Neuroscience
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Extracellular purines and pyrimidines are important signaling molecules that mediate diverse biological functions via cell surface purinergic receptors. Although purinergic modulation to olfactory activity has been reported, cell-specific expression and action of purinergic receptors deserve further exploration. We physiologically characterized expression of purinergic receptors in a set of olfactory sensory neurons that are responsive to both acetophenone and benzaldehyde (AB-OSNs). ⋯ Activation of P2X1 receptors had more profound inhibitory effects on benzaldehyde-evoked intracellular calcium elevation than on acetophenone-evoked responses within the same neurons, and the reverse was true when P2Y2 receptors were activated. Cross-adaptation data showed that acetophenone and benzaldehyde bound to the same olfactory receptor. Thus, our study has demonstrated that purinergic signaling of P2X and P2Y receptors has different effects on olfactory transduction mediated by a defined olfactory receptor and the consequences of purinergic modulation of olfactory activity might depend on stereotypic structures of the odorant-receptor complex.
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Comparative Study
Differential cavitation, angiogenesis and wound-healing responses in injured mouse and rat spinal cords.
The vascular disruption, blood vessel loss and cavitation that occur at spinal cord injury (SCI) epicenters in mice and rats are different, but few studies have compared the acute SCI response in the two species. This is of interest since key elements of the rat SCI response are shared with humans. In this study, we investigated acute SCI responses and characterized changes in pro- and anti-angiogenic factors and matrix deposition in both species. ⋯ We conclude that the more robust angiogenesis/wound-healing response in the mouse attenuates post-injury wound cavitation. Although the spinal cord functions that were monitored post-injury were similarly affected in both species, we suggest that the quality of the angiogenesis/wound-healing response together with the diminished lesion size seen after mouse SCI may protect against secondary axon damage and create an environment more conducive to axon sprouting/regeneration. These results suggest the potential therapeutic utility of manipulating the angiogenic response after human SCI.