Neuroscience
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Sound envelope plays a crucial role in perception: ramped sounds (slow attack and quick decay) are louder in strength and longer in subjective duration than damped sounds (quick attack and slow decay) even if they are equal in intensity and physical duration. To explain the asymmetrical perception, the perceptual constancy hypothesis supposes that the listener eliminates the slow decay of damped sounds from the judgment of perception, while the persistence of perception hypothesis supposes asymmetrical neural responses after the source has stopped. To understand neural mechanisms underlying the perceptual asymmetry, we explored response properties of the primary auditory cortex (A1) neurons during ramped and damped stimuli in awake cats. ⋯ The former needs a short (<2.5 ms) period of stimulus duration for evoking maximal peak responses, while the latter needs a long (20 ms) period, suggesting that the timescale of processing underlies differential sensitivity between the cell types. The findings suggest that perceptual constancy is not yet be executed at A1 because the specific cells distinguishing the direction of amplitude change (attack or decay) are lacking in A1. On the other hand, there is evidence of persistence of perception: overall response duration during ramped sound reached 1.4 times longer than that during damped sound, originating mainly from the response asymmetry of the edge cell (sensitive to the quick decay of ramped sounds but not to the slow decay of damped sounds), and neuronal persistence of excitation after the termination of ramped sounds was substantially longer than that of damped sounds, corresponding to the psychological evidence of persistence of perception.
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Neuropeptide Y (NPY) is present in the superficial laminae of the dorsal horn and inhibits spinal nociceptive processing, but the mechanisms underlying its anti-hyperalgesic actions are unclear. We hypothesized that NPY acts at neuropeptide Y1 receptors in the dorsal horn to decrease nociception by inhibiting substance P (SP) release, and that these effects are enhanced by inflammation. To evaluate SP release, we used microdialysis and neurokinin 1 receptor (NK1R) internalization in rat. ⋯ To determine the contribution of increased Y1 receptor-G protein coupling, we measured [(35)S]GTPγS binding simulated by [Leu(31), Pro(34)]-NPY in mouse dorsal horn. CFA inflammation increased the affinity of Y1 receptor G-protein coupling. We conclude that Y1 receptors contribute to the anti-hyperalgesic effects of NPY by mediating the inhibition of SP release, and that Y1 receptor signaling in the dorsal horn is enhanced during inflammatory nociception.
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This study investigates the role of phonology in reading logographic Chinese. Specifically, whether phonological information is obligatorily activated in reading Chinese two-character compounds was examined using the masked-priming paradigm with event-related potential (ERP) recordings. Twenty-two native Cantonese Chinese speakers participated in a lexical decision experiment. ⋯ In addition, attenuation in ERP amplitudes was found in the Semantic-related condition in the window of 250-500 ms (N400). However, no significant results (neither behavioral nor ERP) were found in the Syllable-related condition. These results suggest that phonological activation is not mandatory and the role of phonology is minimal at best in reading Chinese two-character compounds.
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During a study of spinal cord injury (SCI), mice in our colony were treated with the anthelmintic fenbendazole to treat pinworms detected in other mice not involved in the study. As this was not part of the original experimental design, we subsequently compared pathological and functional outcomes of SCI in female C57BL/6 mice who received fenbendazole (150 ppm, 8 mg/kg body weight/day) for 4 weeks prior to moderate contusive SCI (50 kdyn force) as compared to mice on the same diet without added fenbendazole. The fenbendazole-treated mice exhibited improved locomotor function, determined using the Basso mouse scale, as well as improved tissue sparing following contusive SCI. ⋯ Autoantibodies produced following SCI contribute to the axon damage and locomotor deficits. Fenbendazole pretreatment reduced the injury-induced CD45R-positive B cell signal intensity and IgG immunoreactivity at the lesion epicenter 6 weeks after contusive SCI in mice, consistent with a possible effect on the immune response to the injury. Fenbendazole and related benzimadole antihelmintics are FDA approved, exhibit minimal toxicity, and represent a novel group of potential therapeutics targeting secondary mechanisms following SCI.
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Autophagy is responsible for the bulk degradation of cytoplasmic contents including organelles through the lysosomal machinery. Neonatal hypoxia-ischemia (HI) causes cell death in the brain by caspase-dependent and independent pathways. Ischemic insults also increase the formation of autophagosomes and activate autophagy. ⋯ In the hippocampus, both HI males and all females had increased numbers of autolysosomes suggesting activation of autophagy but with no effect on lysosome numbers, or Beclin-1 or LC3B protein levels. Males and females had increases in caspase 3/7 activity in their cortices and hippocampi following HI, though the increases were three to sixfold greater in females. The present data: (a) confirm greater caspase activation in the brains of females compared to males following HI; (b) suggest a partial failure to degrade LC3B-II protein in cortical but not hippocampal lysosomes of females as compared to males following neonatal HI; (c) all females have greater basal autophagy activity than males which may protect cells against injury by increasing cell turnover and (d) demonstrate that autophagy pathways are disturbed in regional- and sex-specific patterns in the rat brain following neonatal HI.