Neuroscience
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The dorsal raphe nucleus (DRN) participates in stress responses and in mood regulation via its ascending release of serotonin (5-HT) onto neural circuits within the forebrain. Although the 5-HT DRN region is easily defined via 5-HT-expressing DRN neurons, the neuroarchitecture and microcircuitry that confer its multifunctionality have remained incompletely understood and have required further investigation. ⋯ Furthermore, corticosterone administration into male rats as a rodent model of depression induced significantly higher c-Fos expression in 5-HT3AR-positive GABAergic neurons compared to that in 5-HT neurons within the DRN. Taken together, our findings suggest that 5-HT3AR-positive GABAergic neurons in the DRN participate in responses to stress hormones in a rat model of depression.
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The pulvinar is a higher-order thalamic relay and a central component of the extrageniculate visual pathway, with input from the superior colliculus and visual cortex and output to all of visual cortex. Rodent pulvinar, more commonly called the lateral posterior nucleus (LP), consists of three highly-conserved subdivisions, and offers the advantage of simplicity in its study compared to more subdivided primate pulvinar. Little is known about receptive field properties of LP, let alone whether functional differences exist between different LP subdivisions, making it difficult to understand what visual information is relayed and what kinds of computations the pulvinar might support. ⋯ SIGNIFICANCE STATEMENT: The pulvinar has a perplexing role in visual cognition as no clear link has been found between the functional properties of its neurons and behavioral deficits that arise when it is damaged. The pulvinar, called the lateral posterior nucleus (LP) in rats, is a higher order thalamic relay with input from the superior colliculus and visual cortex and output to all of visual cortex. By characterizing single-cell response properties in anatomically distinct subdivisions we found two separate visual feature processing channels in the pulvinar, one in lateral LP related to higher speed processing which likely derives from superior colliculus input, and the other in rostromedial LP for motion processing derived through input from visual cortex.
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Vascular endothelial cells were activated during acute ischemic brain injury, which could induce neural progenitor cell proliferation and migration. However, the mechanism was still unknown. In the current study, we explored whether vascular endothelial cells promoted neural progenitor cell proliferation and whether migration occurs via exosome communication. ⋯ BrdU/nestin-positive cells in Exos group rats were significantly increased (p < 0.05) in the peri infarct area, the ipsilateral DG zone of the hippocampus, and the ventral sub-regions of SVZ when compared with the rats in the control group. Further, in vitro study demonstrated that neural progenitor cell proliferation and migration were activated after exosomes treatment, and cell apoptosis was attenuated compared to the control (p < 0.05). Our study suggested that exosomes should be essential for the reconstruction of neuronal vascular units and brain protection in an acute ischemic injured brain.
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Store-operated Ca2+ entry (SOCE) contributes to Ca2+ refilling of endoplasmic reticulum (ER), but also provides Ca2+ influx involved in physiological and pathological signalling functions. Upon depletion of Ca2+ store, the sensor protein stromal interaction molecule (STIM) activates Orai1, forming an ion-conducting pore highly selective for Ca2+. SOCE-associated regulatory factor (SARAF) associates with STIM1 to facilitate a slow form of Ca2+-dependent inactivation of SOCE or interacts with Orai1 to stimulate SOCE in STIM1-independent manner. ⋯ The expression of Stim1 and SARAF, mainly localised in NeuN-immunopositive neurons, was reduced in the ischemic cortex. Interestingly, neuroprotection by ischemic PC prevented the reduction of SARAF expression in the lesioned cortex and this could be interpreted as a compensatory mechanism to restore ER Ca2+ refilling in neurons in the absence of STIM1. Thus, preventing SARAF downregulation may represent a pivotal mechanism implicated in neuroprotection provided by ischemic PC and should be exploited as an original target for novel stroke therapies.
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The transition of neuronal burst firing from the interictal to ictal state contributes to seizure initiation in human temporal lobe epilepsy. The low-Mg2+ model of seizure is characterized by initial spontaneous interictal bursting events, which later developed into ictaform discharges. Both experimental and clinical studies point to a complex link between spreading depolarization (SD) and epileptiform field potentials (EFP), including SD-induced epileptic seizures. ⋯ In addition, SD significantly accelerated the transition from interictal to ictal state compared to the control tissues. Ictal activities after induction of SD exhibited a significantly longer duration. This study revealed that SD accelerates interictal-to-ictal transitions and facilitates development of ictaform discharges, possibly via the enhancement of neural synchronization, and points to the potential role of SD in seizure initiation.