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.

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 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.

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.