Cytoskeleton Markers in the Spinal Cord and Mechanoreceptors of Thick-Toed Geckos after Prolonged Space Flights

Spaceflight may cause hypogravitational motor syndrome (HMS). However, the role of the nervous system in the formation of HMS remains poorly understood. The aim of this study was to estimate the effects of space flights on the cytoskeleton of the neuronal and glial cells in the spinal cord and mechanoreceptors in the toes of thick-toed geckos (Chondrodactylus turneri GRAY, 1864). Thick-toed geckos are able to maintain attachment and natural locomotion in weightlessness. Different types of mechanoreceptors have been described in the toes of geckos. After flight, neurofilament 200 immunoreactivity in mechanoreceptors was lower than in control. In some motor neurons of flight geckos, nonspecific pathomorphological changes were observed, but they were also detected in the control. No signs of gliosis were detected after spaceflight. Cytoskeleton markers adequately reflect changes in the cells of the nervous system. We suggest that geckos’ adhesion is controlled by the nervous system. Our study revealed no significant disturbances in the morphology of the spinal cord after the prolonged space flight, supporting the hypothesis that geckos compensate the alterations, characteristic for other mammals in weightlessness, by tactile stimulation.

Non-thermal plasma application enhances the recovery of transected sciatic nerves in rats

This experimental research aimed to investigate the effects of non-thermal plasma on nerve regeneration after transected nerve damage using the sciatic nerve in Wistar albino (A) rats. The experiments were performed on 27 Wistar A rats. The rats underwent surgery for right sciatic nerve exposure and were divided into three groups (each group, n = 9) according to sciatic nerve transected injury (SNTI) and non-thermal plasma application: a non-nerve damage (non-ND) group, a only nerve damage without non-thermal plasma application (ND) group, and a nerve damage with non-thermal plasma application (ND + NTP) group. Subsequent to SNTI and immediate suture, non-thermal plasma was administered three times per week for eight weeks. Evaluation for functional recovery was performed using the static sciatic index measured over the full treatment period of eight weeks. The sciatic nerve specimens were obtained after euthanasia and third day from the last non-thermal plasma application. The sciatic nerve tissues were subjected to histological analysis. Behavior analysis presented that the ND + NTP group showed improved static sciatic index compared with the nerve damage group. Histopathological findings demonstrated that the ND + NTP group had more dense Schwann cells and well-established continuity of nerve fibers, greater than the nerve damage group. Immunohistochemistry showed that the ND + NTP group had increased levels of markers for microtubule-associated protein 2 (MAP2), tau, S100 calcium-binding protein B, and neurofilament-200 and regulated the overexpression of CD68 and MAP2. These results indicated that non-thermal plasma enhanced the motor function and restored the neuronal structure by accelerating myelination and axonal regeneration. Additionally, non-thermal plasma was confirmed to have a positive effect on the recovery of SNTI in rats.

The peripheral and central expression of CGRP and IB4 in chronic pain from MIA-induced TMJOA rats

Background Chronic pain is the prevalent symptom that drives temporomandibular joint osteoarthritis (TMJOA) patients to ask for medical care, yet present alleviator remain less effective. This study aimed to investigate the actual TMJOA related chronic pain and the peripheral and central response in a TMJOA animal model. Methods This study firstly determined appropriate MIA dose based on pain behavior assessment with automated electronic von frey in rats. TMJOA pain correlated condylar structure alteration was evaluated by histological staining and Micro-CT. Then, the period of TMJOA chronic pain was further explored by assessing the alteration of glial fibrillary acidic protein (GFAP) positive astrocytes and ionized calcium binding adaptor molecule 1 (Iba1) positive microglia numbers in trigeminal spinal nucleus (TSN) and carrying out non-steroidal anti-inflammatory drugs (NSAIDS) pharmacological efficacy experiment. Finally, expression of neurofilament 200 (NF200), calcitonin gene-related peptide (CGRP), isolectin B4 (IB4) in trigeminal ganglion (TG) and TSN was detected by immunofluorescence. Results 1 mg/50 µl of MIA was considered as an appropriate dose. MIA induced gradual alteration of condylar structure correlated to TMJ mechanical allodynia. GFAP and IBA-1 positive cell numbers upregulated on 2, 3, 4 weeks after MIA injection. NSAIDS pharmacological efficacy disappeared on 10 days post MIA injection. Up-regulation of CGRP and IB4 was found in TG and TSN on 2 and 4 weeks, while expression of NF200 remained unchanged. Conclusion MIA induced TMJOA related chronic pain period emerges on 2 weeks after MIA injection. CGRP, IB4 positive afferent in both peripheral and central nervous system may involve in TMJOA related chronic pain in rats.

Genetic basis for developmental toxicity due to statin intake using embryonic stem cell differentiation model

The in utero environment is a key factor controlling the fate of the growing embryo. The deleterious effects of statins during the fetal development are still not very well understood. Data from animal studies and retrospective studies performed in pregnant women give conflicting reports. In this study, using in vitro differentiation model of embryonic stem cells, which mimic the differentiation process of the embryo, we have systematically exposed the cells to lipophilic statins, simvastatin, and atorvastatin at various doses and at critical times during differentiation. The analysis of key genes controlling the differentiation into ecto-, meso- and endodermal lineages was assessed by quantitative polymerase chain reaction. Our results show that genes of the mesodermal lineage were most sensitive to statins, leading to changes in the transcript levels of brachyury, Flk-1, Nkx2.5, and α/β-myosin heavy chain. In addition, changes to endodermal marker α-fetoprotein, along with ectodermal Nes and Neurofilament 200 kDa, imply that during early differentiation exposure to these drugs leads to altered signaling, which could translate to the congenital abnormalities seen in the heart and limbs.

Myelinated Afferents Are Involved in Pathology of the Spontaneous Electrical Activity and Mechanical Hyperalgesia of Myofascial Trigger Spots in Rats

Myofascial trigger points (MTrPs) are common causes for chronic pain. Myelinated afferents were considered to be related with muscular pain, and our clinical researches indicated they might participate in the pathology of MTrPs. Here, we applied myofascial trigger spots (MTrSs, equal to MTrPs in human) of rats to further investigate role of myelinated afferents. Modified pyridine-silver staining revealed more nerve endings at MTrSs than non-MTrSs (P<0.01), and immunohistochemistry with Neurofilament 200 indicated more myelinated afferents existed in MTrSs (P<0.01). Spontaneous electrical activity (SEA) recordings at MTrSs showed that specific block of myelinated afferents in sciatic nerve with tetrodotoxin (TTX) led to significantly decreased SEA (P<0.05). Behavioral assessment showed that mechanical pain thresholds (MPTs) of MTrSs were lower than those of non-MTrSs (P<0.01). Block of myelinated afferents by intramuscular TTX injection increased MPTs of MTrSs significantly (P<0.01), while MPTs of non-MTrSs first decreased (P<0.05) and then increased (P>0.05). 30 min after the injection, MPTs at MTrSs were significantly lower than those of non-MTrSs (P<0.01). Therefore, we concluded that proliferated myelinated afferents existed at MTrSs, which were closely related to pathology of SEA and mechanical hyperalgesia of MTrSs.