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Biomedical subjects

A Miwa

Publications and source records attributed to A Miwa.

At least 181 records · Page 10Linked to original sources
PubMed1985

Spider toxin (JSTX) blocks glutamate synapse in hippocampal pyramidal neurons.

Effects of spider toxin (JSTX)--a specific blocker of glutamate receptors--on single pyramidal neurons of the hippocampus were studied using tissue slices in vitro. JSTX blocked the synaptic response in CA1 pyramidal cells evoked by Schaffer collateral stimulation without affecting the antidromic spike potential. The toxin suppressed glutamate-induced cell firings whereas it had little effect on aspartate-induced responses. The results suggest that glutamate is a neurotransmitter of the Schaffer collateral input to CA1 pyramidal neurons.

Animals↗
PubMed1985

Renal adenoma incidentally found in removed kidney in a patient with transitional cell carcinoma of the renal pelvis.

Concurrent primary renoparenchymal or renal pelvic neoplasms of different histology in the same kidney appear to be unusual. We herein report on a 75-year-old man in whom a tiny renal adenoma, a transitional cell carcinoma of the renal pelvis, ipsilateral ureter papillomas and transitional carcinoma of the urinary bladder were found. The clinicopathologic findings of this patient as well as the oncogenesis of renal tumours are discussed.

Adenoma↗
PubMed1985

Evidence for L-glutamate as the neurotransmitter of the squid giant synapse.

The effect of a spider toxin (JSTX), a specific blocker of glutamate receptors, was studied in the squid stellate ganglion. JSTX irreversibly blocked the excitatory postsynaptic potential in a dose-dependent manner. The toxin neither affected the spike in the postsynaptic nor the presynaptic fibers. Spontaneous miniature potentials recorded from thin stellate nerves were suppressed by the toxin. Iontophoretically applied L-glutamate depolarized the postsynaptic membrane of the giant axon and this potential was also blocked by JSTX. Kainic acid also depolarized the postsynaptic membrane but this was partially blocked by JSTX, indicating that JSTX differentiated kainate receptor from glutamate one. The results strongly suggest that L-glutamate is the neurotransmitter in the giant synapse of squid.

Animals↗
PubMed1985

Membranous glomerulonephritis associated with enterococcal endocarditis.

An autopsy case of membranous glomerulonephritis associated with enterococcal endocarditis was reported. Although enterococcal antigen was not identified in glomerular deposits, the eluate from the patient's renal tissue was shown to specifically recombine with cells of the enterococcus isolated from his own ante mortem blood. Hypocomplementemia, circulating immune complexes and antienterococcal antibodies were also observed. These findings suggest that enterococcus-related immune complexes played a role in the pathogenesis of glomerulonephritis associated with enterococcal endocarditis in this patient.

Aged↗
PubMed1985

Induction of rat pancreatic B-cell tumors by the combined administration of streptozotocin or alloxan and poly(adenosine diphosphate ribose) synthetase inhibitors.

Streptozotocin and alloxan were administered to Wistar rats in combination with poly(adenosine diphosphate ribose) synthetase inhibitors. Ten to 16 months after the injection of streptozotocin (50 mg/kg body weight i.v.) and 3-aminobenzamide (345 mg/kg i.v.), streptozotocin (50 mg/kg) and nicotinamide (350 mg/kg i.p.), streptozotocin (50 mg/kg) and picolinamide (250 mg/kg i.p.), alloxan (40 mg/kg i.v.) and nicotinamide (350 mg/kg), alloxan (40 mg/kg) and 3-aminobenzamide (345 mg/kg), and alloxan (40 mg/kg) and picolinamide (250 mg/kg), pancreatic islet cell tumors developed in 100, 98, 60, 26, 22, and 20% of surviving rats, respectively. However, after the single injection of streptozotocin and alloxan, islet cell tumors developed in 42 and 11% of surviving rats, respectively. The tumors were rich in B-granules on electron micrographs and contained as large amounts of proinsulin messenger RNA as normal pancreatic islets. The results indicate that poly(adenosine diphosphate ribose) synthetase inhibitors enhance the tumorigenic effect of streptozotocin and alloxan on islet B-cells.

Adenoma, Islet Cell↗
PubMed1984

Spider toxin (JSTX) on the glutamate synapse.

A new neurotoxin (JSTX) was separated from spider (Nephila clavata, Joro spider) venom. JSTX irreversibly suppressed the excitatory postsynaptic potential (EPSP) and the glutamate potential in the lobster neuromuscular junction with high degree of specificity. The threshold concentration for suppressing EPSPs corresponds to a small fraction of the toxin in a venom gland, roughly estimated as low as 10(-10) M/l. 10(-10) M/l. In the giant synapse of squid stellate ganglion JSTX suppressed EPSPs without affecting the antidromic response. Glutamate-induced membrane depolarization was blocked by JSTX. In mammalian brain slice preparation, JSTX suppressed the orthodromic spike response but failed to affect on the antidromic spike in the hippocampal pyramidal neuron of CA1 and CA3 region. The above results strongly support the view that the squid giant synapse and synapses in the hippocampal pyramidal neuron are mediated by glutamate.

Animals↗
PubMed1983

Effects of a spider toxin on the glutaminergic synapse of lobster muscle.

We studied the effect of neurotoxin (JSTX) separated from spider venom on the lobster neuromuscular junction. JSTX selectively suppressed excitatory post-synaptic potentials (e.p.s.p.s) without affecting the inhibitory post-synaptic potentials (i.p.s.p.s). The effect of JSTX was dose-dependent. The threshold dose for suppressing e.p.s.p.s corresponded to a small fraction of the toxin amount in a venom gland. At high concentration, JSTX irreversibly blocked e.p.s.p.s. The reduction in amplitude of extracellularly recorded e.p.s.p.s after JSTX application followed an exponential time course. The rate of suppression increased proportionally with the toxin concentration. JSTX blocked the glutamate potential in the post-synaptic membrane but it failed to affect the aspartate-induced depolarization. Kainic acid potentiated the glutamate-induced depolarization but it was without effect in the presence of JSTX. Depolarization produced by quisqualic acid is suppressed by the toxin. Our results suggest that the spider venom contains specific blockers of glutamate receptors in crustacean neuromuscular junctions.

Animals↗