40 results about "Neuronal excitation" patented technology

Induced movement in a patient is detected and correlated with a TMS stimulating pulse so as to determine the patient's motor threshold stimulation level. Direct visual or audible feedback is provided to the operator indicating that a valid stimulation has occurred so that the operator may adjust the stimulation accordingly. A search algorithm may be used to direct a convergence to the motor threshold stimulation level with or without operator intervention. A motion detector is used or, alternatively, the motion detector is replaced with a direct motor evoked potential (MEP) measurement device that measures induced neurological voltage and correlates the measured neurological change to the TMS stimulus. Other signals indicative of motor threshold may be detected and correlated to the TMS stimulus pulses. For example, left / right asymmetry changes in a narrow subset of EEG leads placed on the forehead of the patient or fast autonomic responses, such as skin conductivity, modulation of respiration, reflex responses, and the like, may be detected. The appropriate stimulation level for TMS studies are also determined using techniques other than motor cortex motor threshold methods. For example, a localized ultrasound probe may be used to determine the depth of cortical tissue at the treatment site. When considered along with neuronal excitability, the stimulation level for treatment may be determined. Alternatively, a localized impedance probe or coil and detection circuit whose Q factor changes with tissue loading may be used to detect cortical depth.

The invention provides microfabricated devices and methods for directing the growth of a cell process to form an artificial synapse. The devices are called artificial synapse chips. The artificial synapse comprises a nanofabricated aperture (about 50–100 nm in size) that connects the cell process to a chemical or electrical means of neuronal excitation. Such an aperture width mimics the length scales of a natural synapse and thus emphasizes the localized spatial relationship between a neuron and a stimulation source. The invention further provides devices and methods for regenerating a nerve fiber into an electrode. The invention thus provides a regeneration electrode that uses a novel neural interface for stimulation and that uses novel surface methods for directing neuronal growth making possible in vivo connection of the devices to neural circuitry in a retina and other anatomical locations.

Embodiments of the technology described herein relate, at least in part, to methods of modulating the activity of a neuron by contacting the neuron with a photo-sensitive TrpA1 agonist and then illuminating the neuron with electromagnetic radiation. Also described herein are photo-sensitive TrpA1 agonists.

Neuronal excitation and inhibition of the brain is tracked in the hippocampal CA1 network during a latent period, wherein biomarkers are observed which include a sustained increase in the firing rate of the excitatory postsynaptic field activity, paired with a subsequent decrease in the firing rate of the inhibitory postsynaptic field activity; the mean amplitude profiles of both fEPSP and fEPSP field potential activity during the latent period have characteristic shapes; both excitatory and inhibitory CA1 field activity firing rates are observed to follow a circadian rhythm that drifts during epileptogenesis; the circadian rhythms described are in-phase in controls and anti-phase during epileptogenesis; and the fEPSP rate drifts from a circadian rhythm to a greater extent than the fEPSP rate. An additional biomarker is a change in a circadian rhythm of core body temperature. Therapeutic measures can include thermal, chemical, or electrical modulation, in an open or closed loop process.

The invention provides application of an ErbB receptor stimulant to preparation of a medicament for treating epilepsy. The ErbB receptor stimulant has the advantages: the inhibiting effect of the ErbB4 stimulant NRG1 on epilepsy is disclosed, the organism of epilepsy is studied intensively, a research direction for studying a novel effective 'target' and a molecule of an epilepsy inhibiting medicament is provided, and a basis is laid for the screening of a novel medicament for treating brain diseases based on neuronal excitability changes.

The invention is directed to compositions and methods for treating or reducing the likelihood of the development of epilepsy in an individual. The method comprises administering to the central nervous system of an individual in need of such treatment a therapeutically effective amount of an agent capable of increasing the expression and / or activity of miR-128.

Use of a CB1 receptor antagonist and / or inverse agonist, preferably rimonabant, for the preparation of drugs useful for increasing motor neuron excitability in the cerebral cortex and / or in the brain stem and / or at the spinal level, as well as a method for increasing motor neuron excitability through the administration of a CB1 antagonist / inverse agonist receptors, and to the use of a pharmaceutical composition which comprises a CB1 receptor antagonist and / or inverse agonist, preferably rimonabant, for increasing motor neuron excitability in the cerebral cortex and / or in the brain stem and / or at the spinal level.

The invention discloses application of growth promoting factor (OPN and IGF1) overexpression in combination with embryo spinal nerve stem cell (NSCs) transplantation and a small molecule compound (CLP290) in preparation of a medicine for treating spinal cord injury. A medicine kit for treating spinal cord injury comprises AAV-OPN, AAV-IGF1, NSCs and CLP290. The invention also discloses applicationof OPN and IGF1 overexpression in combination with NSCs transplantation and the small molecule CLP290 in treatment of spinal cord injury. OPN and IGF1 overexpression, NSCs transplantation and small molecule CLP290 intervention are combined for treating spinal cord injury, the intrinsic regeneration capacity of neurons is enhanced, meanwhile, interrupted upstream and downstream neural loops are rebuilt, the excitability of inhibitory neurons is adjusted, and functional recovery after spinal cord injury is promoted.

