15 results about "Inhibitory neuron" patented technology

The embodiment of the invention relates to the technical field of artificial intelligence, and discloses an image analysis method and device based on a pulse neural network, computer equipment and a computer readable storage medium, and the method comprises the steps: obtaining a to-be-analyzed image; inputting the to-be-analyzed image into a pulse neural network based on suppression neurons; the neural network comprises an SNN module based on convolution, an SNN module based on Transform, a pulse self-feedback suppression module and a reasoning module. The suppression pulse self-feedback module comprises at least one suppression neuron and is used for dynamically issuing suppression pulses to adjust the membrane potential state of surrounding excitation neurons; neurons of the pulse neural network carry out signal transmission through integer pulses. The neurons comprise an SNN module based on convolution, and excitation neurons and inhibition neurons in the SNN module based on Transform; and outputting an analysis result. By means of the mode, the model prediction precision is improved, and computing resources are remarkably reduced.

This invention provides a method, system, electronic device, and storage medium for analyzing the energy consumption of neural networks based on ion channel regulation. It constructs a neural network dynamics model containing excitatory and inhibitory neurons. The neuronal membrane potential dynamics equation is defined by a set of differential equations for various voltage-gated ion currents (fast sodium ion current, continuous sodium ion current, slow potassium ion current, etc.) and leakage current. By adjusting the unit area conductivity parameter and / or inactivation time constant parameter of the voltage-gated ion channels in the model, the external intervention effect is simulated. After obtaining membrane potential sequence data through simulation, the total energy consumption, synaptic energy consumption ratio, average discharge rate, and average synchronization rate between neurons of the model are calculated. Finally, a quantitative correlation model between parameter changes and the above indicators is established, clarifying the coupling effect of the target ion channel dynamics characteristics on the neural network discharge behavior pattern and energy metabolism.

The present invention relates generally to compositions and methods for modulating cell activity using multi-characteristic opsin proteins (MCOs). In addition, the present invention provides methods of treating conditions associated with dorsal root ganglion (DRG), anterior clasps cortex (ACC), or spinal cord activity, including neuropathic pain. Particular embodiments include methods of modulating an inhibitory pathway to inhibit chronic neuropathic pain. The method may use a photosensitive optogenetic actuator with inhibitory neuron specificity. Embodiments also include an optogenetic pain regulator device that can regulate the frequency and intensity of optogenetic stimulation.

This invention describes artificial expression constructs for regulating gene expression in target types of central nervous system cells. By using the artificial expression constructs of this disclosure, it is possible to express or modify the expression of synthetic genes in spinal motor neurons, including SpP1 spinal motor neurons, Parg spinal motor neurons, Ogdh1 spinal motor neurons, and ChAT spinal motor neurons; α motor neurons, including Chodl spinal motor neurons; γ motor neurons; spinal excitatory motor neurons, including Mafa excitatory neurons, Esrrg Trhr excitatory neurons, and Slc17a6 spinal excitatory neurons; spinal inhibitory neurons, including Slc6a5 spinal inhibitory neurons; whole spinal neurons, including Esrrg spinal motor neurons and types of neurons found throughout the spinal cord; cerebrospinal fluid contact neurons, including Poln spinal motor neurons; and non-neuronal cells of the spinal cord, including astrocytes and oligodendrocytes.

The invention provides a neural stem cell induced differentiation and clinical application method for intractable epilepsy, and relates to the technical field of biological medicine, the induced differentiation method comprises the following steps: S1, cell source and preparation: adopting induced pluripotent stem cells from a patient; s2, constructing an induced differentiation system, differentiating the induced pluripotent stem cells into GABA (gamma-aminobutyric acid) inhibitory interneurons, and differentiating the GABA inhibitory interneurons; s3, purifying and amplifying the cells, adopting immunomagnetic bead sorting, and purifying and enriching the cells expressing the GABA energy neuron marker; s4, cell quality control; according to the method, the autologous induced pluripotent stem cells of the patient are taken as a source, immunological rejection is avoided, the transplanting safety is improved, and moreover, the high-purity GABAergic neurons can more effectively supplement damaged inhibitory neurons in the brain of the epileptic and reconstruct the inhibition balance of a neural network, so that the epileptic seizure is more effectively controlled.

Embodiments of the present application relate to the technical field of artificial intelligence, and disclose an image analysis method and device based on a pulse neural network, computer equipment and a computer readable storage medium, the method comprising: acquiring an image to be analyzed; inputting the image to be analyzed into a pulse neural network with inhibitory neurons; the neural network comprising a convolution-based SNN module, a Transformer-based SNN module, an inhibitory pulse self-feedback module and an inference module; the inhibitory pulse self-feedback module comprising at least one inhibitory neuron for dynamically emitting inhibitory pulses to regulate the membrane potential state of surrounding excitatory neurons; signal transmission between neurons of the pulse neural network is performed through integer pulses; the neurons comprise excitatory neurons and inhibitory neurons in the convolution-based SNN module and the Transformer-based SNN module; and outputting an analysis result. In the above manner, the embodiments of the present application improve the prediction accuracy of the model and significantly reduce the computing resources.

