The invention provides a method of modulating electrophysiological activity of an excitable cell. The method involves causing exogenous expression of a glycine receptor (GlyR) protein in an excitable cell of a subject. Thereafter, the excitable cell is exposed to an allosteric modulator of the GlyR protein. Modulation of the exogenous GlyR protein (an ion channel) in response to the allosteric modulator modulates the electrophy-stological activity of the excitable cell. The method can be used to control pain in a subject. The invention further provides a replication-defective HSV vector comprising an expression cassette encoding a GlyR protein, stocks and pharmaceutical compositions containing such vectors, and a transgenic animal.

The present invention relates to: A schizophrenia animal model wherein the model is a mouse in which an anoctamin 1 (ANO1) gene is knocked out in cholinergic neurons of a medial habenula; and a preparation method therefor and the like. The schizophrenia animal model according to the present invention targets the medial habenula which is brain tissue playing a major role in the pathogenesis of schizophrenia, and it has been confirmed that when the ANO1 gene is specifically knocked out in the cholinergic neurons of the medial habenula, positive, negative and cognitive symptoms of schizophrenia are observed, thereby confirming that schizophrenia has been induced. Therefore, the animal model of the present invention is expected to be effectively useful in schizophrenia pathogenesis research and therapeutic agent development and screening.

The present disclosure is directed to a method of treating neurological disorder comprising measuring c-reactive protein in a patient and peripherally administering to the patient a DN-TNF polypeptide that inhibits the activity of soluble TNF-but not transmembrane TNF-.

Provided are a posttraumatic stress disorder (PTSD) animal model in which dopamine receptor subtype 4 (D4R) is damaged or deficient, a method for preparing the same, a method for screening a drug for treating PTSD using the same, and a pharmaceutical composition for treating PTSD comprising a drug detected by the screening method. As it is identified that a specific type of dopamine receptor is associated with a mechanism for fear memory expression induced by long-term depression (LTD), the understanding of pathogenesis of PTSD may be heightened, the animal model exhibiting similar clinical conditions of PTSD and the method for preparing the same may be applied in analyses for stability and effectiveness of a therapeutic agent for PTSD and screening of a therapeutic drug. Further, an agonist of D4R contained in the composition has been approved by the US FDA and clinically used for psychiatric diseases such as schizophrenia, and thus may be immediately used for clinical applications for PTSD symptoms.

The present invention provides a suppression type antisense oligonucleotide targeting TDP-43 mRNA, containing a nucleotide sequence complementary to a sequence consisting of at least 10 continuous nucleotides in a nucleotide sequence shown in any of SEQ ID NOs: 2-4, and a promotion type antisense oligonucleotide targeting TDP-43 mRNA, containing a nucleotide sequence complementary to a sequence consisting of at least 10 continuous nucleotides in a nucleotide sequence shown in SEQ ID NO: 5.

Provided herein, in some embodiments, are methods for modulating expression and/or activity of transient receptor potential cation channel subfamily C, member 3 (TRPC3), as well as methods of treating Alzheimer's disease.

Method for controlling for the appearance of seizures in the mammalian brain comprising modifying the abundance of a specific miRNA-miR-211, for uses in preventing seizures and providing a model system to examine the effect of a drug or a treatment to seizures.

Disclosed are a protein and a gene each of which is a factor involved in latent infection with a herpesvirus. An antibody against the factor was detected in approximately 50% of patients suffering from mental disorders, whereas the antibody was hardly detected in healthy persons. Further, a mouse having SITH-1 introduced therein developed a mental disorder such as a manic-depressive illness or depression-like disorder. Based on these findings, it is possible to provide a method for objectively determining a mental disorder and an animal model of a mental disorder.

The present invention relates to the engineering an animal model, preferably mammalian models, more preferably a rat model representing Charcot-Marie-Tooth disease 2A (CMT2A) harboring the p.Arg364Trp or p.His361Tyr Mfn2 mutation, whose human counterpart results in a severe, early-onset axonal neuropathy. A model having the p.Arg364Trp Mfn2 mutation is based on a mutation made using zinc finger endonuclease technology in fertilized rat eggs. Cohorts of mutants and wild type littermates were characterized behaviorally and shown to develop multiple motor deficits that worsened over time. Separate cohorts of mutant and wild type rats sacrificed at 7, 40, and 48 weeks and analyzed by light microscopy showed a reduced density of myelinated axons and active axonal degeneration in distal but not proximal nerves, as well as axonal degeneration in the fasciculus gracilis of the cervical spinal cord at 40 and 48 weeks. These findings were not present in the 7-week-old cohort of Mfn2 mutants, or in wild type rats at 7 or 40 weeks. A model having the p.His361Tyr Mfn2 mutation is based on a mutation made using CRISPR/Cas9 gene editing technology. This mutation showed abnormalities in gait dynamics at 8 weeks and a lengthening of the gait cycle at 16 weeks. A genetically authentic animal model for CMT2A developing a progressive axonal neuropathy is a valuable tool for examining the pathogenesis and treatment of CMT2A.

Methods for producing new neurons in the brain in vivo are provided according to aspects of the present invention which include introducing NeuroD1 into a glial cell, particularly into a reactive astrocyte or NG2 cell, thereby converting the reactive glial cell to a neuron. Methods of producing a neuronal phenotype in a glial cell are provided according to aspects of the present invention which include expressing exogenous NeuroD1 in the glial cell, wherein expressing exogenous NeuroD1 includes delivering an expression vector, such as a viral expression vector, including a nucleic acid encoding the exogenous NeuroD1 to the glial cell.