This feature is closely related to its structure and physico-chemical properties, which can lead to the opening of new structure–function relationship studies of peptides for pharmacological applications. Agelaia MP-I, like the Mastoparan peptide, is a peptide capable of interacting with different components of cells (phospholipids, receptors, ionic channels) and promoting the degranulation of different granulocytes. As such, AMP-I showed a positive and non-lytic effect upon pancreatic beta cell function. In contrast to Mastoparan, AMP-I did not affect KATP nor L-type Ca2+ channel activity in pancreatic

beta cells, suggesting a different mechanism for this compound screening assay peptide, possibly by a G protein interaction due to the structural and physicochemical similarity of this peptide with Mastoparan-X, as obtained by modeling. This CFTR activator study may open interesting new structure–activity relationship perspectives for peptides with pharmacological interest for future studies related to metabolic endocrine disease. The structural analyses were developed at the Laboratory of Structural Biology and Zoology (LSBZ) – Biological Institute of UNESP – Rio Claro/SP, while the biological assays were assayed at the Endocrine Pancreas Laboratory – Biology Institute of UNICAMP – Campinas/SP.

This research was supported by FAPESP (2011/51684-1), and CAPES grants. MSP and EMC are researchers of CNPq. “
“Phoneutria nigriventer, popularly known as armed spider, causes most of the human accidents by venomous spiders in Southeast of Brazil. The venom of this spider is a cocktail of toxins, having peptides, free

amino acids, histamine and serotonin. Most of the toxins that have been purified from this venom act on ion channels (for review see Gomez et al., 2002), including voltage gated sodium (Na+), calcium (Ca2+) and potassium (K+) channels. Clinically, P. nigriventer accidents graded as severe (less than 1%) may cause convulsions particularly in children or debilitated victims ( Bucaretchi et al., 2000). Recent findings in experimental models have shown that the systemic injection of P. nigriventer venom (PNV) in rats causes blood–brain barrier (BBB) permeability, with hippocampal BBB greatly susceptible to venom ( Le Sueur et al., 2003). It has been also shown that envenoming causes neuroinflammation in the cerebellum and hippocampus and neuron many activation (induction of Fos + neurons) in some brain regions, which though showed differential regional and time-course modulation ( Rapôso et al., 2007; da Cruz-Höfling et al., 2007, 2009). This BBB permeation was transient being thereafter gradually restored. However, the cellular events which course with the alterations of permeability at the blood–brain interface and how the repair occurs were not determined yet ( da Cruz-Höfling et al., 2009). One of the growth factors with seminal involvement in the process of brain repair is the vascular endothelial growth factor (VEGF).