39 results about "Interneuron" patented technology

A method to control respiration generally comprising generating a confounding neuro-electrical signal that is adapted to confound or (suppress) at least one interneuron that induces a reflex action and transmitting the confounding neuro-electrical signal to the subject, whereby the reflex action is abated. In one embodiment, the confounding neuro-electrical signal is adapted to confound at least one parasympathetic action potential that is associated with the target reflex action, e.g., bronchial constriction.

Provided herein are compositions and methods for disrupting at least one reward-related behavior in an individual through the use of light-responsive opsin proteins used to control the polarization state of the cholinergic interneurons of the nucleus accumbens or the striatum.

One aspect of the invention provides a method of predicting a seizure in a subject comprising: (a) recording single neuron activity for a plurality of interneurons within the subject's mesial temporal lobe; (b) recording local field potential (LFP) within the subject's mesial temporal lobe; (c) measuring interneuron synchrony within the subject's mesial temporal lobe; and (d) detecting a pattern of interneuron activity and interneuron synchrony within the subject's mesial temporal lobe associated with an increased likelihood of a seizure. Another aspect of the invention provides a method for preventing a seizure in a subject comprising: (a) performing any one of the methods described herein; and (b) upon detection of the pattern, administering a therapeutically effective intervention to the subject to prevent onset of a seizure. Another aspect of the invention provides a non-transitory computer readable medium containing computer-readable program code including instructions for performing any of the methods described herein.

Methods and systems for generating MGE precursor cells in vitro as well as compositions of enriched MGE precursor cells are provided. The methods and systems provide efficient production of MGE precursors. The methods and systems disclosed herein provide functional MGE precursors which differentiate into functional GABAergic interneurons.

A system for automated construction of an artificial neural network architecture is provided. The system includes a set of interfaces and data links configured to receive and send signals, wherein the signals include datasets of training data, validation data and testing data, wherein the signals include a set of random number factors in multi-dimensional signals X, wherein part of the random number factors are associated with task labels Y to identify, and nuisance variations S. The system further includes a set of memory banks to store a set of reconfigurable deep neural network (DNN) blocks, hyperparameters, trainable variables, intermediate neuron signals, and temporary computation values including forward-pass signals and backward-pass gradients. The system further includes at least one processor, in connection with the interface and the memory banks, configured to submit the signals and the datasets into the reconfigurable DNN blocks, wherein the at least one processor is configured to execute a Bayesian graph exploration using the Bayes-Ball algorithm to reconfigure the DNN blocks such that redundant links are pruned to be compact by modifying the hyperparameters in the memory banks. The system realizes nuisance-robust variational Bayesian inference to be transferable to new datasets in semi-supervised settings.

The present disclosure provides systems and methods for at least one of preventing, reducing, and treating a level of or change in at least one of amyloid-β (Aβ) peptide, C-terminal fragment-β (β-CTF), β-secretase (BACE1), γ-secretase, neuroinflammation, and/or dementia (e.g., Alzheimer's disease or age-related decline) in a subject by inducing synchronized gamma oscillations in the brain of the subject using, for example, a stimulus-emitting device to emit a stimulus (e.g., light, sound, and/or haptic) at a frequency (e.g., about 40 Hz) that synchronously activates in vivo a specific cell type (e.g., fast-spiking-parvalbumin (FS-PV) immunoreactive interneurons) and/or brain region (e.g., a sensory cortex and/or hippocampus) of the subject.

Provided are compositions and methods for prophylaxis and/or therapy of disorders that involve seizures. The compositions and methods relate to a recombinant adeno-associated virus (rAAV) comprising a I56i enhancer sequence, and a sequence encoding hM3Dq modified muscarinic receptor (Gq-DREADD). The method includes introducing the rAAV into interneurons of an individual such that Gq-DREADD is expressed in interneurons of the individual. The method can further comprise administering to the individual an agonist of the Gq-DREADD, such for reducing or preventing seizures.

Methods of generating spinal cord glutamatergic interneurons (V2a interneurons) from human pluripotent stem cells (hPSCs) are provided. A method of the present disclosure may include culturing a first population of hPSCs in vitro in a neural induction medium that includes: a retinoic acid signaling pathway activator; a sonic hedgehog (Shh) signaling pathway activator; and a Notch signaling pathway inhibitor, wherein the culturing results in generation of a second population of cultured cells containing CHX10+ V2a interneurons. Also provided are non-human animal models that include the hPSC-derived spinal cord glutamatergic interneurons, and methods of producing the non-human animal models.

It has been discovered that pharmacological inhibition of K+ channels (using the FDA-approved broad-spectrum K+ channel antagonist 4-AP) positively benefitted smn mutant phenotypes, a result that is consistent with the defective excitability of motor circuits by their interneuron or sensory neuron inputs being a critical consequence of SMN depletion. Based on these observations, certain embodiments of the invention are directed to methods of treatment of SMA by administering therapeutically effective amounts of one or more potassium channel antagonists, including 4-aminopyridine, 4-(dimethylamino)pyridine, 4-(methylamino)pyridine, and 4-(aminomethyl)pyridine. Other embodiments are directed to new pharmaceutical formulations comprising two or more potassium channel antagonists.

