Neuroscience
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Timing of Modulation of Corticospinal Excitability by Heartbeat Differs with Interoceptive Accuracy.
Interoceptive inputs are ascending information from the internal body. Cortical activities have been shown to be elicited by interoceptive inputs from the heartbeat at approximately 200-600 ms after the R wave, and sensory processing is modulated by the heartbeat within the time window. However, the influence of interoceptive inputs and their timing on corticospinal excitability has not yet been fully elucidated. ⋯ Conversely, we found a significant negative correlation between the modulation of corticospinal excitability at 400 ms after the R wave and interoceptive accuracy. These results indicated that the corticospinal excitability was modulated at 200-400 ms after the R wave (systolic phase) and that the timing of excitatory or inhibitory states in the corticospinal pathway differed with interoceptive accuracy. Although the neural mechanism remains unclear, these findings may aid in determining new factors influencing corticospinal excitability.
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Our choices are often informed by temporally integrating streams of sensory information. This has been well demonstrated in the visual and auditory domains, but the integration of tactile information over time has been less studied. We designed an active touch task in which participants explored a spheroid-shaped object to determine its inclination with respect to the horizontal plane (inclined to the left or the right). ⋯ The behavioral results were fit with a bounded accumulation model and an independent sampling model that assumes no sensory accumulation. The results of model fits favor an accumulation-to-bound mechanism and suggest that participants integrate the first 600 ms of 1800 ms-long stimuli. This means that the somatosensory system benefits from longer streams of information, although it does not make use of all available evidence.
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The fact that neurobiological research is reliant upon laboratory-reared rodents is well known. The following paper discusses this topic broadly, but also aims to highlight other species used in the study of the nervous system and the evolution of animal species usage from the end of World War II through recent investigations. ⋯ Such a limitation in animal species causes many difficulties in the development of new therapies for various neuropsychiatric diseases. Based on numerous scientific publications, the advantages of using a greater diversity of species in neuroscience and the disadvantages of focusing on mice and rats are presented.
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Synaptic plasticity, such as long term potentiation (LTP) and long term depression (LTD), underlies the cellular mechanism of learning and memory. Chemical-induced LTP (cLTP), which facilitates biochemical analysis of molecular changes in brain slices or neuronal cultures, has been accepted as an in vitro model to explore synaptic plasticity. cLTP, by either forskolin and rolipram (F&R) or glycine, is thought to be dependent on NMDA receptor. ⋯ Furthermore, an increased phosphorylation level of GluA1 at serine 845 by F&R-induced LTP rather than glycine-induced LTP was dependent on the activation of GluN2B, which is supported by the results from GluN2B antagonists, small interfering peptide and CRISPR-Cas9-mediated knock out of GluN2B. Taken together, we reveal the significant role of GluN2B in F&R-induced LTP, uncovering the role of GluN2B subunit of NMDA receptor in a specified cLTP.
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Ischemic postconditioning (PostC) is an endogenous neuroprotective strategy for cerebral ischemia induced by low activation of glutamate receptors. We have previously shown that the application of the mGluR1/5 agonist (S)-3,5-dihydroxyphenylglycine (DHPG) 5 min after 30 min of oxygen and glucose deprivation (OGD) reduces CA1 damage in organotypic hippocampal slices by activating the PI3K-Akt signalling pathway. In order to extend these data, we analysed the production of reactive oxygen species (ROS) and the glycogen synthase kinase 3β (GSK3β) signalling pathway. ⋯ This reduction was prevented by the PI3K inhibitor LY294002, indicating that there is a link between the PI3K/Akt pathway and the formation of ROS in the protective mechanisms of PostC. DHPG PostC also induces a transient increased in GSK3β phosphorylation and inactivation that is followed by nuclear accumulation of β-catenin, that probably lead to the up-regulation of neuroprotective genes. Our results propose GSK3β as new target for neuroprotection, therefore, we verified that the two GSK3β inhibitors N-(3-Chloro-4-methylphenyl)-5-(4-nitrophenyl)-1,3,4-oxadiazol-2-amine (TC-G 24) and LiCl are neuroprotective agents in OGD and also can be used as PostC agents.