P.0358 Synergistic anticonvulsant effect of carbamazepine and mono-/bicyclic terpenoids on pentylenetetrazole-induced seizures

2021 ◽  
Vol 53 ◽  
pp. S260-S261
Author(s):  
M. Nesterkina ◽  
I. Kravchenko
2009 ◽  
Vol 22 (2) ◽  
pp. 115-124
Author(s):  
Anna Zadrożniak ◽  
MichaŁ K. Trojnar ◽  
Marcin P. Trojnar ◽  
Żaneta Kimber-Trojnar ◽  
Monika Dudra-Jastrzębska ◽  
...  

1983 ◽  
Vol 48 (4) ◽  
pp. 1173-1186 ◽  
Author(s):  
Václav Bártl ◽  
Jiří Holubek ◽  
Emil Svátek ◽  
Marie Bartošová ◽  
Miroslav Protiva

Reactions of 10-(4-aminopiperazino)-10,11-dihydrodibenzo[b,f]thiepins XIVa-XIVd with benzaldehyde, 3,4-dimethoxybenzaldehyde, 4-dimethylaminobenzaldehyde, salicylaldehyde, 3-ethoxy-4-hydroxybenzaldehyde, 2-(2-dimethylaminoethoxy)benzaldehyde, 3-(2-dimethylaminoethoxy)benzaldehyde and 3-ethoxy-4-(2-dimethylaminoethoxy)benzaldehyde afforded a series of 19 hydrazones IIIa-Xc. Some of them showed the expected anticonvulsant effect but only towards pentetrazole; antagonism of maximal electroshock seizures was not observed. In general, the products have a character of tranquillizers: in higher does they produce central depression, potentiate the thiopental sleeping time, have hypothermic action; in single cases antiamphetamine, antireserpine, antihistamine and cataleptic effects were observed. The water-soluble salts of the basic hydrazones VIIIa, VIIIc, IXc and Xc, administered parenterally, showed a rather high acute toxicity and revealed also adrenolytic and hypotensive activity.


1989 ◽  
Vol 54 (1) ◽  
pp. 225-228 ◽  
Author(s):  
Irena Červená ◽  
Jiří Holubek ◽  
Emil Svátek ◽  
Jan Metyš ◽  
Martin Valchář ◽  
...  

Heating of 4-methoxydibenzo[b,e]thiepin-11(6H)-one with pyridine hydrochloride to 225 to 235 °C effected demethylation and gave IV. Its sodium salt reacted with 3-dimethylaminopropyl chloride in ethanol and afforded the 4-(3-dimethylaminopropoxy) compound II. The isomeric ether III was prepared via the 4-(4-bromobutoxy) compound V. Hydrochloride of II (VÚFB-17 033) inhibited mildly the binding of [3H]desipramine in rat hypothalamus, had antireserpine activity in rats, mild anticonvulsant effect, and antihypoxic effect in the test of nitrogen anoxia in mice.


2009 ◽  
Vol 41 (1) ◽  
pp. 41 ◽  
Author(s):  
Radha Goel ◽  
Amit Goel ◽  
Anshu manocha ◽  
KK Pillai ◽  
RashmiS Srivastava

2005 ◽  
Vol 82 (1) ◽  
pp. 74-81 ◽  
Author(s):  
Anshu Manocha ◽  
Krishna Kishore Sharma ◽  
Pramod Kumari Mediratta

2010 ◽  
Vol 19 (4) ◽  
pp. 568-574 ◽  
Author(s):  
Abbas Ghasemi ◽  
Mohammad Saberi ◽  
Mehdi Ghasemi ◽  
Hamed Shafaroodi ◽  
Leila Moezi ◽  
...  

PEDIATRICS ◽  
1983 ◽  
Vol 71 (3) ◽  
pp. 467-468
Author(s):  
JOHN M. FREEMAN

In Reply.— Coen is correct. Seizures are a sign of CNS disorders, and adequate diagnosis and appropriate specific therapy are always indicated. However, as our study showed, most seizures occurring during the first three or four days of life are related to hypoxia and/or asphyxia and there is no specific therapy. Whether seizures per se cause brain damage in humans remains a matter of debate. Whether the problem of anticonvulsant effect on neurons is of significance in vivo remains to be proven.


2012 ◽  
pp. 619-628 ◽  
Author(s):  
E. SZCZUROWSKA ◽  
P. MAREŠ

The activation of metabotropic glutamate receptors subtype 4 (mGluR4) potentiates models of absence seizures in adult rats. These seizures are age-dependent, but data concerning the role of mGluR4 in immature brain is insufficient. N-phenyl-7-(hydroxyimino)cyclopropa[b]chromen-1acarboxamide (PHCCC), which is a positive allosteric modulator of these receptors, was used in three different models of seizures in immature rats: 1) convulsions induced by high doses of pentetrazol (PTZ; a model of generalised tonic-clonic seizures); 2) rhythmic electro-encephalographic (EEG) activity induced by low doses of PTZ (a model of absence seizures); and 3) electrically elicited cortical afterdischarges (ADs, a model of myoclonic seizures). We administered four doses of PHCCC (1, 3, 10 and 20 mg/kg) in PTZ-induced convulsions and two doses (3 and 10 mg/kg) in the two electrophysiological models of freely moving rats with implanted electrodes. Every dose and age group consisted from 8 to 10 rats. PTZ-elicited convulsions were not significantly influenced by PHCCC. In contrast, PHCCC potentiated the effect of a subconvulsant dose (60 mg/kg) of PTZ. The 10-mg/kg dose of PHCCC significantly prolonged the duration of PTZ-induced rhythmic activity episodes and shortened the intervals between individual episodes in 25-day-old rats (P25). In contrast, this potentiation was not seen in P18 rats. Cortical ADs were significantly prolonged with repeated stimulations by both doses of PHCCC in P12 and P18 animals. P25 rats exhibited only slightly longer AD durations. In conclusion, we did not find any anticonvulsant effect of PHCCC. On the contrary, proconvulsant action was demonstrated in all three models in immature rats.


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