The present inventors found an inhibitory neuron-specific promoter sequence which, although having a shorter length than the mGAD65 promoter, does not impair any of the promoter activity, specificity for inhibitory neurons, and gene expression efficiency, which is specifically a promoter consisting of DNA having a promoter activity, comprising: a base sequence of a Dlx1 binding site and / or a Dlx2 binding site in a glutamic acid decarboxylase (GAD) promoter; and a base sequence of a region ranging from a 5′ end of exon 1 to a transcription start site (TSS) in a glutamic acid decarboxylase (GAD).

Artificial expression constructs are provided.SOLUTION: Artificial expression constructs are provided that selectively regulate gene expression in selected central nervous system cell types. Such artificial expression constructs can be used to selectively express synthetic genes or alter the expression of genes in inhibitory neocortical GABAergic neurons, including somatostatin GABAergic neurons, parvalmine GABAergic neurons, vasoactive intestinal peptide GABAergic neurons, Lamp5GABA GABAergic neurons, or in some instances astrocytes.SELECTED DRAWING: Figure 2-1

To provide expression constructs, vectors, and methods that result in protein expression selectively within inhibitory neurons for the purpose of rescuing defective Nav1.1 channel function.SOLUTION: Provided is a method of treating Dravet Syndrome in a subject in need thereof, comprising intravenously administering a therapeutically effective amount of at least two adeno-associated viral (AAV) vectors, each viral vector comprising an expression construct comprising (i) an enhancer; (ii) a promoter; and (iii) a coding sequence that results in expression of a fragment of human SCN1A, the AAV vectors are associated with a capsid that crosses the blood brain barrier, and the human SCN1A fragments encoded by the coding sequences being expressed selectively within inhibitory GABAergic interneurons and result in rescue of Nav1.1 channel function within inhibitory GABAergic interneurons in need thereof following the intravenous administering.SELECTED DRAWING: Figure 1A

Artificial expression constructs are described that selectively regulate gene expression in selected central nervous system cell types and can be used to selectively express synthetic genes or modify gene expression in somatostatin GABAergic neurons, parvalbumin GABAergic neurons, vasoactive intestinal peptide GABAergic neurons, Lamp5 GABAergic neurons, or, in some examples, inhibitory neocortical GABAergic neurons, including astrocytes.

Artificial expression constructs are provided.SOLUTION: Artificial expression constructs are provided that selectively regulate gene expression in selected central nervous system cell types. Such artificial expression constructs can be used to selectively express synthetic genes or alter the expression of genes in inhibitory neocortical GABAergic neurons, including somatostatin GABAergic neurons, parvalmine GABAergic neurons, vasoactive intestinal peptide GABAergic neurons, Lamp5GABA GABAergic neurons, or in some instances astrocytes.SELECTED DRAWING: Figure 2-1

Described herein is a gene therapy platform to restore GABAergic inhibition and improve cognition in neurodevelopmental disorders, epilepsies, sensory disorders, aging, and Alzheimer's disease, by increasing expression of the transcription factor Meis2 in parvalbumin-expressing inhibitory neurons (PV INs).

Transplantation of inhibitory neuronal precursor cells can reactivate a targeted, time-limited critical phase plasticity stage in a receptor brain region. Restoration of such young plasticity creates a therapeutic environment that facilitates circuit recombination and has continuously proved that cognitive and dysfunction can be ameliorated. It is notable that the critical phase plasticity is sufficient to reactivate only by overexpression of Calb1 in adult inhibitory neurons by viral vectors, without the need for transplantation. Accordingly, described herein are methods and compositions for enhancing Calb1 expression as a therapeutic pathway to reactivate plasticity.

The present application relates to the medical technical field, disclose a spike recognition model construction method, spike recognition method, device and equipment, the construction method includes: obtaining electroencephalogram signal;The electroencephalogram signal is segmented, and the spike electroencephalogram signal section is obtained;The spike electroencephalogram signal section is pulse coded, and the pulse sequence is obtained;Based on the pulse sequence and neuron dynamics mechanism, the initial neuron model is constructed;Based on the synaptic plasticity adjustment mechanism inside neuron, the initial neuron model is updated, and the adaptive neuron model is constructed;Based on the adaptive neuron model, the pulse neural network is constructed, and the pulse neural network is used for feature mapping of the pulse sequence;Based on the synaptic plasticity adjustment mechanism inside neuron, the pulse neural network is updated, and the target spike recognition model is obtained.The target spike recognition model, both excitatory neurons and inhibitory neurons, ensure the rationality of pulse neural network feature mapping, improve the accuracy of identifying non-invasive traceable type epilepsy-like spike.

Provided is a novel pharmaceutical agent for glioma.　This glioma therapeutic agent is characterized by comprising, as an active ingredient, a synaptic activator of an inhibitory neuron. This synaptic activator is, for instance, a GABA receptor agonist, and specifically, a benzodiazepine compound such as diazepam.