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1 l response to a GABA(A) receptor antagonist, pentylenetetrazole.
2 ures induced by pilocarpine, kainic acid, or pentylenetetrazole.
3 istration of the GABA(A) receptor antagonist pentylenetetrazole.
4 convulsant drugs: caffeine (250mg/L; 1.3mM), pentylenetetrazole (1.5g/L; 11.0mM) and picrotoxin (100m
6 d severity of seizures induced by kainate or pentylenetetrazole, and both necrosis and apoptosis of h
7 mice where the effects of the proconvulsant pentylenetetrazole are attenuated by acutely increasing
9 ic rat brain regions by the convulsive drug, pentylenetetrazole, as well as by the anticonvulsant dru
10 , did not interfere with seizures induced by pentylenetetrazole, bicucculine, picrotoxin, and strychn
11 at electrographic seizure events, induced by pentylenetetrazole, can be reliably distinguished from e
12 uration or scores of the seizures induced by pentylenetetrazole, DHA significantly prolonged the seiz
13 norhabditis elegans (Lis-1) and Danio rerio (pentylenetetrazole) highlight a reductionist approach.
14 ound persistently enhanced susceptibility to pentylenetetrazole-induced convulsions 15 weeks after TB
15 25 (LY3130481), was fully protective against pentylenetetrazole-induced convulsions in rats without t
16 and delayed the onset of chemical convulsant pentylenetetrazole-induced generalized convulsive seizur
17 ad no effect on Kv2.1 channels, and moderate pentylenetetrazole-induced seizure activity in adult mic
18 ompound 33 was also found to be effective in pentylenetetrazole-induced seizure model (ED50 PTZ = 123
19 is the most effective anticonvulsant against pentylenetetrazole-induced seizures (ED50, 37 mg/kg; PI
22 ned using a completely independent paradigm, pentylenetetrazole-induced tonic-clonic seizures, exclud
24 KO mice to seizures induced by kainic acid, pentylenetetrazole, or flurothyl, although DKO mice were
25 rent convulsant mechanisms (4-Aminopyridine, Pentylenetetrazole, Pilocarpine and Strychnine) resulted
26 tion patterns, transient seizure activity by pentylenetetrazole provoked only a brief c-Jun phosphory
27 NA interference (RNAi) was performed using a pentylenetetrazole (PTZ) exposure paradigm to induce con
29 s in vivo in 2 and 14-day old piglets during pentylenetetrazole (PTZ) seizures using 31P nuclear magn
32 manifest increased aggressiveness and higher pentylenetetrazole (PTZ)-induced seizure propensity.
33 bility, we administered the GABAA antagonist pentylenetetrazole (PTZ; 0.3 or 1.0 mg/kg/day) to arrhyt
34 controls and their ictal activity following pentylenetetrazole (PTZ; 85 mg/kg i.p.) was compared to
35 al electroshock (MES) test, the subcutaneous pentylenetetrazole (scPTZ) test, and the six-hertz (6 Hz
37 vity induced by intraperitoneal injection of pentylenetetrazole was recorded from microwire electrode
38 oxidation in the cerebral cortex induced by pentylenetetrazole was significantly attenuated by DHA,
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