Musical and vocal emotion perception for cochlear implants users.

Cochlear implants can successfully restore hearing in profoundly deaf individuals and enable speech comprehension. However, the acoustic signal provided is severely degraded and, as a result, many important acoustic cues for perceiving emotion in voices and music are unavailable. The deficit of cochlear implant users in auditory emotion processing has been clearly established. Yet, the extent to which this deficit and the specific cues that remain available to cochlear implant users are unknown due to several confounding factors. Here we assessed the recognition of the most basic forms of auditory emotion and aimed to identify which acoustic cues are most relevant to recognize emotions through cochlear implants. To do so, we used stimuli that allowed vocal and musical auditory emotions to be comparatively assessed while controlling for confounding factors. These stimuli were used to evaluate emotion perception in cochlear implant users (Experiment 1) and to investigate emotion perception in natural versus cochlear implant hearing in the same participants with a validated cochlear implant simulation approach (Experiment 2). Our results showed that vocal and musical fear was not accurately recognized by cochlear implant users. Interestingly, both experiments found that timbral acoustic cues (energy and roughness) correlate with participant ratings for both vocal and musical emotion bursts in the cochlear implant simulation condition. This suggests that specific attention should be given to these cues in the design of cochlear implant processors and rehabilitation protocols (especially energy, and roughness). For instance, music-based interventions focused on timbre could improve emotion perception and regulation, and thus improve social functioning, in children with cochlear implants during development.

Molecular cloning and characterization of Phoneutria nigriventer toxins active on calcium channels.

The aim of the present study was the molecular cloning of toxins active on calcium channels expressed by the spider Phoneutria nigriventer. Clones encoding the toxins Pn3-3A, Pn3-4A, Tx3-5, Pn3-5A, Tx3-6, Pn3-6A and Pn3-6B were identified from a cDNA library derived from the venom gland of this spider, revealing toxins of 49, 76, 45, 39, 55 and 58 amino acids residues, respectively, with polypeptide precursors being composed of three major portions: a signal peptide, a propeptide and finally, the mature toxin. A high degree of homology with the amino acid sequence was found between Pn3-3A and the neurotoxin Tx3-3 (identity of 79%), and between Pn3-4A and the neurotoxin Tx3-4 (identity of 95%). The deduced amino acid sequence for the mature polypeptides Tx3-5 and Tx3-6 confirms the polypeptide sequence previously published for these neurotoxins. In addition, the toxin Pn3-5A showed 58% identity to the Tx3-5 amino acid sequence, and the toxins Pn3-6A and Pn3-6B showed 85 and 33% identity, respectively, to the Tx3-6 amino acid sequence.

Phoneutria nigriventer toxin Tx3-1 blocks A-type K+ currents controlling Ca2+ oscillation frequency in GH3 cells.

GH3 cells present spontaneous Ca2+ action potentials and oscillations of intracellular Ca2+, which can be modified by altering the activity of K+ or Ca2+ channels. We took advantage of this spontaneous activity to screen for effects of a purified toxin (Tx3-1) from the venom of Phoneutria nigriventer on ion channels. We report that Tx3-1 increases the frequency of Ca2+ oscillations, as do two blockers of potassium channels, 4-aminopyridine and charybdotoxin. Whole-cell patch clamp experiments show that Tx3-1 reversibly inhibits the A-type K+ current (I(A)) but does not block other K+ currents (delayed-rectifying, inward-rectifying, and large-conductance Ca2+-sensitive) or Ca2+ channels (T and L type) in these cells. In addition, we describe the sequence of a full cDNA clone of Tx3-1, which shows that Tx3-1 has no homology to other known blockers of K+ channels and gives insights into the processing of this neurotoxin. We conclude that Tx3-1 is a selective inhibitor of I(A), which can be used to probe the role of this channel in the control of cellular function. Based on the effect of Tx3-1, we suggest that I(A) is an important determinant of the frequency of Ca2+ oscillations in unstimulated GH3 cells.

Cloning, cDNA sequence analysis and patch clamp studies of a toxin from the venom of the armed spider (Phoneutria nigriventer).

The cDNAs (Tx3-2 and Pn3A) encoding precursor of toxin Tx3-2 and an isoform called Pn3A have been isolated from a library constructed from stimulated venom glands of the spider Phoneutria nigriventer. The cDNA of Tx3-2 reveals the presence of a signal peptide of 21 amino acids and of an intervening propeptide (with 16 amino acids) preceding the toxin sequence, which was followed by additional amino acid residues at the C-terminus (C-terminal peptide), implying post-translational modifications of the synthesised peptide. The deduced amino acid sequence for the mature toxin confirms the previous sequence published. In addition, by using the whole-cell patch clamp technique, we have determined that purified Tx3-2 decreases L-type currents present in GH3 cells. Finally, the presence of the cDNA Pn3A, with high sequence identity with Tx3-2, reveals the existence of a putative new toxin showing, at the cDNA level, 85.4% identity in its whole segment.