14 results about "Glutamatergic" patented technology

The invention relates to the technical field of nerve cell marking and regulation and control, in particular to a nerve cell living body selective protein modification probe capable of penetrating a blood brain barrier and application of the nerve cell living body selective protein modification probe. The protein body part specifically targets a living glutamic acid energetic neuron cell membrane, the protein body part and / or a modified part thereof can regulate and control the function of the glutamic acid energetic neuron, and a coding sequence of the protein body part comprises a sequence as shown in SEQ ID NO: 1 or a sequence having at least 85% identity with the SEQ ID NO: 1. The protein modified probe provided by the invention provides a new feasible thought for developing in-vivo nerve cell selective markers and regulation tools which are non-gene transfection of blood brain barrier penetration, are high in biological safety, are more stable and are easy to obtain and have nerve cell specific type selectivity.

To provide artificial expression constructs for selectively modulating gene expression in selected central nervous system cell types.SOLUTION: As target central nervous system cell populations, there are neocortical glutamatergic layer 5 neurons, for example, neocortical glutamatergic layer 5 extratelencephalic-projecting (L5 ET) neurons. In certain applications, aspects of the present disclosure can be used to deliver therapeutic payloads to upper motor neurons associated with, for example, Amyotrophic Lateral Sclerosis (ALS) or other neurodegenerative diseases in which L5 ET neurons are involved.SELECTED DRAWING: Figure 4B

The present invention provides a method and device for treating motor dysfunction after spinal cord injury by targeting the lateral hypothalamus (LHA). Specifically, in the present invention, by performing electrical stimulation on glutamatergic neurons in the dorsal part of the caudal LHA, the LHA-PnO-spinal cord circuit is activated to modulate limb motor function in patients with spinal cord injury. The method of the present invention has small side effects and can serve as a potential approach for restoring voluntary motor function in patients with spinal cord injury.

The invention relates to a composition for inducing reprogramming of mesenchymal stem cells and application of the composition, and belongs to the technical field of biological medicine. According to the present invention, it is firstly found that the composition of CHIR99021, Y27632, SB431542 and purmorphamine can induce the reprogramming of mesenchymal stem cells into cholinergic motor neurons and glutamic acid energy interneurons, the cholinergic motor neurons are mainly adopted, and the induction efficiency of the composition is the highest; and inoculating the mesenchymal stem cells onto the silk fibroin scaffold, adding CYSP for induced culture, and finding that the induced neuron-like cells wrap the periphery of silk fibroin fibers to form a transplantable neuron network. When the neural network is transplanted into a spinal cord injury rat model, the deposition of collagen in a spinal cord injury cavity of a rat transplanted with the neural network is reduced, host neurons are saved, nerve fiber regeneration is promoted, and the injured spinal cord is repaired.

The application discloses application of human amniotic epithelial stem cells in preparation of a medicine for treating depressive diseases. The human amniotic epithelial stem cells are obtained by mechanically separating the inner surface amnion of discarded placental tissue, and then subjected to trypsin digestion, centrifugation, resuspension and harvesting in sequence after washing; and a human amniotic epithelial stem cell scheme for treating depression; the cells are widely sourced, free of ethical controversy, low in immunogenicity and non-tumorigenic, and provide a new safe and effective approach for treating depression; the cell preparation can be administered through intravenous injection, intrathecal injection or nasal delivery, and the mechanism of action is to inhibit the overactivation of glial cells, reduce the depressive-related neuroinflammatory response, and thus improve the neuronal microenvironment. The application can effectively promote hippocampal neurogenesis (increase in DCX positive cells), regulate 5-hydroxytryptaminergic neurons and glutamatergic neuron activity, restore the steady state of neural networks, and significantly improve the depressive behavior of model mice.

Methods of use, pharmaceutical formulations, and labeled versions of compounds are provided of compounds that penetrate the blood-brain barrier and influence the balance of excitatory versus inhibitory neurotransmission by enantiomer selective modulation of glutamate and GABA metabolism. In some embodiments, a glutamatergic false neurotransmitter is S-2-methylglutamate (S-2MeGlu). In some embodiments a GABAergic false neurotransmitters is R-4 aminopentanomic acid (4APA) or S-4 aminopentanomic acid (S-4APA), with high penetration of the blood brain barrier and low toxicity, therein providing useful pharmacologic or imaging agents.

Artificial expression constructs for modulating gene expression in targeted central nervous system cell types are described. The artificial expression constructs can be used to express synthetic genes or modify gene expression in forebrain glutamatergic neurons.

