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Abstract: (307 Views)
Introduction: Even though neuropeptide Y (NPY) is involved in learning and memory and the role of the Y1 receptor is well understood, the role of the Y2 receptor (Y2R) is still up for debate. NPY may also have a role in autophagy, according to some studies. In this study, we investigated whether NPY and its Y2R inhibitor could modulate memory or affect beclin-1 expression in a rat model of Alzheimer’s disease.
Methods: Intracerebroventricular (i.c.v) injections of amyloid-beta (Aβ1-42, 2µg/µl/side) were used to create an animal model of Alzheimer's disease. NPY (10 ng/µl, 10 µl, i.c.v) was administered 30 minutes before the retrieval. BIIE-0246 as a Y2 antagonist was injected 15 minutes before NPY injection in the targeted groups. BIIE-0246 was used at three different concentrations (20 nM, 200 nM, and 2 µM). Passive avoidance memory and novel object recognition were both evaluated. Then, beclin-1 protein expression was determined in the hippocampus using a western blot.
Results: It was discovered that NPY improves passive avoidance and cognitive memory in Aβ treated animals. Injecting BIIE-0246 before NPY did not reverse the improving effect of NPY on passive avoidance and Novel Object Recognition memories. Furthermore, compared to sham-operated animals, Aβ treatment significantly reduced the hippocampal expression of beclin-1 protein (P≤0.05), and NPY or NPY Y2 receptor inhibitors did not affect beclin-1.
Conclusion: In Aβ-induced memory impairment, it is thought that NPY can improve both aversive and cognitive memory. The blockade of NPY Y2 receptors by BIIE-0246 did not affect NPY's memory-enhancing impact.
Methods: Intracerebroventricular (i.c.v) injections of amyloid-beta (Aβ1-42, 2µg/µl/side) were used to create an animal model of Alzheimer's disease. NPY (10 ng/µl, 10 µl, i.c.v) was administered 30 minutes before the retrieval. BIIE-0246 as a Y2 antagonist was injected 15 minutes before NPY injection in the targeted groups. BIIE-0246 was used at three different concentrations (20 nM, 200 nM, and 2 µM). Passive avoidance memory and novel object recognition were both evaluated. Then, beclin-1 protein expression was determined in the hippocampus using a western blot.
Results: It was discovered that NPY improves passive avoidance and cognitive memory in Aβ treated animals. Injecting BIIE-0246 before NPY did not reverse the improving effect of NPY on passive avoidance and Novel Object Recognition memories. Furthermore, compared to sham-operated animals, Aβ treatment significantly reduced the hippocampal expression of beclin-1 protein (P≤0.05), and NPY or NPY Y2 receptor inhibitors did not affect beclin-1.
Conclusion: In Aβ-induced memory impairment, it is thought that NPY can improve both aversive and cognitive memory. The blockade of NPY Y2 receptors by BIIE-0246 did not affect NPY's memory-enhancing impact.
Type of Manuscript: Experimental research article |
Subject:
Neurophysiology/Pharmacology
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