin. Invest. Tomonori Kaifu, et al. 111:323 doi:10.1172/JCI16923 [Go to this article.]

Figure 6
Reduced startle response, impaired sensorimotor gating, and aberrant GABAergic mIPSC’s in DAP12^–/– mice. (a) DAP12^–/– mice (white bars) displayed significantly lower startle responses than did wild-type mice (black bars). F(1, 18) = 5.790, P < 0.05. The average startle responses at 100 and 110 dB were significantly lower in knockout mice. (b) DAP12^–/– mice (white bars) displayed significantly lower prepulse (pp) inhibition than did wild-type mice (black bars). F(1, 18) = 5.061, P < 0.05. This effect was attributable to the acoustic startle pulse (p) stimulus of 100 dB. In a and b, the data are presented as mean ± SEM (n = 10, *P < 0.05). (c) Schematic illustration of a neural circuit for negative feedback giving rise to prepulse inhibition. The thalamus receives inhibition by GABAergic neurons. (d) Developmental change in the decay time constant of spontaneous mIPSC’s recorded from laterodorsal thalamic neurons in the presence of tetrodotoxin; 6-cyano-7-nitroquinoxaline-2,3-dione; D(−)-2-amino-5-phosphonopentanoic acid; and strychnine. The mean decay time constants of mIPSC’s recorded from DAP12^–/– mice (open circles) were 12.2 ± 0.7 ms (n = 5) and 10.9 ± 0.2 ms (n = 4) at P20 and P62, respectively, whereas those from wild-type mice (filled circles) were 17.3 ± 1.1 ms (n = 4) and 8.1 ± 1.0 ms (n = 4) at P19 and P64, respectively. The numbers of neurons tested are given in parentheses. The decay time matched a monoexponential time course. The current traces on the left are the averaged mIPSC’s (from 491–999 events) at each age of wild-type or DAP12^–/– mice.