, 1997a). Moreover, U1-TRTX-Lsp1b, obtained through heterologous expression, was shown to block L-type Ca2+ channel in BC3H1 cells ( Dutra et al., 2008). Therefore, the segment -CKCXDKDNKD- was postulated to act upon the selectivity of these toxins ( Diego-Garcia et al., 2010). The other toxins listed in Fig. 3 have not had their biological activities or molecular targets described in the literature yet. However, it is noteworthy that U3-TRTX-Cj1b does not show effects

on voltage gated ion currents in rat dorsal ganglia neurons – tetrodotoxin-sensitive and tetrodotoxin-resistant sodium channels, potassium and calcium channels (Chen et al., 2008). Besides the presence of conserved regions,

the analysis reveals some peculiarities of μ-TRTX-An1a primary LBH589 datasheet structure, when compared selleck kinase inhibitor to similar toxins. The presence of two extra segments formed by residues Asp13–Lys17 and Asp27–Lys30 should be highlighted. The presence of a Lys12–Asp13–Gly14 motif inside a long segment between CysII and CysIII is also relevant. The former fact leads to the hypothesis that this peptide could have similar activities to disintegrins, a peptide family present in the venom of various vipers that selectively block integrin receptor functions (Calvete et al., 2005). Considering the previously reported anti-insect activity of μ-TRTX-An1a (Borges, 2008) and its similarity to other toxins bearing insect neurotoxic activity, we evaluated the effect

of μ-TRTX-An1a on cockroach DUM neurons, by using electrophysiology. All DUM neurons tested in this study exhibited spontaneous electrical activity whose electrophysiological characteristics have previously been studied (Grolleau and Lapied, 2000; Wicher et al., 2001). As illustrated in Fig. 4, after 10 min of treatment, bath application of the toxin (100 nM) produced a slight depolarization associated with an increase of spontaneous firing frequency associated with a reduction of the action potential amplitudes (Fig. 4). After 15 min of application, toxin produced a substantial Edoxaban membrane depolarization during which DUM neuron beating activity further increased in frequency. Finally, after 20 min of toxin application, the spikes disappeared giving only slow wave of depolarization. The toxin-induced depolarizing effect of the DUM neuron membrane potential was well illustrated in Fig. 5. When the isolated cell body was superfused with μ-TRTX-An1a (100 nM for 12 min), the amplitude of the action potential elicited by a depolarizing current pulse (0.6 nA for 50 ms) was reduced. This effect was associated with a depolarization of the resting membrane potential (Fig. 5; arrow).