Neuroscience letters
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Neuroscience letters · Sep 2019
ReviewGene editing based hearing impairment research and therapeutics.
Hearing impairment affects 1 in 500 newborns worldwide and nearly one out of three people over the age of 65 (WHO, 2019). Hereditary hearing loss is the most common type of congenital deafness; genetic factors also affect deafness susceptibility. ⋯ CRISPR-Cas9 and base editors (BEs) are newly developed gene editing technologies that can facilitate gene studies in the inner ear and provide therapeutic approaches for hearing impairment. Here, we present recent applications of gene editing in the inner ear.
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Neuroscience letters · Aug 2019
MiR-34a is differentially expressed in dorsal root ganglia in a rat model of chronic neuropathic pain.
Recent evidence shows that numerous microRNAs (miRNAs) regulate pain-related genes in chronic pain. The aim of the present study was to further explore the regulation of miRNAs and their effect on the expression of pain-associated target genes in experimental neuropathic pain. ⋯ Peripheral mononeuropathic pain in rats was associated with distinct alterations of miRNA expression in the ipsilateral DRG. Notably, miR-34a was time-dependently down regulated. We validated SCN2B and VAMP-2 as new targets of miR-34a. While SCN2B expression was only marginally altered, VAMP-2 expression was increased. The present study underlines that the induction and maintenance of neuropathic pain is accompanied by expression changes of miRNAs in the peripheral nervous system, adding several previously unreported miRNAs, including miR-34a.
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Neuroscience letters · Aug 2019
The relationship between sensitivity to pain and conditioned pain modulation in healthy people.
The relationship between sensitivity to pain and conditioned pain modulation (CPM) - a paradigm reflecting the activity of the endogenous descending analgesic system - is still unclear. This study aimed at investigating CPM magnitude in two distinct subgroups of healthy subjects, presenting low vs. high sensitivity to pain (LSP vs. HSP, respectively), by employing two different thermal paradigms of CPM. ⋯ These findings show that regardless of the thermal CPM paradigm employed, healthy individuals exhibiting low sensitivity to pain have a low pain inhibition profile and vice-versa. It is suggested that in healthy subjects, pain sensitivity predisposes the magnitude of CPM and not the other way around.
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Neuroscience letters · Aug 2019
EEG signal based classification before and after combined Yoga and Sudarshan Kriya.
Nowadays, the style of living is restless and busy which has resulted in increased stress among many people. Stress causes various mental and health illness such as depression, anxiety, mood disorders, and aggressive behavior. Yoga and Sudarshan Kriya (SK) meditation are healthy ways to eradicate stress from people's lives. ⋯ Further, Artificial Neural Network (ANN) has been applied on aforementioned statistical parameters to classify subjects as meditators and non-meditators. The experimental results indicated that the proposed method achieved 87.2% accuracy for classification and could be further extended to construct an accurate classification system for detection of meditators and non-meditators. This study forms a scientific foundation to encourage the use of meditation in clinical practices.
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Neuroscience letters · Aug 2019
Connexin 43 contributes to temporomandibular joint inflammation induced-hypernociception via sodium channel 1.7 in trigeminal ganglion.
We previously demonstrated that sodium channel 1.7 (Nav1.7) in trigeminal ganglion (TG) was a critical factor in temporomandibular joint (TMJ) inflammation-induced hypernociception, but the mechanism underlying inflammation-induced upregulation of Nav1.7 remained unclear. Glial-neuron interaction plays a critical role in pain process and connexin 43 (Cx43), a gap junction protein expressed in satellite glial cells (SGCs) has been shown to play an important role in several pain models. In the present study, we investigate the role of Cx43 in TMJ inflammation-induced hypernociception and its possible impact on neuronal Nav1.7. ⋯ The expression of Cx43, glial fibrillary acidic protein (GFAP), and Nav1.7 increased greatly compared with controls. In addition, pretreatment with Cx43 blockers in TMJ-inflamed rats could alleviate mechanical hypernociception, inhibit SGCs activation and IL-1βrelease, and thus block the upregulation of Nav1.7. These findings indicate that the propagation of SGCs activation via Cx43 plays a critical role in Nav1.7-involved mechanical hypernociception induced by TMJ inflammation.