Devices, systems and methods are disclosed for treating or preventing an autism spectrum disorder, a pervasive developmental disorder, or a disorder of psychological development. The methods comprise transmitting impulses of energy non-invasively to selected nerve fibers, particularly those in a vagus nerve. The nerve stimulation may be used as a behavior conditioning tool, by producing euphoria in an autistic individual. Vagus nerve stimulation is also used to modulate circulating serotonin levels in a pregnant woman so as to reduce the risk of having an autistic child; modulate the levels of growth factors within a child; promote balance of neuronal excitation / inhibition; modulate the activity of abnormal resting state neuronal networks; increase respiratory sinus arrhythmia; and avert episodes of motor stereotypies with the aid of forecasting methods.

The invention discloses a system and a method for simulating biological neuron dynamics to realize logical operation. The system for simulating biological neuron dynamics to realize logical operation comprises an input module, an electric coupling module, a laser response module and an output module. The system for simulating biological neuron dynamics to realize logical operation is based on the Fano laser, on one hand, compared with a traditional laser, the system has more stable characteristics, so that the excitability of simulated neurons can be more stable through an electric signal modulation injection technology, and unnecessary relaxation oscillation phenomena cannot be generated; and thus, the information processing speed is increased. Meanwhile, on the basis of avoiding extra light injection, the structure simplification is realized, especially in a large neural network for realizing complex tasks. And secondly, the Fano laser is extremely small in size, extremely low in energy consumption, higher in speed, simple in structure, low in cost and easy to control.

The invention discloses a neural network circuit structure capable of changing nerve cell excitement, which comprises a neural network structure and a parameter interface module, and is characterizedin that the neural network structure is connected with the parameter interface module. According to the invention, the nonlinear state of neuronal excitement during learning of people can be fully approximated; The self-learning capability is achieved, and unknown or uncertain systems can be learned; All quantitative or qualitative information is equipotential distributed and stored in each neuronin the emotional neural network, so that the robustness and the fault tolerance are very high; And a parallel distribution processing method is adopted, so that the high-speed solution searching andoptimizing capability is achieved, the high-speed operation capability of a computer can be exerted, a large number of operations can be carried out quickly, and the learning efficiency is greatly improved.

The invention discloses the application of a chemical genetic drug composition in preparing a drug for preventing and treating propofol addiction. The propofol addiction mainly involves two classic addictive behaviors, behavioral sensitization and self-administration. The present invention fully proves that after long-term repeated use of propofol in rats, addictive behavior will be produced, which is mainly caused by the excitation of neurons in the medial prefrontal cortex (mPFC area) of the cortex; Inhibits the hyperexcitable state of mPFC region induced by propofol, thereby inhibiting propofol-addictive behavior in rats. The chemical genetic drug composition provided by the invention has the advantages of good effect, strong controllability and the like, and provides a new therapeutic drug for the treatment, research, development and prevention of propofol addiction.

The invention provides a fusion polypeptide with a cerebral ischemia resistant effect and application thereof. The fusion polypeptide has a peptide chain fragment sequence of YGRKKRRQRRRGDPV. The polypeptide provided by the invention can rapidly and effectively enter cells; through interfering with the signal conduction of CAPON, the neuron excitatory toxicity injury induced by glutamic acid is obviously inhibited; the cerebral ischemia injury of MCAO model rats can be effectively resisted. The polypeptide has good application prospects in the preparation of medicine for treating cerebrovascular diseases.

The invention discloses an application of a chemical genetics pharmaceutical composition in preparation of a medicine for preventing and treating propofol addiction. The propofol addiction mainly relates to two classic addiction behaviors of behavior sensitization and self-administration. The invention fully proves that the addiction behaviors are generated after propofol is repeatedly used for along time for a rat, and the addiction behaviors are mainly caused by excitation of neurons of the prefrontal cortex (mPFC region) on the inner side of the cortex; and the mPFC region high excitationstate caused by the propofol can be effectively inhibited by utilizing the chemical genetics pharmaceutical composition, so that the propofol addiction behaviors of the rat is inhibited. The chemicalgenetics pharmaceutical composition provided by the invention has the advantages of good effect, strong controllability and the like, and provides a new therapeutic medicine for treating, researchingand developing and preventing propofol addiction.

The invention discloses the application of CDN1163 in preparing a medicine for relieving or treating neuropathic pain. The CDN1163 can act on neuropathic pain including one or more of central neuropathic pain and peripheral neuropathic pain, and improve chronic sciatic nerve compression in rats. Mechanical pain sensitivity and thermal pain sensitivity caused by sexual injury, improve neuronal shrinkage and astrocyte activation in lumbar intervertebral foramen 5 dorsal root ganglia, inhibit neuronal excitation in lumbar intervertebral foramina 4-6 dorsal root ganglia It can effectively reduce the symptoms of neuropathic pain, and repeated injections can significantly reverse mechanical hyperalgesia and thermal hyperalgesia, and there is no sign of tolerance, and the therapeutic effect can be maintained after drug withdrawal. and difficult-to-treat neuropathic pain medications.