Neuroscience
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In the present study we investigated the effects of anodal transcranial direct current stimulation over the auditory cortex (AC) on the perception of rapidly changing acoustic cues. For this purpose, in 15 native German speakers the left or right AC was separately stimulated while participants performed a between-channel gap detection task. ⋯ Our data indicate a left hemispheric dominance for the processing of rapid temporal cues in auditory non-speech sounds. Moreover, we demonstrate the ability of non-invasive brain stimulation to change human temporal information processing in the auditory domain.
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Melatonin is a neurohormone associated with circadian rhythms. A diurnal rhythm in olfactory sensitivity has been previously reported and melatonin receptor mRNAs have been observed in the olfactory bulb, but the effects of melatonin in the olfactory bulb have not been explored. First, we corroborated data from a previous study that identified melatonin receptor messenger RNAs in the olfactory bulb. ⋯ Via qPCR, we observed that messenger RNAs encoding melatonin receptors and melatonin biosynthesis enzymes fluctuated in the olfactory bulb across 24h. Together, these data show that melatonin receptors are present in the olfactory bulb and likely affect olfactory function. Additionally, these data suggest that melatonin may be locally synthesized in the olfactory bulb.
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Precise regulation of the chloride homeostasis crucially determines the action of inhibitory transmitters GABA and glycine and thereby endows neurons or even discrete neuronal compartments with distinct physiological responses to the same transmitters. In mammals, the signaling mediated by GABAA/glycine receptors shifts during early postnatal life from depolarization to hyperpolarization, due to delayed maturation of the chloride homeostasis system. While the activity of the secondary active, K(+)-Cl(-)-extruding cotransporter KCC2, renders GABA/glycine hyperpolarizing in auditory brainstem nuclei of altricial rodents, the mechanisms contributing to the initially depolarizing transmembrane gradient for Cl(-) in respective neurons remained unknown. ⋯ Our data identify the 1Na(+):1K(+):2Cl(-) cotransporter 1 (NKCC1) as the major Cl(-)-loader responsible for depolarizing action of GABA/glycine at postnatal days 3-5 (P3-5). Extracellular GABA/muscimol elicited calcium signaling through R-, L-, and T-type channels, which was dependent on bumetanide- and [Na(+)]e-sensitive Cl(-) accumulation. The "adult like", low intracellular Cl(-) concentration is established during the second postnatal week, through a mechanism engaging the NKCC1-down regulation between P5 and P15 and ongoing KCC2-mediated Cl(-)-extrusion.
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It is important to clarify the neural mechanisms underlying fatigue sensation. There have been several studies which identified brain regions in which the level of the neural activities was correlated with the subjective level of fatigue. However, the neural activity evoked when we evaluate our level of fatigue may not be related to the subjective level of fatigue. ⋯ The proportion of participants in whom ECDs were observed in the PCC in the evaluation session was significantly higher than that in the control session (McNemar test). In addition, the intensities of the ECDs were positively associated with the extent to which the participants successfully evaluated the fatigue in their right hand in the evaluation session. These data suggest that the PCC is involved in the neural substrates associated with self-evaluation of physical fatigue.
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Eugenol is a bioactive plant extract used as an analgesic agent in dentistry. The structural similarity of eugenol to cinnamaldehyde, an active ligand for transient receptor potential ankyrin 1 (TRPA1), suggests that eugenol might produce its effect via TRPA1, in addition to TRPV1 as we reported previously. In this study, we investigated the effect of eugenol on TRPA1, by fura-2-based calcium imaging and patch clamp recording in trigeminal ganglion neurons and in a heterologous expression system. ⋯ In addition, eugenol response was observed in trigeminal ganglion neurons from TRPV1 knockout mice and human embryonic kidney 293 cell lines that express human TRPA1, which was inhibited by TRPA1-specific antagonist HC-030031. Eugenol-evoked TRPA1 single channel activity and eugenol-induced TRPA1 currents were dose-dependent with EC50 of 261.5μM. In summary, these results demonstrate that the activation of TRPA1 might account for another molecular mechanism underlying the pharmacological action of eugenol.