Disease relevance of C13931

• This QA/Glu reaction is inhibited by islet-activating protein (IAP, pertussis toxin), but was not blocked by Joro spider toxin (JSTX), a specific blocker of traditional ionotropic QA/Glu receptors [1].
• Joro-spider toxin (JSTX) blocked myocardial excitatory junctional potentials evoked by the cardiac ganglion [2].

Psychiatry related information on C13931

• At higher doses (more than 12 nmol/brain), JSTX-3 increased motor activities and induced characteristic symptoms [3].

High impact information on C13931

• Using an 'ex vivo' approach in mice, we show that a single injection of cocaine caused strong rectification and conferred sensitivity to the polyamine Joro spider toxin (JST) of AMPAR-mediated excitatory postsynaptic currents (AMPAR EPSCs), indicating the recruitment of receptors that lack GluR2 [4].
• Both a general antagonist of AMPA/kainate receptors (CNQX) and a specific antagonist of calcium-permeable AMPA receptors (joro spider toxin) reduced formation of SOD-1 proteinaceous aggregates and prevented death of motor neurons expressing SOD-1 mutants [5].
• Pretreatment with a selective calcium-permeable AMPA/KA receptor antagonist (5nmol joro spider toxin), but not an NMDA receptor antagonist (25nmol d-2-amino-5-phosphonovalerate, AP-5), blocked thermal stimulus-evoked increases in phosphorylated PKA and PKC, in addition to increased cytosolic GLUR1 [6].
• 4. At the standard membrane potential (-60 mV), recovery from the blockage by JSTX-3 was very slow [7].
• 1. The effect of synthetic joro spider toxin (JSTX-3) on alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor channels in cultured rat hippocampal neurones was investigated using the whole-cell patch-clamp technique [7].

Chemical compound and disease context of C13931

• This presynaptic glutamate potential (PGP) was insensitive to Joro spider toxin (JSTX), a spider toxin which specifically blocks the postsynaptic glutamate receptor, but was blocked by pertussis toxin island activating protein (IAP) in a dose-dependent manner [8].

Biological context of C13931

• When the myogenic activity of the heart muscle was pharmacologically isolated from the ganglionic drive by applying a glutamatergic antagonist, Joro spider toxin (JSTX), the spontaneous muscle contraction caused a hyperpolarizing deflection in the CG neuron [9].
• The synthetic arylamine spider toxins JSTX-3, argiotoxin-636, and argiotoxin-659 were 26 to 73 times more potent at antagonizing the NMDA receptor-mediated EPSP (IC50 values ranging from 12 to 24 microM) than the AMPA receptor-mediated population spike (IC50 values ranging from 612 to 878 microM) [10].
• These observations suggest that JSTX-3 blocks excitatory synaptic transmission mainly by suppressing non-NMDA-receptor-mediated EPSCs, and that the JSTX-3-insensitive component is mediated at least in part by NMDA receptors in the hippocampal slice [11].
• Following determination of the structure of JSTXs, a main component JSTX-3 with its analogs was chemically synthesized and used for the study of structure-activity relationships [12].
• CaN activation appears to be dependent on seizure-induced activation of Ca2+-permeable AMPA receptors (AMPARs), because the upregulation of CaN activation and GABA(A)R inhibition were attenuated by GYKI 52466 [1-(4-aminophenyl)-4-methyl-7,8-methylenedioxy-5H-2,3-benzodiazepine hydrochloride] or Joro spider toxin [13].

Anatomical context of C13931

• The block by JSTX-3 was observed in pyramidal cells where the EPSCs showed linear peak current-voltage (I-V) relations in the control [11].
• JSTX-3 was injected into lateral ventricles of chronically cannulated mice at a dose of 22.2 pmol/brain, which did not produce any apparent behavioral changes [14].
• Differential blocking action of Joro spider toxin analog on parallel fiber and climbing fiber synapses in cerebellar Purkinje cells [15].
• Histochemical study utilizing the interaction of biotinylated JSTX-3 with avidin showed specific binding of the toxin in rat cerebellum and hippocampus [16].

Associations of C13931 with other chemical compounds

• EPSPs evoked by stimulation of parallel fibers were effectively blocked by perfusion of a slice with the synthetic analog of Joro spider toxin, 1-naphthylacetyl-spermine (NAS) at 250 microM [15].

Gene context of C13931

• Anti-calreticulin induced extracellular Ca(2+) influx in cultured neuron cells was blocked partially by N-methyl-D-aspartate receptor (NMDAR) antagonist 2-amino-5-phosphonovaleric acid (AP5) and spider polyamine toxin JSTX-3, which is recognized as a blocker of glutamatergic nervous system [17].
• Simultaneous measurements of kainate-activated Ca2+ fluxes and inward currents, using fura-2 microfluorimetry under voltage clamp conditions, suggested the existence of GluR2 containing channels which are permeable to Ca2+ and insensitive to Joro spider toxin (JSTx) [18].
• Prior to mGluR-LTD, AMPAR mediated excitatory postsynaptic currents (EPSCs) showed strong rectification at positive potentials and were sensitive to Joro spider toxin (JST), a selective blocker of GluR2-lacking AMPARs [19].
• The allodynia induced by ACRO-A (500 ng x kg(-1)) was not inhibited by Joro spider toxin or NMDA receptor antagonists [20].

Analytical, diagnostic and therapeutic context of C13931

• The purification was carried out in two steps: affinity chromatography using a spider toxin (Joro spider toxin; JSTX) immobilized on a lysine-agarose column, and a Mono Q anion exchange column [21].
• Passive membrane properties were analyzed before and after perfusion with the 0-Mg2+ ACSF and the application of toxin JSTX-3 [22].

References