Changes in early endosomes in rat hippocampal CA1 neurons after transient global cerebral ischaemia.

Introduction: Transient global ischaemia in rodents causes selective loss of hippocampal CA1neurons, but the potential involvement of endocytic pathways has not been fully explored. The aim of this study was to investigate the changes in early endosomes in the CA1 subfield after ischaemia and reperfusion.

Materials And Methods: A four-vessel occlusion (4-VO) model was established in Wistar rats to induce 13 minutes of global cerebral ischaemia.

Roux-en-Y Gastric Bypass Improves Insulin Sensitivity in Obese Rats with Type 2 Diabetes Mellitus by Regulating the Grin3a/AMPK Signal Axis in Hypothalamic Arcuate Nucleus.

Objective: The objective of this study was to explore the effects and related mechanisms of Roux-en-Y gastric bypass (RYGB) on insulin sensitivity in obese rats with type 2 diabetes mellitus (T2DM).

Methods: The obese T2DM rat model was constructed by feeding a high-fat diet and injecting streptozotocin (STZ), and treated with RYGB. Grin3a shRNA was injected into the bilateral hypothalamic arcuate nucleus (ARC) to knockdown the Grin3a expression on T2DM rats.

A novel detection method for neuronal death indicates abnormalities in intracellular membranous components in neuronal cells that underwent delayed death.

Acute neuronal degeneration is always preceded under the light and electron microscopes by a stage called microvacuolation, which is characterized by a finely vacuolar alteration in the cytoplasm of the neurons destined to death. In this study, we reported a method for detecting neuronal death using two membrane-bound dyes, rhodamine R6 and DiOC(3), which may be associated with the so-called microvacuolation. This new method produced a spatiotemporally similar staining pattern to Fluoro-Jade B in kainic acid-damaged brains in mice.

The Association of lncRNA and mRNA Changes in Adipose Tissue with Improved Insulin Resistance in Type 2 Obese Diabetes Mellitus Rats after Roux-en-Y Gastric Bypass.

Objective: Roux-en-Y gastric bypass (RYGB) has shown good effects in improving obesity and type II diabetes mellitus (T2DM), but the underlying mechanisms remain unclear. This study explored the changes of related lncRNAs, mRNAs, and signaling pathways in white adipose tissue of T2DM rats after RYGB based on RNA-Seq sequencing, with the aim to provide a theoretical basis for RYGB treatment.

Methods: T2DM rat models were established by continuous feeding with a high-fat diet and injection of streptozotocin (STZ), after which they underwent RYGB or sham surgery.

Different changes in pre- and postsynaptic components in the hippocampal CA1 subfield after transient global cerebral ischemia.

To date, ischemia-induced damage to dendritic spines has attracted considerable attention, while the possible effects of ischemia on presynaptic components has received relatively less attention. To further examine ischemia-induced changes in pre- and postsynaptic specializations in the hippocampal CA1 subfield, we modeled global cerebral ischemia with two-stage 4-vessel-occlusion in rats, and found that three postsynaptic markers, microtubule-associated protein 2 (MAP2), postsynaptic density protein 95 (PSD95), and filamentous F-actin (F-actin), were all substantially decreased in the CA1 subfield after ischemia/reperfusion (I/R). Although no significant change was detected in synapsin I, a presynaptic marker, in the CA1 subfield at the protein level, confocal microscopy revealed that the number and size of synapsin I puncta were significantly changed in the CA1 stratum radiatum after I/R.

What can cerebrospinal fluid testing and brain autopsies tell us about viral neuroinvasion of SARS-CoV-2.

To provide instructive clues for clinical practice and further research of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection, we analyzed the existing literature on viral neuroinvasion of SARS-CoV-2 in coronavirus disease 2019 (COVID-19) patients. To date, SARS-CoV-2 has been detected in the cerebrospinal fluid (CSF) or brain parenchyma in quite a few patients, which provide undeniable evidence for the neuroinvasive potential of this novel coronavirus. In contrast with the cerebrum and cerebellum, the detection rate of SARS-CoV-2 was higher in the olfactory system and the brainstem, both of which also showed severe microgliosis and lymphocytic infiltrations.

Neurological involvement in the respiratory manifestations of COVID-19 patients.

The peculiar features of coronavirus disease 2019 (COVID-19), caused by Severe Acute Respiratory Syndrome Coronavirus-2 (SARS-CoV-2), are challenging the current biological knowledge. Early in Feb, 2020, we suggested that SARS-CoV-2 may possess neuroinvasive potential similar to that of many other coronaviruses. Since then, a variety of neurological manifestations have been associated with SARS-CoV-2 infection, which was supported in some patients with neuroimaging and/or cerebrospinal fluid tests.

Evidence of central nervous system infection and neuroinvasive routes, as well as neurological involvement, in the lethality of SARS-CoV-2 infection.

The outbreak of coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2), has become a significant and urgent threat to global health. This review provided strong support for central nervous system (CNS) infection with SARS-CoV-2 and shed light on the neurological mechanism underlying the lethality of SARS-CoV-2 infection. Among the published data, only 1.

