Zahra Kiasalari; Mohsen Khalili; Mehrdad Roghani; Abbas Ahmadi; Monireh Mireie
Volume 9, Issue 2 , April 2014, , Pages 138-148
Abstract
Background and Objective: N-Methyl-D-aspartate (NMDA) antagonists such as piperidines are the most important antiepileptic drugs. Considering the fact that piperidine derivatives such as phencyclidine (PCP) and its new derivative, 1-[1-(3-methoxyphenyl) (tetralyl)] piperidine (PCP1), have different potencies, ...
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Background and Objective: N-Methyl-D-aspartate (NMDA) antagonists such as piperidines are the most important antiepileptic drugs. Considering the fact that piperidine derivatives such as phencyclidine (PCP) and its new derivative, 1-[1-(3-methoxyphenyl) (tetralyl)] piperidine (PCP1), have different potencies, the antiepileptic effects of mentioned drugs were investigated in the present study.
Methods: Fifty male mice weighing 25-30 g were randomly selected and divided into five experimental groups: 1- Control 2- Pentylentetrazole-kindled mice, 3- Positive control group which received valproate, and groups 4 and 5, which received PCP and PCP1, respectively. Kindling was down by 11 periods injection of PTZ every second day for 22 days. At the 12th injection, all kindled group were tested for PTZ challenge dose. The exhibited phases of seizure (0-6) were observed and noted till 30 minutes after PTZ injection. Finally, the malondialdehyde, superoxide dismutase and nitric oxide levels of the animal’s brain tissues were determined and compared with others.
Results: PCP1 could have a prominent anti-convulsion effect compared to PCP, especially in the reduction of phase 2 duration time and seizure score in challenge dose. Our additional experiments showed that there was a significant reduction in NO level in PCP1 treated animals.
Conclusion: Administration of the new piperidine derivate, PCP1 could have yielded a prominent anti-convulsion effect in grand epilepsy. Regarding to the changes in conformation of PCP1 as a non-competitive antagonist of NMDA receptor, it may block the NMDA receptors potentially more effectively than phencyclidine.
Mohsen Khalili; Zahra Kiasalari; Batol Rahmati; Jamshid Narenjkar
Volume 5, Issue 1 , January 2010, , Pages 27-33
Abstract
Background and Objectives: There is well established the beneficial effects of Crocus sativus extract in learning and memory improvement. In the present study the effect of this plant in memory behavioral impairment and forbrain histological damage induced by STZ-icv model of Alzheimer disease ...
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Background and Objectives: There is well established the beneficial effects of Crocus sativus extract in learning and memory improvement. In the present study the effect of this plant in memory behavioral impairment and forbrain histological damage induced by STZ-icv model of Alzheimer disease were investigated. Materials and Methods: This study was conducted at Shahed University (Tehran) in 2007. Forty five male rats were divided into three 15 number groups: 1- Control which received CSF bilaterally two times in 1 and 3 days (10 µl in each injection ) 2- STZ-icv, streptozotocin (3 mg/kg) dissolved in CSF was injected (icv) to the animals. 3- STZ+CSE, the STZ-icv animals received the plant extract (30 mg/kg; i.p) one other day as treatment ones. All of the animal groups were weighted and subjected to memory behavioral passive avoidance test and brain histological damage analysis. Results: STZ caused selective injury to the fornix and hippocampus and an enlargement as well as loss of ependymal cell in third ventricle. However, STZ-icv treated animals with CSE (30 mg/kg, i.p) one other day starting one day pre-surgery for three weeks show higher correct choice and lower errors in shuttle box test than vehicle-treated STZ-injected rats. But the same CSE treatment rats did not show any antagonizing effects on STZ-icv induced histological impairment. Conclusion: Our findings provide an explanation for effectiveness of CSE in preventing the cognitive deficits caused by STZ-icv in rats, which mediated by enzymes, metabolisms (glucose utilization) and other biochemical pathways, but not via histological injury repair.
