7 results about "Inhibitory neuron" patented technology

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.

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.

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.