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Figure 2 | Molecular Autism

Figure 2

From: Haploinsufficiency of the autism-associated Shank3 gene leads to deficits in synaptic function, social interaction, and social communication

Figure 2

Altered basal synaptic properties in Shank3 heterozygous mice. (A) Reduced α-amino-3-hydroxyl-5-methyl-4-isoxazole-propionic acid (AMPA) receptor responses in Shank3 heterozygous mice. Slices were incubated in the presence of 2-amino-5-phosphonopentanoic acid (APV) and mean field excitatory postsynaptic potential (field EPSP) slope as a function of fiber volley is shown for slices derived from wild-type and heterozygous mice. The inset shows representative traces for a given stimulus intensity (0.5 mA) in the input/output (I/O) graph (arrow indicates the trace from wild-type; scale: 10 ms, 0.5 mV). (B) Normal N-methyl-D-aspartic acid (NMDA) receptor responses in Shank3 heterozygous mice. Slices were incubated in the presence of 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX), and mean field EPSP slope as a function of fiber volley is shown. (C) Miniature excitatory postsynaptic currents (mEPSCs) from wild-type and Shank3 heterozygous mice. Left: Amplitude of mEPSCs. *P < 0.01. Right: Frequency of mEPSCs. *P < 0.03. (D) Sample traces of mEPSCs. Scale: 1 s, 40 pA. (E) Cumulative probability of mEPSC amplitude. (F) Paired-pulse ratio. Left: Representative EPSC traces from Shank3 heterozygous (red) and wild-type (black) mice, with traces normalized to the first EPSC for comparison. *P < 0.05. WT, wild-type mice; Het, Shank3 heterozygous mice.

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