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“School of Cognitive Sciences”

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Paper   IPM / Cognitive Sciences / 12175
School of Cognitive Sciences
  Title:   B1-noradrenergic system of the central amygdala is involved in state-dependent memory induced by a cannabinoid agonist, WIN55,212-2, in rat
1.  Maryam Ghiasvand
2.  Ameneh Rezayof
3.  Shamseddin Ahmadi
4.  Mohammad Reza Zarrindast
  Status:   Published
  Vol.:  225
  Year:  2011
  Pages:   1-3
  Supported by:  IPM
In the present study, we investigated effects of intra-central amygdala (intra-CeA) administrations of a B 1-receptor agonist and antagonist, isoprenaline (isoproterenol) and atenolol respectively, on state-dependent memory induced by a cannabioid agonist, WIN55,212-2. This study used a step-through inhibitory avoidance task to assess memory in male Wistar rats. The results showed that post-training intra-CeA administrations of different doses of WIN55,212-2 (0.01, 0.05, 0.1 and 0.25 ug/rat) decreased memory as revealed by a decrease in memory retrieval on the test day. The decrease in retrieval induced by post-training WIN55,212-2 (0.25 ug/rat) was reversed by pre-test administration of the same dose of the drug, which was suggestive of drug-induced state-dependent memory. Although pre-test intra-CeA administrations of isoprenaline (0.01, 0.025 and 0.05 g/rat) alone had no effect, its co-administrations at doses of 0.025 and 0.05 ug/rat with an ineffective dose of WIN55,212-2 (0.1 ug/rat) restored memory retrieval that impaired by post-training WIN55,212-2 (0.25 ug/rat). The results also showed that pre-test intra-CeA administrations of atenolol (0.01, 0.05 and 0.1 g/rat) alone had no effect, but at dose of 0.1 g/rat disrupted state-dependent memory induced by WIN55,212- 2. Moreover, the improving effect of isoprenaline (0.025 g/rat) on retrieval of state-dependent memory induced by WIN55,212-2 (0.1 ug/rat) was prevented by intra-CeA co-injections of atenolol. Taken together, our results suggest that the CeA may be potentially critical for statedependent memory induced by WIN55,212-2 and the B 1-noradrenergic receptor mechanism(s) interact with the cannabinergic system in the modulation of this kind of memory in the CeA.

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