Oxytocin inhibits pentylentetrazol-induced seizures in the rat
► Epilepsy is characterized as recurrent seizures arising from abnormal electrical activity. ► PTZ-induced seizures result in electrographic, molecular and endocrine responses in the brain. ► Oxytocin (OT) is a neurohypophysial nonapeptide synthesized in hypothalamus. ► It was found that OT has an i...
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Veröffentlicht in: | Peptides (New York, N.Y. : 1980) N.Y. : 1980), 2013-02, Vol.40, p.141-144 |
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Sprache: | eng |
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Zusammenfassung: | ► Epilepsy is characterized as recurrent seizures arising from abnormal electrical activity. ► PTZ-induced seizures result in electrographic, molecular and endocrine responses in the brain. ► Oxytocin (OT) is a neurohypophysial nonapeptide synthesized in hypothalamus. ► It was found that OT has an inhibitory effect on seizures via EEG recording. ► OT could be used to treat epilepsy patient.
We aimed to reveal the anti-convulsant effects of oxytocin (OT) in pentylenetetrazol (PTZ)-induced seizures in rats. Thirty rats were randomly divided into 5 equal groups. Using stereotaxy, we implanted electroencephologram (EEG) electrodes in the left nucleus of the posterior thalamus. After 2 days, the first and second groups were used as the control and PTZ (35mg/kg) groups, respectively. We administered 40, 80 and 160nmol/kg OT+35mg/kg PTZ to the rats, constituting the third, fourth, and fifth groups, respectively, for 5 days. At the end of 5 days, we recorded EEGs via bipolar EEG electrodes. After 12h, all groups except the first received 70mg/kg PTZ and we determined the dose–response ratio. Racine's Convulsion Scale was used to evaluate seizures. The spike–wave complex percentage in the EEG was determined as 0% for the first group, 38.6%±7.2 for the second group, 36.4%±5.6 for the third group, 4.3%±1.8 for the fifth group and 4.1%±1.1 for the fifth group. The fourth and fifth groups had significantly decreased spike–wave complex percentages compared to the second group (p |
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ISSN: | 0196-9781 1873-5169 |
DOI: | 10.1016/j.peptides.2012.12.003 |