شماره ركورد :
90082
عنوان مقاله :
هسته آميگدال بر تشنجهاي ناشي از كنيدلينگ هيپوكمپ در موشهاي صحرايي A1 تاثير فعاليت گيرنده هاي آدنوزيني
عنوان به زبان ديگر :
Effect of Amygdala Adenosine A, Receptors on Kindled Seizures in Rats
پديد آورندگان :
ميرنجفي زاده ، جواد نويسنده Mirnajafi-Zadeh, javad , محمدحسين پورغلامي ف يعقوب فتح الهي، مترجم ,
رتبه نشريه :
-
تعداد صفحه :
8
از صفحه :
275
تا صفحه :
282
كليدواژه :
Kindling , 1,3-dimethyl-8-cyclopenthylxanthine , N^6-cyclohexyladenosine , تشنج , هيپوكمپ , كنيدلينگ , سيكلوهگزيل آدنوزين , آميگدال , 1،3 دي متيل , 8 سيكلوپنتل گزانتين , N6 , Seizure , Hippocampus , Amygdala
چكيده لاتين :
Epilepsy is a common neural abnormality. Many investigations on the role of antiepileptic agents using experimental model of epilepsy have been done. On the other hand, adenosine is a neuromodulator which exert antiepileptic effects via its Al receptors. In this study effects of intra amygdala infusion of a selective adenosine Al receptor agonist (N6-cyclohexyladenosine; CHA) and a selective adenosine Al receptor antagonist (1,3-dimetyl-8-cyclopenthylxanthine; CPT) on hippocampal kindled seizure were investigated. All animals had a tripolar electrode implanted into the CAI region of the hippocampus and a guide cannula attached to a monopolar electrode into the amygdala. One week after surgery, the animals were given by electrical stimulation of the CAI region of the hippocampus to be kindled and prepared for drug injections. The drugs were dissolved in artificial cerebrospinal fluid. Data showed that intra-amygdala injection of CHA (5nM-1mM; 1miu lit/2min) reduced hippocampal secondary afterdischarge duration and amygdala afterdischarge duration significantly. On the other hand intraamygdala infusion of CPT (0.5 and1miu M) had no significant effect on seizure parameters. Also, intraamygdala CPT pretreatment before CHA, inhibited the CHA effects. Therefore, it may be suggested that in hippocampal kindling, the amygdala has a relaying role in spreading afterdischarge especially in producing hippocampal reactivity and secondary afterdischarges and the activity of adenosine A1 receptors of the amygdala reduced this.
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