1403/02/06
شمس الدین احمدی

شمس الدین احمدی

مرتبه علمی: دانشیار
ارکید: 0000-0003-0300-3226
تحصیلات: دکترای تخصصی
اسکاپوس: 12141695900
دانشکده: دانشکده علوم پایه
نشانی: سنندج، دانشگاه کردستان، دانشکده علوم پایه، گروه علوم زیستی
تلفن: 08733664600 (2510)

مشخصات پژوهش

عنوان
Activation of cannabinoid CB1 receptors in the central amygdala impairs inhibitory avoidance memory consolidation via NMDA receptors
نوع پژوهش
JournalPaper
کلیدواژه‌ها
Central amygdala - Memory consolidation - ACPA - NMDA - D-AP5 - Rat
سال
2011
مجله Neurobiology of Learning and Memory
شناسه DOI
پژوهشگران Maryam Ghiasvand ، Ameneh Rezayof ، Mohammad Reza Zarrindast ، Shamseddin Ahmadi

چکیده

In the present study, we investigated the influence of bilateral intra-central amygdala (intra-CeA) microinjections of N-methyl-D-aspartate (NMDA) receptor agents on amnesia induced by a cannabinoid CB1 receptor agonist, arachydonilcyclopropylamide (ACPA). This study used a step-through inhibitory (passive) avoidance task to assess memory in adult male Wistar rats. The results showed that intra-CeA administration of ACPA (2 ng/rat) immediately after training decreased inhibitory avoidance (IA) memory consolidation as evidenced by a decrease in step-through latency on the test day, which was suggestive of drug-induced amnesia. Post-training intra-CeA microinjections of NMDA (0.0001, 0.001 and 0.01 µg/rat) did not affect IA memory consolidation. However co-administration of NMDA with ACPA (2 ng/rat) prevented the impairment of IA memory consolidation that was induced by ACPA. Although post-training intra-CeA administration of the NMDA receptor antagonist, D-(-)-2-amino-5-phosphonopentanoic acid (D-AP5; 0.01, 0.05 and 0.1 µg/rat) alone had no effect, its co-administration with an ineffective dose of ACPA (1 ng/rat) impaired IA memory consolidation. Post-training intra-CeA microinjection of an ineffective dose of D-AP5 (0.01 µg/rat) prevented an NMDA response to the impaired effect of ACPA. These results suggest that amnesia induced by intra-CeA administration of ACPA is at least partly mediated through an NMDA receptor mechanism in the Ce-A.