The invention provides an illumination regulating and controlling composition for specifically regulating and controlling internuncial neuron activity of hypothalamus and an application of the illumination regulating and controlling composition. The internuncial neuron activity of the hypothalamus is specifically regulated and controlled by an optogenetic regulation and control technology to affect an anxiety behavior. The illumination regulating and controlling composition for specifically regulating and controlling the internuncial neuron activity of the hypothalamus comprises a virus vector and an illumination device, wherein the virus vector is used for infecting photoesthetic genes carried by internuncial neurons or precursor cells of the internuncial neurons; the carrier comprises a promoter, the photoesthetic genes and a green fluorescence marker gene; the promoter is a VGAT promoter; and the illumination device is used for carrying out illumination regulation and control on the infected internuncial neuron cells or precursor cells of the internuncial neuron cells to change the activity. According to the technique provided by the invention, the internuncial neurons of the hypothalamus can be accurately and specifically regulated and controlled; and anxiety-like behaviors can be effectively affected.

Provided herein are methods of generating hindbrain cells, including respiratory hindbrain cells, from pluripotent stem cells. Also provided are methods of generating a three-dimensional organoid comprising a population of hindbrain cells including a heterogeneous population of interneurons.

As a result of screening for genes that are selectively expressed in fetal mouse brain region by subtraction method, the present inventors obtained a cDNA fragment encoding Corl1. The expression of Corl1 was examined by RT-PCR, in situ hybridization, and immunostaining using polyclonal antibodies. The results demonstrated that Corl1 was especially expressed at a high level of selectively in the central nervous system during embryonic stages. The expression patterns of Corl1 determined using various markers in embryonic spinal cord were compared to identify types of neurons expressing Corl1. The results revealed that Corl1 was specifically expressed in spinal cord interneurons dI4, dI5, dILA, and dILB. Accordingly, the present invention provides for discrimination between dI4 and dI6, neurons which previously could only be discriminated based on developmental location, using the expression of Corl1 as an indicator.

The invention relates to a method of neuron-imitating enterprise data hierarchy representation and a system thereof. The method includes: acquiring enterprise data; dividing the enterprise data on thebasis of neuron categories according to perceiving neurons, interneurons and motor neurons; acquiring upper/lower-level relationships of the enterprise data according to connection relationships between the perceiving neurons, the interneurons and the motor neurons, and acquiring enterprise upper/lower-level data; and carrying out data hierarchy dividing on the enterprise data according to the connection relationships and the enterprise upper/lower-level data to acquire an enterprise data hierarchy. According to the method, utilizing a human brain neural-network to build the enterprise data hierarchy is realized, guaranteeing atomicity of the data is facilitated, redundancy of data storage is reduced, comprehensiveness and organization of evaluation of an enterprise service institution ororganization on an enterprise are improved, and correctness, accuracy and high efficiency of the original data hierarchy are more efficiently guaranteed.

Provided are therapeutic virus vectors, particularly, recombinant adeno-associated virus (rAAV) vectors, designed to contain an enhancer sequence that specifically restricts expression of an effector gene (e.g., an SCN1A-encoding polynucleotide, Gq-DREADD-encoding polynucleotide, or PSAM-encoding polynucleotide) contained in the vector to PV-expressing GABAergic interneuron or to neuron cell populations in the brain. The rAAV vectors, compositions and methods thereof are useful for treating subjects afflicted with neuropathologies, seizures, pharmacologically-intractable forms of epilepsy including Dravet syndrome (DS), a form of infantile epilepsy associated with severe seizures, cognitive impairment and premature death, as the cause of DS involves loss of function of a sodium channel encoded by the SCN1A gene. The described vectors restore expression of effector genes to the appropriate interneuron or neuron cell populations with specificity and sensitivity, advantageously to address the root cause of the disease by restoring the excitation-inhibition balance by means of gene-therapy (with SCN1A) or pharmacogenetics.

Artificial expression constructs for selectively modulating gene expression in selected central nervous system cell types are described. The artificial expression constructs can be used to selectively express synthetic genes or modify gene expression in GABAergic interneurons.

The invention relates to a double-electrode electronic system for reconstructing a gait motion function. The double-electrode electronic system comprises an instruction acquisition system, a pulse signal generation system, two biological stimulation electrodes and a reference electrode. The instruction acquisition system generates a control instruction according to instruction information and sends the control instruction to the pulse signal generation system; the pulse signal generation system generates a pulse signal according to the control instruction and sends the pulse signal to the biological stimulation electrodes; alternate electric pulse excitation is carried out on two key sites for inducing gait motion in spinal cord by the biological stimulation electrodes, the key sites for generating coordinated action of an inherent intermediate neural network for generating lower limb rhythm motion in spinal cord nerves are activated, and reconstruction of a lower limb gait motion function is effectively carried out in a mode of being closer to physiological conditions. The electronic system can be applied to animal experiments or rehabilitation training.