The invention provides a method and equipment for treating dyskinesia after spinal cord injury by targeting lateral hypothalamus LHA. Specifically, an LHA-PnO-spinal cord loop is activated by performing electrical stimulation on glutamicergic neurons on the back side of the tail of the outer hypothalamus, and the limb movement function of a patient with spinal cord injury is adjusted. The method is small in side effect and can be used as a potential means for the spinal cord injury patient to recover the autonomous movement function.

The application discloses an olfactory training system for activating a motor-olfactory-hippocampal neural network and application, the system comprises a plurality of different odor sources, the odor source is used for alternating olfactory stimulation to stroke patients, so as to improve the cognitive function and / or olfactory function of the patient. The application firstly discloses that the function connection of the motor-olfactory-cognitive brain area is disordered after stroke, the function of the VIP neuron of the motor cortex (MO) around the infarction is inhibited; the VIP neuron of the MO region dominates the GABA neuron of the dorsal peripeduncular area (DP) through an inhibitory pathway, activating the pathway can remove the inhibition of the glutamatergic pyramidal neuron of the DP, enhance the excitatory input to the hippocampal CA3 region, and restore the olfaction and spatial memory. The application proves that the structured olfactory training can activate the loop, and significantly improve the cognitive function of the stroke patient. The application provides a simple and non-invasive stroke rehabilitation strategy.

This pest control composition contains a component (1) and a component (2), wherein: the component (1) is an isoxazoline-based or metadiamide-based compound; and the component (2) is a phenylpyrazole-based compound, a compound acting as a mitochondrial electron transfer system complex III inhibitor, a compound acting as a glutamic-acid-activated chlorine ion channel allosteric modulator, a compound acting as a nicotinic acetylcholine receptor competitive modulator, a compound acting as a chord organ TRPV channel modulator, a compound acting as an acetyl CoA carboxylase inhibitor, a pyrethroid-based compound, benzpyrimoxan, fluhexafon, tyclopyrazoflor, indazapyroxamet, tiapyrachlor, flupyroxystrobin, or cybenzoxasulfyl.

The invention discloses a method for promoting neuronal maturation by using a transcription factor MSC and application thereof. The method comprises the following steps: overexpressing the transcription factor MSC in glutamic acid energetic neurons; the transcription factor MSC has a nucleotide sequence as shown in SEQ ID NO: 1. According to the method, through overexpression of the transcription factor MSC, the maturation speed of nerve cells can be remarkably increased, the maturity of mature neurons is improved, and therefore a more efficient tool is provided for research and treatment of nervous system diseases.

The invention discloses application of human amniotic epithelial stem cells in preparation of drugs for treating depression diseases. The human amniotic epithelial stem cells are harvested after being subjected to pancreatin digestion, centrifugation and resuspension in sequence after being cleaned by mechanically separating an amnion on the inner surface of a discarded in-vitro placenta tissue; and a human amniotic epithelial stem cell regimen for the treatment of depression; the cell is wide in source, free of ethical dispute, low in immunogenicity and free of tumorigenicity, and a novel safe and effective way is provided for depression treatment. The cell preparation can be administered through intravenous injection, intrathecal injection or nasal delivery, and the action mechanism of the cell preparation is that the cell preparation can inhibit excessive activation of glial cells and relieve depression-related neuroinflammatory response, so that the neuron microenvironment is improved. The traditional Chinese medicine composition can effectively promote hippocampal neurogenesis (DCX positive cell increase and the like), regulate the activity of 5-hydroxytryptamine neurons and glutamic acid neurons to restore the steady state of a neural network, and remarkably improve the depression-like behavior of a model mouse.

The invention provides a mutant of gtf1 gene coding glycosyl transferase and application of the mutant in preparation of NMN, belongs to the technical field of molecular biology, and particularly provides the mutant of the gtf1 gene coding glycosyl transferase, the amino acid mutation site is that the 150th lysine of the amino acid sequence SEQ ID NO.3 of the gtf1 gene coding glycosyl transferase is mutated into glutamic acid; the invention provides a mutant, a coding gene of the mutant is shown as SEQ ID NO.2, a recombinant bacterium containing the coding gene of the mutant is further provided, and it is found for the first time that the 150th lysine of gtf1 gene coding glycosyl transferase in escherichia coli is mutated into glutamic acid, generation of by-products can be reduced, and the yield of NMN can be increased.