ライフサイエンスコーパス: pentylenetetrazol

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1 ), but not a GABAA receptor channel blocker (pentylenetetrazol).

2 increased sensitivity to the chemoconvulsant pentylenetetrazol.

3 kg, i.v.), kainic acid (12.0 mg/kg, i.v.) or pentylenetetrazol (100-250 mg/kg, i.p).

4 lsant potencies of systemically administered pentylenetetrazol (30-50 mg/kg) and NMDA (50-100 mg/kg).

5 hold dose (40 mg/kg) of the chemo-convulsant pentylenetetrazol and events recorded over 1 h.

6 eizures or alter the convulsant potencies of pentylenetetrazol and NMDA.

7 elevated seizure response to the convulsant pentylenetetrazol compared with sham mice, associated wi

8 Caudolateral SNr lesions did not affect pentylenetetrazol-enhanced convulsions.

9 study, we evaluated the effects of 15 daily pentylenetetrazol-induced convulsions in immature rats b

10 kainic acid, as well as greater severity of pentylenetetrazol-induced convulsions.

11 ronal excitability and the susceptibility to pentylenetetrazol-induced seizure in mice.

12 Aged apoE4 TR mice progressed through pentylenetetrazol-induced seizure stages more rapidly th

13 We have used pentylenetetrazol-induced seizure that produces synchron

14 ed plus-maze and increased susceptibility to pentylenetetrazol-induced seizures were apparent 96 h (b

15 nger (NCX) may contribute to the etiology of pentylenetetrazol-induced seizures.

16 sant activity of systemic AMPA, kainate, and pentylenetetrazol is not mediated by GluK1 kainate recep

17 e, and maximal electroshock and subcutaneous pentylenetetrazol (Metrazol) in rats.

18 ic alcohol exposure, and seizure response to pentylenetetrazol or an audiogenic stimulus.

19 M and (2) disinhibiting the slice using 3 mM pentylenetetrazol or combined application of 10 microM g

20 ids displayed anticonvulsant activity in the pentylenetetrazol (PTZ) and maximal electroshock (MES) t

21 investigate behavioral seizure responses to pentylenetetrazol (PTZ) and to map the location of genes

22 tion are consistent with the decrease in the pentylenetetrazol (PTZ) seizure threshold which was prev

23 d plasma THDOC concentrations and raised the pentylenetetrazol (PTZ) seizure threshold.

24 CIE treatment also increased the ability of pentylenetetrazol (PTZ) to inhibit GABA mediated 36Cl- i

25 ing seizure susceptibility to the convulsant pentylenetetrazol (PTZ), given via timed tail vein infus

26 muli: 2,2,2-trifluroethyl ether (flurothyl), pentylenetetrazol (PTZ), kainic acid, and high-decibel s

27 olecular consequences of seizures induced by pentylenetetrazol (PTZ), which is a widely used convulsa

28 Pentylenetetrazol (PTZ)-induced seizures occurred with s

29 nic seizures and less EEG activity following pentylenetetrazol (PTZ; 70 mg/kg, IP) administration tha

30 ncidence of tonic-clonic seizures induced by pentylenetetrazol (PTZ; 70 mg/kg, IP) administration.

31 The GABA antagonist pentylenetetrazol restored learning without restoring ci

32 d a significantly lower seizure threshold to pentylenetetrazol than controls.

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