Neuroscience
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Leptin is an important hormone that regulates food intake and energy homeostasis by acting on central and peripheral targets. In the gustatory system, leptin is known to selectively suppress sweet responses by inhibiting the activation of sweet sensitive taste cells. Sweet taste receptor (T1R2+T1R3) is also expressed in gut enteroendocrine cells and contributes to nutrient sensing, hormone release and glucose absorption. ⋯ This effect was inhibited by a leptin antagonist (mutant L39A/D40A/F41A) and by ATP gated K(+) (KATP) channel closer glibenclamide, suggesting that leptin affects sweet taste responses of enteroendocrine cells via activation of leptin receptor and KATP channel expressed in these cells. Moreover, leptin selectively inhibited sweet-induced but not bitter-induced glucagon-like peptide-1 (GLP-1) secretion from STC-1 cells. These results suggest that leptin modulates sweet taste responses of enteroendocrine cells to regulate nutrient sensing, hormone release and glucose absorption in the gut.
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Guess who's coming to dinner: Brain signatures of racially biased and politically correct behaviors.
The ability to share feelings with those of someone in pain is affected by the racial difference between the target and the onlooker. A differential empathic activation for race (DEAR effect) in favor of in-group members has been documented in the brain pain matrix. However, we are also capable of unbiased responses that manifest politically correct behaviors toward people of a different race. ⋯ On the other hand, during the response phase a significant out-group specific DEAR effect emerged in the prefrontal cortices. This latter effect was coupled with a revealing behavioral pattern: while the magnitude of the painful experience attributed to Caucasians and Africans was the same, our participants were significantly slower when judging the pain experience of the African actors. We propose a model that logically integrates these two contrasting forces at the neurobiological and behavioral level.
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Iron-overload can cause cognitive impairment due to blood-brain barrier (BBB) breakdown and brain mitochondrial dysfunction. Although deferiprone (DFP) has been shown to exert neuroprotection, the head-to-head comparison among iron chelators used clinically on brain iron-overload has not been investigated. Moreover, since antioxidant has been shown to be beneficial in iron-overload condition, its combined effect with iron chelator has not been tested. ⋯ All treatments, except DFX, attenuated these impairments. Moreover, combined therapy provided a greater efficacy than monotherapy. These findings suggested that iron-overload induced brain iron toxicity and a combination of an iron chelator with an antioxidant provided a greatest efficacy for neuroprotection than monotherapy.
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Sigma receptor (σR), a unique receptor family, is classified into three subtypes: σR1, σR2 and σR3. It was previously shown that σR1 activation induced by 1μM SKF10047 (SKF) suppressed N-methyl-d-aspartate (NMDA) receptor-mediated responses of rat retinal ganglion cells (GCs) and the suppression was mediated by a distinct Ca(2+)-dependent phospholipase C (PLC)-protein kinase C (PKC) pathway. In the present work, using whole-cell patch-clamp techniques in rat retinal slice preparations, we further demonstrate that SKF of higher dosage (50μM) significantly suppressed AMPA receptor (AMPAR)-mediated light-evoked excitatory postsynaptic currents (L-EPSCs) of retinal ON-type GCs (ON GCs), and the effect was reversed by the σR1 antagonist BD1047, suggesting the involvement of σR1. ⋯ Calcium imaging further revealed that SKF (50μM) did not change intracellular calcium concentration in GCs and persisted to suppress L-EPSCs when intracellular calcium was chelated by BAPTA. The SKF (50μM) effect was intact when protein kinase A (PKA) and phosphatidylinostiol (PI)-PLC signaling pathways were both blocked. We conclude that the SKF (50μM) effect is Ca(2+)-independent, PKG-dependent, but not involving PKA, PI-PLC pathways.
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The rat has long been considered an important model system for studying neural mechanisms of auditory perception and learning, and particularly mechanisms involving auditory thalamo-cortical processing. However, the functional topography of the auditory thalamus, or medial geniculate body (MGB) has not yet been fully characterized in the rat, and the anatomically-defined features of field-specific, layer-specific and tonotopic thalamo-cortical projections have never been confirmed electrophysiologically. ⋯ We also demonstrated that microstimulation in the MGv elicited cortical activation in layer-specific, region-specific and tonotopically organized manners. To our knowledge, the present study has provided the first and most compelling electrophysiological confirmation of the anatomical organization of the primary thalamo-cortical pathway in the rat, setting the groundwork for further investigation.