Abstract
Background: 17β-Estradiol modulates nociception by binding to the estrogen receptors and also by allosteric interaction with other membrane-bound receptors like the NMDA receptors. The paragigantocellularis lateralis nucleus (LPGi) is also involved in the pain modulation. In this study, the role of NMDA receptors of the LPGi nucleus has been investigated in the 17β-estradiol-induced pain modulation in the ovariectomized rats.
Materials and Methods: In this study, the female Wistar rats in the range of 200-270 gr were used. In order to study the role of the NMDA receptors in the 17β-estradiol-induced pain modulation in the ovariectomized rats, primarily, rats were bilaterally ovariectomized and immediately cannulation of the LPGi nucleus was performed. Then, drugs were injected and 15 minutes later 50 μl of 5% formalin was injected into the rat's hind paw; and formalin-induced paw jerking behaviour was recorded for 60 min.
Results: The results of the present study showed that the intra-LPGi injection of 17β-estradiol significantly reduced the paw jerking behavior both in the first and in the second phases of formalin test. Pretreatment of the LPGi nucleus by NMDA receptor antagonist (AP5) neutralized the antinociceptive effect of 17β-estradiol on the paw jerking frequency in the both phases of formalin test; and induced hyperalgesia in the both phases of this behavior.
Conclusion: These results indicated that the intra-LPGi injection of 17β-estradiol produces modest analgesia on the formalin-induced inflammatory pain. Therefore, it can be concluded that the NMDA receptors of the paragigantocellularis lateralis nucleus are probably involved in the antinociceptive effect of 17β-estradiol in the ovariectomized rats.
 

Background and Aim: The purpose of this study was to investigate the stimulatory and protective effects of Methylphenidate (MPD) on the experimental epilepsy induced by intraperitoneal injection of Pentylenetetrazole (PTZ) in adult male rats.
Methods & Materials: In this study, 15 male rats (weight, 200-250 gr) dividied into one control group (n=5) received normal saline and two treatment groups; the first group (n=5) received MPD with a dose of 2.5 mg/kg and the second group (n=5) received MPD with a dose of 5 mg/kg by gavage. After anesthesia with ketamine-xylazin combination and animal skull surgery, the recorded electrodes were inserted into the cranium in the stratum striatum layer of the CA1 region of the hippocampus, and epileptic activity was induced by intraperitoneal injection of PTZ (80 mg/kg) and the epileptiform activity was evaluated in terms of the number of spikes per time unit and their amplitudes by eTrace software.
Ethical Considerations: This study with an ethics code of FVMT.REC.1397.67 was approved by the Research Ethics Committee of the Faculty of Veterinary Medicine at University of Tabriz. 
Results: Oral MPD at 2.5 and 5 mg/kg doses increased the number of spikes up to 576 and 613, respectively, compared to the control group (330 spikes), which were statistically significant. Amplitude of PTZ-induced epileptic activity after treatment with 2.5 and 5 mg/kg MPD reached 1254 and 1085 respectively compared to control group (1051), which were not statistically significant.
Conclusion: The doses of oral MPD used in this study potentiate seizure activity. Therefore, the use of this drug in people with a background of seizure or suffering from some types of seizure should be cautious, and the evaluation of its effect in these patients need further studies.