101 results about "Sensory neuron" patented technology

The present invention relates to the discovery of a novel molecular pathway involved in long-term hyperexcitability of sensory neurons, which, in higher animals, is associated with persistent pain. It is based on the discovery that, following injury to an axon of a neuron, an increase in nitric oxide synthase activity results in increased nitric oxide production, which, in turn, activates guanylyl cyclase, thereby increasing levels of cGMP. Increased cGMP results in activation of protein kinase G (“PKG”), which then is retrogradely transported along the axon to the neuron cell body, where it phosphorylates MAPKerk.

The present invention relates generally to the field of cell biology of stem cells, more specifically the directed differentiation of pluripotent or multipotent stem cells, including human embryonic stem cells (hESC), somatic stem cells, and induced human pluripotent stem cells (hiPSC) using novel culture conditions. Specifically, methods are provided for obtaining neural tissue, floor plate cells, and placode including induction of neural plate development in hESCs for obtaining midbrain dopamine (DA) neurons, motorneurons, and sensory neurons. Further, neural plate tissue obtained using methods of the present inventions are contemplated for use in co-cultures with other tissues as inducers for shifting differentiation pathways, i.e. patterning.

A method for rapidly screening small molecules to identify small molecules that stimulate axon regeneration and outgrowth from adult sensory neurons. The method generally comprises preparing a purified individualized dorsal root ganglia cell suspension (DRG), coating well surfaces of a suitably prepared multi-well microplate with the DRG, then dispensing dosages of selected small molecules into selected wells. The microplates are incubated under sterile conditions at about 37° C. for at least 24 hours. The DRG suspension in each well is then morphometrically assessed to assess the extent of axon regeneration and outgrowth that occurred, and the effects of the selected small molecules are determined by comparison to control treatments. The method is suitable for screening chemically derived small molecules and biologically derived small molecules.

Disclosed herein are methods, sequences and nucleic acid molecules used to treat pain. Specifically, the methods and sequences include locally administering molecules that suppress the expression of amino acid sequences that encode for Na_v1.7 channels or that otherwise inhibit the function of Na_v1.7 channels. Local suppression of Na_v1.7 channel levels and/or function will occur in the peripheral sensory neurons of the dorsal root ganglia.

V An anomalous effect detector (100, 130, 300, 800, 830, 840, 900, 930) responsive to an influence of mind comprises a source of non-deterministic random numbers, SNDRN, (104, 134, 310), a phase-sensitive filter (108, 140, 170, 320), and a results interface (110, 160, 340). In some embodiments, the phase-sensitive filter comprises a complex filter (170). An artificial sensory neuron (802, 810, 820, 906) comprises a SNDRN. Preferably, several artificial sensory neurons (802, 906) are grouped in a small volume. An analog artificial sensory detector (800) comprises a plurality of analog artificial sensory neurons (802), an abstracting processor (804) and a control or feedback unit (806). Some embodiments include an artificial neural network (850). An artificial consciousness network (900) contains a plurality of artificial neural networks (902, 914). One of the artificial neural networks (914) comprises an activation pattern meta-analyzer. An artificial consciousness device comprises a cluster (936) of artificial consciousness networks, a sensory input device (932) to provide sensory input signals (933) to the input of one or more ANNs in ACD (930), and an output device (938).

Devices, systems and methods are provided for the targeted treatment of abnormal sensory conditions. In such conditions, physical stimuli is transduced into neuronal impulses that are subsequently transmitted to the central nervous system for processing. Such transduction is achieved by primary sensory neurons in the dorsal root ganglions. Subcellular structures on primary sensory neurons can significantly modulate the function of these neurons, thereby affecting the transduction and reducing the abnormal sensory experiences. Thus, devices, systems and methods are provided for neuromodulating subcellular structures on primary sensory neurons of the dorsal root ganglions.

One embodiment is directed to a system for controllably managing pain in the afferent nervous system of a patient having a targeted tissue structure that has been genetically modified to have light sensitive protein, comprising a light delivery element configured to direct radiation to at least a portion of a targeted tissue structure; a light source configured to provide light to the light delivery element; and a controller operatively coupled to light source; wherein the targeted tissue structure comprises a sensory neuron of the patient; and wherein the controller is configured to be automatically operated to illuminate the targeted tissue structure with radiation such that a membrane potential of cells comprising the targeted tissue structure is modulated at least in part due to exposure of the light sensitive protein to the radiation.

Diagnostic assessment and therapeutic treatment of pelvic pain disorders, including bladder disorders, bowel disorders, and/or reproductive tissue or organ disorders that are characterized by increased expression of the neuropeptides CGRP and/or PACAP. Additionally, applicants have developed a transgenic nonhuman model for pelvic pain disorders, where the transgenic animal expresses in bladder sensory neurons a recombinant neuropeptide implicated in the pelvic pain disorder.

Methods and systems described herein can be used to automatically turn on and off stimulation of a target dorsal root ganglion (DRG) and/or adjust stimulation parameters. At least one of an input signal (indicative of an electrical field resulting from an electrical signal propagated by adjacent distal sensory nerve fibers toward the target DRG), an output signal (indicative of an electrical field resulting from an electrical signal propagated by adjacent proximal sensory nerve fibers away from the target DRG) or a DRG signal (indicative of an electrical field produced by cell bodies of primary sensory neurons within the target DRG and resulting from an electrical signal propagated by sensory nerve fibers within the target DRG) is/are obtained and analyzed. Delivery of electrical stimulation is turned on and off and/or at least one of pulse amplitude, pulse width and/or pulse repetition rate is/are adjusted based on results of the analysis.

