Skip to main content
. 2010 Feb 4;107(8):3876–3881. doi: 10.1073/pnas.0912531107

Fig. 3.

Fig. 3.

NAS selectively activates TrkB receptor. (A and B) TrkB−/− and TrkC−/− cortical neurons were treated with serotonin and various metabolites (100 nM). (A) NAS but not serotonin specifically activated TrkB in wild-type but not TrkB-null neurons, whereas TrkA was not activated in either neuron. (B) NAS induced TrkB activation but not TrkA activation in both wild-type and TrkC knockout neurons. (C) NAS activates TrkB F616A mutant. Cortical neurons from TrkB F616A knockin mice were prepared and pretreated with 1NMPP1 (100 nM) for 2 h, followed by stimulation with NAS. Cell lysates were analyzed by immunoblotting with anti-p-TrkB. NAS-mediated TrkB phosphorylation was selectively blocked by 1NMPP1 but not K252a, whereas serotonin had no effect. (D) NAS suppresses kainic acid (KA) -induced neuronal cell death in TrkB F616A mutant mice, which can be blocked by 1NMPP1. TrkB F616A mice were pretreated with 1NMPP1 (50 μM) or water 1 day before the experiment. NAS (20 mg/kg, i.p.) and melatonin (1 mg/kg, i.p.) were injected into TrkB F616A mice 1 h before KA (20 mg/kg). Brain lysates were prepared 4 h after KA treatment and analyzed by immunoblotting with anti-active caspase 3 and anti-p-TrkB.