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1 ), but not a GABAA receptor channel blocker (pentylenetetrazol).
2 increased sensitivity to the chemoconvulsant pentylenetetrazol.
3 eizure threshold was assessed in response to pentylenetetrazol (1% solution, i.v.) in adolescence (~P
4 kg, i.v.), kainic acid (12.0 mg/kg, i.v.) or pentylenetetrazol (100-250 mg/kg, i.p).
5 lsant potencies of systemically administered pentylenetetrazol (30-50 mg/kg) and NMDA (50-100 mg/kg).
6  exhibited decreased latency to seizure upon pentylenetetrazol administration.
7 t of y-aminobutyric acid receptor antagonist pentylenetetrazol also showed signs of reducing the RI.
8 hold dose (40 mg/kg) of the chemo-convulsant pentylenetetrazol and events recorded over 1 h.
9 eizures or alter the convulsant potencies of pentylenetetrazol and NMDA.
10 e model by kindling with the chemoconvulsant pentylenetetrazol and observed that the mouse model exhi
11 namics resolved SD evoked by an injection of pentylenetetrazol as a bilateral wave of hypoperfusion a
12  elevated seizure response to the convulsant pentylenetetrazol compared with sham mice, associated wi
13      Caudolateral SNr lesions did not affect pentylenetetrazol-enhanced convulsions.
14  study, we evaluated the effects of 15 daily pentylenetetrazol-induced convulsions in immature rats b
15  kainic acid, as well as greater severity of pentylenetetrazol-induced convulsions.
16 ronal excitability and the susceptibility to pentylenetetrazol-induced seizure in mice.
17        Aged apoE4 TR mice progressed through pentylenetetrazol-induced seizure stages more rapidly th
18                                 We have used pentylenetetrazol-induced seizure that produces synchron
19 ed plus-maze and increased susceptibility to pentylenetetrazol-induced seizures were apparent 96 h (b
20                            Mutants displayed pentylenetetrazol-induced seizures, confirming epilepsy
21 nger (NCX) may contribute to the etiology of pentylenetetrazol-induced seizures.
22 sant activity of systemic AMPA, kainate, and pentylenetetrazol is not mediated by GluK1 kainate recep
23 e, and maximal electroshock and subcutaneous pentylenetetrazol (Metrazol) in rats.
24 ic alcohol exposure, and seizure response to pentylenetetrazol or an audiogenic stimulus.
25 M and (2) disinhibiting the slice using 3 mM pentylenetetrazol or combined application of 10 microM g
26 ithout injections) and animals injected with pentylenetetrazol (PTZ) and euthanized at different time
27 ids displayed anticonvulsant activity in the pentylenetetrazol (PTZ) and maximal electroshock (MES) t
28  investigate behavioral seizure responses to pentylenetetrazol (PTZ) and to map the location of genes
29 tomatic stages and be further exacerbated by pentylenetetrazol (PTZ) kindling.
30 tion are consistent with the decrease in the pentylenetetrazol (PTZ) seizure threshold which was prev
31 d plasma THDOC concentrations and raised the pentylenetetrazol (PTZ) seizure threshold.
32  CIE treatment also increased the ability of pentylenetetrazol (PTZ) to inhibit GABA mediated 36Cl- i
33                        Under the exposure of Pentylenetetrazol (PTZ), an epilepsy-inducing drug, clea
34 l electroshock (MES), 6 Hz (32/44 mA), acute pentylenetetrazol (PTZ), and PTZ-kindling.
35 ing seizure susceptibility to the convulsant pentylenetetrazol (PTZ), given via timed tail vein infus
36 muli: 2,2,2-trifluroethyl ether (flurothyl), pentylenetetrazol (PTZ), kainic acid, and high-decibel s
37 olecular consequences of seizures induced by pentylenetetrazol (PTZ), which is a widely used convulsa
38                                      Using a pentylenetetrazol (PTZ)-induced epilepsy rat model (n =
39                                              Pentylenetetrazol (PTZ)-induced seizures occurred with s
40 ever, seizure severity and susceptibility to pentylenetetrazol (PTZ)-induced seizures were significan
41 nic seizures and less EEG activity following pentylenetetrazol (PTZ; 70 mg/kg, IP) administration tha
42 ncidence of tonic-clonic seizures induced by pentylenetetrazol (PTZ; 70 mg/kg, IP) administration.
43                          The GABA antagonist pentylenetetrazol restored learning without restoring ci
44 sceptibility to tonic-clonic seizures in the pentylenetetrazol seizure model, whereas adeno-associate
45 d a significantly lower seizure threshold to pentylenetetrazol than controls.
46 xcitability and reduced seizure threshold to pentylenetetrazol treatment.