Tools for modelling biological processes.
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Publications and source records attributed to John Keane.
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Neural coding of sensory input is a major unsolved issue in neuroscience. Current experimental methods rely on neural activity recording or visualization following sensory stimulation. Most of them, however, do not include behavioral correlates on the actual perception by the animal. We present a novel approach to address olfaction and coding in adult Drosophila. Sensory input was selectively blocked in two subsets of sensory neurons that project to different, albeit overlapping, groups of central targets, by means of tetanus toxin expressed under the control of the yeast transcription factor Gal4. Glomeruli DL1, DL2, VM1, and VM4 were tested following stimulation with benzaldehyde, ethyl acetate, propionic acid, butanol, or acetone at various concentrations. The behavioral response was found to be modified in an odorant-specific and a concentration-dependent manner. Sensory input to DL2 and, to a minor extent, VM1 and/or VM4, appear to be required for benzaldehyde perception, while acetone is processed through DL1. None of these glomeruli, however, seem necessary for butanol perception. In addition, sexual differences were observed for some stimuli. These results demonstrate the behavioral relevance of odor representation as maps of glomerular activity generated in the antennal lobes following specific sensory input. The strategy used here should be useful to characterize olfactory coding, as new and selective Gal4 lines become available.
Mechanical stimulation induces opposite behavioral responses in the adult and dauer pharynx. Tail tap of adults inhibits pharyngeal pumping via a pathway involving the innexin gene unc-7 and components of the glutamatergic pathway encoded by the genes avr-14 and avr-15. Tail tap of dauers stimulates pumping through a mechanism involving G alpha o and G alpha q. The nematocidal drug ivermectin is believed to kill worms by opening a glutamate-gated chloride channel (AVR-15) on pharyngeal muscle, causing complete pumping inhibition. However, ivermectin can also inhibit pumping in the absence of this channel. We propose that one of the ways ivermectin could prevent pumping, in the absence of the AVR-15 ivermectin-binding channel on pharynx muscle, is to target AVR-14 and AVR-15, which are expressed in the inhibitory pathway linking mechanosensation and pumping activity.