Neuroscience
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The capacity to identify unanticipated abnormal cues in a natural scene is vital for animal survival. Stimulus-specific adaptation (SSA) has been considered the neuronal correlate for deviance detection. There have been comprehensive assessments of SSA in the frequency domain along the ascending auditory pathway, but only little attention given to deviance detection in the spatial domain. ⋯ The variability in neuronal spatial discriminability among the TRN population was directly related to response difference (RD) but not variance; meanwhile, further analyses attributed higher spatial sensitivity at deviant locations to larger RD. Astonishingly, a significant correlation was found between the amount of adaptation and deviant discriminability. Collectively, our results suggest that adaptation facilitates rare location discrimination by sharpening the response gap between two locations.
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The polypeptide ghrelin is an endogenous ligand at the growth hormone secretagogue receptor 1a. To ghrelin multiple functions have been ascribed including promotion of gastrointestinal motility. Postprandial ghrelin levels have been reported to be reduced in patients suffering from Parkinson disease (PD). ⋯ Whereas the protective effects of acylated ghrelin required receptor binding, effects of the unacylated form remained unaffected by treatment with a ghrelin receptor antagonist. Importantly, inhibition of ghrelin O-acyltransferase failed to reduce the activity of unacylated ghrelin. Overall, our data suggest that both acylated and unacylated ghrelin afford protection to dopamine neurons but through mechanisms that only partially overlap.
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Bradykinin (BK), a component of the kallikrein-kininogen-kinin system exerts multiple effects via B1 and B2 receptor activation. In the cardiovascular system, bradykinin has cardioprotective and vasodilator properties. We investigated the effect of BK on cardiac-projecting neurons of nucleus ambiguus, a key site for the parasympathetic cardiac regulation. ⋯ BK produced a dose-dependent depolarization of nucleus ambiguus neurons, which was prevented by the B2 receptor antagonist. In vivo studies indicate that microinjection of BK into nucleus ambiguus elicited bradycardia in conscious rats via B2 receptors. In summary, in cardiac vagal neurons of nucleus ambiguus, BK activates B2 receptors promoting Ca2+ influx and Ca2+ release from endoplasmic reticulum, and membrane depolarization; these effects are translated in vivo by bradycardia.
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Little is known about how the central nervous system prepares postural responses differently in anticipated compared to non-anticipated perturbations. To investigate this, participants were exposed to translational and rotational perturbations presented in a blocked (anticipated) and a random (non-anticipated) design. The preparatory setting ('central set') was measured by H-reflexes, motor-evoked potentials (MEPs), and short-interval intracortical inhibition (SICI) shortly before perturbation onset in the soleus of 15 healthy adults. ⋯ As the SLR and MLR are organized at the spinal and the LLR at the cortical level, the preparatory setting seems to mainly influence cortically mediated postural responses. However, the modulation of the H-reflex before anticipated perturbations indicates that supraspinal centers adjusted Ia-afferent transmission for the soleus in a perturbation-specific manner. Intracortical inhibition was also modulated but differentiates to a lesser extent only between perturbation conditions and unperturbed stance.
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Bumetanide is a selective inhibitor of the Na+-K+-Cl--co-transporter 1(NKCC1). We studied whether bumetanide could affect axonal growth and behavioral outcome in stroke rats. Adult male Wistar rats were randomly assigned to four groups: sham-operated rats treated with vehicle or bumetanide, and ischemic rats treated with vehicle or bumetanide. ⋯ Bumetanide treatment also decreased the expressions of NKCC1 and Nogo-A, increased the expressions of KCC2 and BDNF in the perilesional cortex and enhanced the synaptic plasticity in the denervated cervical spinal cord after cerebral ischemia. The behavioral performance of ischemic rats was significantly improved by bumetanide. In conclusion, bumetanide promoted post-stroke axonal sprouting together accompanied by an improved behavioral outcome possibly through restoring and maintaining neuronal chloride homeostasis and creating a recovery-promoting microenvironment by overcoming the axonal growth inhibition encountered after cerebral ischemia in rats.