The invention relates generally to novel genes expressed in normal but not Neurogenin-1-deficient animals. The invention relates specifically to a novel family of G protein-coupled receptors and a novel family of two-transmembrane segment proteins that are expressed in dorsal root ganglia, and a method of screening for genes specifically expressed in nociceptive sensory neurons.

According to the novel human sensory neuron induction culture system provided by the invention, the combination of the small-molecule inhibitor LY2157299 and the growth factor is added into the serum-free basal culture medium, so that compared with a serum-containing induction method, the efficiency of converting pluripotent stem cells into sensory neurons is greatly improved, and the induction efficiency of the pluripotent stem cells is improved. In addition, the expression of various ion channel proteins is obviously improved, so that various induced pluripotent stem cells with different sources are successfully induced into sensory neurons.

In order to identify a factor demonstrating a repellent effect on axon extension of a neuron, lysophosphatidylglucoside (LPG) has been found to have an activity as a chemorepellent effect on axon guidance of a DRG sensory neuron specific to a neuron expressing TrkA, an NGF receptor.

In addition, it has been found out that suppressing the function of LPG makes it possible to suppress a repellent effect of LPG on axon extension of a neuron expressing TrkA. A molecule capable of suppressing the function of LPG can be a composition promoting repairing of a neural circuit in neuronal damages and the like.

The present invention relates to a system for stimulating the sensory cortex of an individual, comprising: means for obtaining a neuronal stimulation signal adapted to provide a movement cue for the individual and means for transmitting the neuronal stimulation signal to an electric contact of a neuronal stimulation electrode that is already implanted into the brain of the individual for a purpose different from providing the movement cue.

The present invention further relates to a system for communicating proprioceptive information to an individual, comprising means for obtaining information about the body posture of the individual; means for determining, based on the obtained information, a neuronal stimulation signal to be applied to at least one afferent axon targeting at least one sensory neuron in the cortex of the individual, wherein the determined neuronal stimulation signal corresponds to the proprioceptive information to be communicated and means for transmitting the determined neuronal stimulation signal to a neuronal stimulation means of the individual adapted to apply the determined neuronal stimulation signal to the at least one afferent axon.

The present invention further relates to a system for communicating movement information to an individual, comprising means for providing a first neuronal stimulation signal to be applied to the cortex of an individual adapted to provide a movement cue for the individual and means for providing a second neuronal stimulation signal to be applied to the cortex of the individual adapted to provide proprioceptive information to the individual, wherein the first and the second neuronal stimulation signal are adapted to be applied together to the cortex of the individual.

Amyotrophic lateral sclerosis (ALS) is a devastating disease that leads initially to death of motor nerves with some progression to death of sensory and autonomic nerves. Experimental work shows that more electrical energy is required to successfully stimulate motor vs. sensory nerve components of a nerve and longer vs. shorter components of a nerve. This discovery explains sparing of the nerves of ocular motion and nerves of rectal and urethral sphincters in patients suffering from ALS and supports the energy hypothesis of ALS. Neurons and peripheral nerves are dependent upon glial cells and oligodendrocytes respectively to support their high energy demands. These supporting cells shuttle lactate to neurons and nerves. Lactate is required to sustain contraction of skeletal muscle. Administration of racemic or L-lactate in an amount greater than the capacity of the liver to oxidize will increase the available lactate to nerves and neurons and improve the symptoms of ALS.

Provided here are new methods to identify specific families of mammalian odorant receptors for odorants or aroma, particularly indole and skatole malodors and their use in assays that may be used to discover compounds that modulate (blocking, enhancing, masking or mimicking compounds) their activity. Orphan mouse odorant receptors are identified from olfactory sensory neurons that respond to target compounds. The resulting receptors as well as their human counterparts can be screened in assays against test compounds to confirm their identity as odorant or aroma receptors, particularly malodor receptors and subsequently discover for example modulators that inhibit the perception of the malodor in humans.

The invention discloses an MSCs (Mesenchymal stem cells) sourced schwann cell trophoblast type axon growth method of sensory neurone. The method comprises the following steps: S1, culturing P2-generation umbilical cord MSCs with umbilical cord wharton jelly of a newborn through an MSCs culture medium; S2, suspending the P2-generation umbilical cord MSCs through the MSCs culture medium; inoculatingto a recombinant human laminin and recombinant human vitronectin coated cell culture plate for culturing until the confluence reaches 60-70%; and preparing neuroepithelium pre-induced cell through aneural differentiation culture medium; S3, culturing P0-generation SCs with the neuroepithelium pre-induced cell through an SCs culture medium; and performing a subculture until P1 generation is obtained; S4, preparing an SCs trophoblast through P1-geneation SCs; and S5, preparing DRG (Dorsal root ganglion) sensory neurone cells; and performing co-culture through the SCs trophoblast and the DRG sensory neurone cells. According to the method, a new ideal is provided for cell therapy on nerve injury and repair of central nervous system.