Objective: 

Oxytocin's (OX) recently attributed features other than its well known endocrine effects have been on the agenda lately. In this study, we hypothesized that OX might possibly exert anticonvulsant effect, and we investigated this in pentylenetetrazol (PTZ) induced generalized seizure and absence seizure rat model, identifying the action by behavioral measurement and thalamic EEG recordings.

Methods: 

Using 60 (8-12 week old) Sprague Dawley male rats, we set 10 groups (n=6 / group), administered i.p. 10, 20, 40, 80 and 120 U/kg OX to Groups 1-5, and saline only to Group 6 (control); 5 minutes later, we administered 70 mg/kg PTZ, and determined the dose-response ratio. Evaluating seizures by using Racine's Convulsion Scale, we determined the absence seizure inducing PTZ dose as 35 mg/kg, and the supressive OX doses as 80 and 120 U/kg. We recorded EEG on the Biopac MP30 System by bipolar EEG electrodes implanted in the left nucleus of posterior thalamus using stereotaxy (AP: -3.6 mm,L: +2.8 mm,V: -5.0 mm; Paxinos). We administered saline only, 35 mg/kg PTZ only, and 80 and 120 U/kg OX plus PTZ to the Groups 7, 8, 9 and 10, respectively. We affirmed electrode location histologically following euthanisation.Processing recordings by "Power Spectral Analysis" using the "Fast Fourier Transform", we determined the percentage dominance of EEG waves.

Results: 

The potent anticonvulsant effect emerging at 40 and 80 U/kg doses (p<0.05) and peaking at 120 U/kg dose of OX, and its significant (p<0.005) overall delta enhancing and theta attenuating effect (p<0.005) were definitely demonstrative.

Conclusions: 

Our results suggest OX as a putative anticonvulsant in treating epilepsy. We aim to identify the specific mechanism mediating this action.