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. Author manuscript; available in PMC: 2010 Apr 1.
Published in final edited form as: Nat Med. 2009 Aug 23;15(10):1208–1214. doi: 10.1038/nm.2019

Figure 1.

Figure 1

LGI1 down-regulates presynaptic release probability at hippocampal MPP-GC excitatory synapses via Kv1 channels during postnatal development. (a) Representative traces showing paired-pulse facilitation (PPF) of evoked MPP-GC postsynaptic currents, a measure of release probability, increases between postnatal days 17 and 23 in control (WT) mice. (b) Western blots showing LGI1 and its receptor, ADAM22, also increase between p17 and p23. (c) Representative traces showing PPF remains low in mature mLGI1 and significantly increases in mature LGI1 OE mice relative to control. (d) Western blot showing increased expression of 64 kDa LGI1 in LGI1 OE mice and expression of 23 kDa mutant LGI1, marked by an arrow on densitometry traces, in mLGI1 mice. (e) Quantification of 64 kDa LGI1 protein density (normalized to β-actin) in WT, LGI1 OE, and mLGI1 mice (n = 7). (f) Kv1 channel blocker α-dendrotoxin (DTX) eliminates the difference in paired-pulse ratio (ppr) in mature mice. (g) Quantification of ppr in WT (black symbols), mLGI1 (red symbols), and LGI1 OE (blue symbols) mice (n = 4 to 25). *: P < 0.05; **: P < 0.01; ***: P < 0.001.