The possible impairment of respiratory-related neural loops may be associated with the silent pneumonia induced by SARS-CoV-2.

As compared to many other viral pulmonary infections, there existed several peculiar manifestations in the COVID-19 patients, including the "silence" of pneumonia in both mild and severe cases and a long intensive care unit stay for those requiring invasive mechanical ventilation. Similar silent pneumonia has been documented in the infectioninduced by H5N1 influenza virus HK483 and was found to result from the direct attack of the virus on the bronchopulmonary C-fibers at the early stage and the final infection in the brainstem at the late stage. The long stay of critical patients in the intensive care unit is possibly due to the depression of central respiratory drive, which resulted in the failure to wean from the mechanic ventilation.

The temporal and spatial changes of microtubule cytoskeleton in the CA1 stratum radiatum following global transient ischemia.

The down-regulation of microtubule proteins has been widely documented in the ischemic brain, but the temporal or spatial alteration of microtubules has not been systematically investigated in the vulnerable areas after ischemia. By examining the stability and distribution of microtubules following transient global ischemia, we found that the biomarkers of stable microtubules, MAP2 and acetylated α-tubulin, became significantly down-regulated in the CA1 stratum radiatum of rat hippocampus and that the neuron-specific microtubule protein, class III β-tubulin, was progressively decreased in the same region. Surprisingly, pan-β-tubulin, which is expressed at a low level in glial cells under physiological conditions, was significantly increased in reactive astrocytes after ischemia.

The temporal and spatial changes of actin cytoskeleton in the hippocampal CA1 neurons following transient global ischemia.

Transient global ischemia usually results in delayed neuronal death in selective brain regions, prior to which a rapid loss of dendritic spines has been widely reported in these regions. Dendritic spines are characterized by a highly branched meshwork of actin cytoskeleton (F-actin), which is extremely vulnerable to the ATP-depleted conditions such as hypoxia/ischemia. However, the ischemia-induced changes of F-actin are still not clarified in the vulnerable brain areas.

The effects of epothilone D on microtubule degradation and delayed neuronal death in the hippocampus following transient global ischemia.

Disruption of microtubule cytoskeleton plays an important role during the evolution of brain damage after transient cerebral ischemia. However, it is still unclear whether microtubule-stabilizing drugs such as epothilone D (EpoD) have a neuroprotective action against the ischemia-induced brain injury. This study examined the effects of pre- and postischemic treatment with different doses of EpoD on the microtubule damage and the delayed neuronal death in the hippocampal CA1 subfield on day 2 following reperfusion after 13-min global cerebral ischemia.

The effects of calcineurin inhibitor FK506 on actin cytoskeleton, neuronal survival and glial reactions after pilocarpine-induced status epilepticus in mice.

After status epilepticus (SE), actin cytoskeleton (F-actin) becomes progressively deconstructed in the hippocampus, which is consistent with the delayed pyramidal cell death in both time course and spatial distribution. A variety of experiments show that calcineurin inhibitors such as FK506 are able to inhibit the SE-induced actin depolymerization. However, it is still unclear what changes happen to the F-actin in the epileptic brain after FK506 treatment.

The unique organization of filamentous actin in the medullary canal of the medulla oblongata.

In the central canal, F-actin is predominantly localized in the apical region, forming a ring-like structure around the circumference of the lumen. However, an exception is found in the medulla oblongata, where the apical F-actin becomes interrupted in the ventral aspect of the canal. To clarify the precise localization of F-actin, the fluorescence signals for F-actin were converted to the peroxidase/DAB reaction products in this study by a phalloidin-based ultrastructural technique, which demonstrated that F-actin is located mainly in the microvilli and terminal webs in the ependymocytes.

Pilocarpine-induced epilepsy is associated with actin cytoskeleton reorganization in the mossy fiber-CA3 synapses.

Dramatic structural changes have been demonstrated in the mossy fiber-CA3 synapses in the post status epilepticus (SE) animals, suggesting a potential reorganization of filamentous actin (F-actin) network occurring in the hippocampus. However, until now the long-term effects of SE on the synaptic F-actin have still not been reported. In this study, phalloidin labeling combined with confocal microscopy and protein analyses were adopted to investigate the effects of pilocarpine treatment on the F-actin in the C57BL/6 mice.

The rearrangement of filamentous actin in mossy fiber synapses in pentylenetetrazol-kindled C57BL/6 mice.

Chemical kindling, as an experimental model of epileptogenesis, is induced by repetitive administration of subconvulsive amount of excitatory drugs. Kindled mice do not typically display spontaneous recurrent seizures, but are instead characterized by enhanced seizure susceptibility to convulsive stimulations. In order to provide insights into the aberrant synaptic plasticity during kindling, this study investigated the effect of pentylenetetrazol (PTZ) kindling on filamentous actin (F-actin) in mossy fiber synapses in C57BL/6 mice.