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IPM
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“School of Cognitive Sciences”

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Paper   IPM / Cognitive Sciences / 12812
School of Cognitive Sciences
  Title:   Possible interaction between opioidergic and cholinergic systems of CA1 in cholestasis-induced amnesia in mice
  Author(s): 
1.  Mohammad Reza Zarrindast
2.  Saereh Hoseindoost
3.  Mohammad Nasehi
  Status:   Published
  Journal: Behavioural Brain Research
  Vol.:  228
  Year:  2012
  Pages:   116-124
  Supported by:  IPM
  Abstract:
Bile duct ligation (BDL) induces primary biliary cirrhosis characterized by cholestasis, impaired liver function and cognition including impairment of memory formation and anxiety-like behaviors. Endogenous opioid and acetylcholine levels are elevated in animal model of cholestasis. In addition, there is no data about the effects of interaction opioidergic and cholinergic systems of dorsal hippocampus (CA1) on amnesia-induced by cholestasis. Male mice weighing 25�??35 g were used in this study. Cholestasis was induced by the ligation of the common bile duct. One-trial step-down and hole-board paradigms were used for the assessment of memory retrieval and anxiety-like behaviors respectively. All drugs injected intra-CA1. The data showed that cholestasis (24 days after BDL) decreased memory retrieval. Sole intra-CA1 injection of higher dose of mecamylamine (0.125, 0.25, 0.5 and 1 µg/mice) and scopolamine (0.125, 0.25, 0.5 1 and 2 µg/mice) but not all doses of naloxone (0.0125, 0.025 and 0.05 µg/mice) decreased memory retrieval in the sham operated BDL. The ineffective doses of naloxone (0.025 and 0.05 µg/mice), mecamylamine (0.5 µg/mice) and scopolamine (0.5 µg/mice) restored cholestasis-induced amnesia 24 days after BDL. Further, all cross co-administration ineffective doses of naloxone (0.0125 µg/mice), mecamylamine (0.125 µg/mice) and scopolamine (0.125 µg/mice) reversed cholestasis-induced amnesia. All doses of the drugs have no effect on exploratory behaviors. The data strongly revealed that synergistic effect between opioidergic and cholinergic systems of CA1 on the modulation of cholestasis-induced amnesia.

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