A research team led by Prof. Jeremy Henley from the University of Bristol discovered that when a certain receptor - the kainate receptor - receives a chemical signal, a small protein called SUMO attaches to the receptor. SUMO inactivates the receptor, inducing a refractory state to other stimuli, making the neuron hypoexcitable for a period of time. Prof. Henley stated that increasing the amount of SUMO protein attached to kainate receptors may lead to a treatment for epilepsy by preventing neuronal hyperactivity.
A research team led by Prof. Jeremy Henley from the University of Bristol discovered that when a certain receptor - the kainate receptor - receives a chemical signal, a small protein called SUMO attaches to the receptor. SUMO inactivates the receptor, inducing a refractory state to other stimuli, making the neuron hypoexcitable for a period of time. Prof. Henley stated that increasing the amount of SUMO protein attached to kainate receptors may lead to a treatment for epilepsy by preventing neuronal hyperactivity.
A research team led by Prof. Jeremy Henley from the University of Bristol discovered that when a certain receptor - the kainate receptor - receives a chemical signal, a small protein called SUMO attaches to the receptor. SUMO inactivates the receptor, inducing a refractory state to other stimuli, making the neuron hypoexcitable for a period of time. Prof. Henley stated that increasing the amount of SUMO protein attached to kainate receptors may lead to a treatment for epilepsy by preventing neuronal hyperactivity.
descoperit ca in momentul in care un anumit receptor receptorul de kainat primeste un semnal chimic, o mica proteina, SUMO (small ubiquitin-like modifier protein) se ataseaza de receptor. SUMO inactiveaza receptorul, inducand o stare refractara la alti stimuli, neuronul devenind astfel hipoexcitabil pentru o perioada de timp. Munca noastra e importanta pentru ca ofera o noua perspectiva si o intelegere mai profunda asupra proceselor de transmitere a informatiei intre celulele nervoase si reglarea acestui flux. Este posibil ca prin marirea cantitatii proteinei SUMO atasata receptorilor de kainat sa se poate ajunge la un tratament al epilepsie prin prevenirea supraexcitarii, declara prof. Henley. In ceea ce priveste receptorii de kainat (KARs), ei sunt receptor ionotropi, non-NMDA, ce raspund la stimularea cu glutamat. Au fost initial identificati ca un tip distinct de receptori, prin activarea lor selectiva de catre kainat, o substanta ce mimeaza efectul glutamatului, izolata din algele rosii Digenea simplex si folosita in deosebirea acestor receptori de restul receptorilor pentru glutamat. KARs sunt mai putin studiati decat ceilalti receptori ionotropi pentru glutamat, AMPA si NMDA. Bicuculline is a light-sensitive competitive antagonist of GABAA receptors. It was originally identified in 1932 in plant alkaloid extracts[1] and has been isolated from Dicentra cucullaria, Adlumia fungosa, Fumariaceae, and several Corydalis species. Since it blocks the inhibitory action of GABA receptors, the action of bicuculline mimics epilepsy. This property is utilized in laboratories across the world in the in vitro study of epilepsy, generally in hippocampal or cortical neurons in prepared brain slices from rodents. This compound is also routinely used to isolate glutamatergic (excitatory amino acid) receptor function. The action of bicuculline is primarily on the ionotropic GABAA receptors, which are ligandgated ion channels concerned chiefly with the passing of chloride ions across the cell membrane, thus promoting an inhibitory influence on the target neuron. These receptors are the major targets for benzodiazepines and related anxiolytic drugs. The half-maximal inhibitory concentration (IC50) of bicuculline on GABAA receptors is 3 M. In addition to being a potent GABAA receptor antagonist, bicuculline can be used to block Ca2+activated potassium channels.[2] Sensitivity to bicuculline is defined by IUPHAR as a major criterion in the definition of GABAA receptors