Abstract:We examine whether Phellodendron amurense (PA) and its major alkaloid compound, berberine (BER), improved memory defects caused by administering scopolamine in rats. Effects of PA and BER on the acetylcholinergic system and pro-inflammatory cytokines in the hippocampus were also investigated. Male rats were administered daily doses for 14 days of PA (100 and 200 mg/kg, i.p.) and BER (20 mg/kg, i.p.) 30 min before scopolamine injection (2 mg/kg, i.p.). Daily administration of PA and BER improved memory impairme… Show more
“…administration of scopolamine, a muscarinic cholinergic receptor antagonist, was exploited as a parmarcological model for AD in rats. Scopolamine interfere with central cholinergic functions and memory circuits, leading to decreased Ach release and subsequent memory, attention, and executive function-related deficits that are seen in aging and dementia [14]. Due to this, scopolamine-induced cognitive dysfunction is extensively used to probe potential therapeutic agents attenuating cognitive deficits [15].…”
AMP-activated protein kinase (AMPK), an important regulator of energy metabolism, is activated in response to cellular stress when intracellular levels of AMP increase. We investigated the neuroprotective effects of AMPK against scopolamine-induced memory impairment in vivo and glutamate-induced cytotoxicity in vitro. An adenovirus expressing AMPK wild type alpha subunit (WT) or a dominant negative form (DN) was injected into the hippocampus of rats using a stereotaxic apparatus. The AMPK WT-injected rats showed significant reversal of the scopolamine induced cognitive deficit as evaluated by escape latency in the Morris water maze. In addition, they showed enhanced acetylcholinesterase (AChE)-reactive neurons in the hippocampus, implying increased cholinergic activity in response to AMPK. We also studied the cellular mechanism by which AMPK protects against glutamate-induced cell death in primary cultured rat hippocampal neurons. We further demonstrated that AMPK WT-infected cells increased cell viability and reduced Annexin V positive hippocampal neurons. Western blot analysis indicated that AMPK WT-infected cells reduced the expression of Bax and had no effects on Bcl-2, which resulted in a decreased Bax/Bcl-2 ratio. These data suggest that AMPK is a useful cognitive impairment treatment target, and that its beneficial effects are mediated via the protective capacity of hippocampal neurons.
“…administration of scopolamine, a muscarinic cholinergic receptor antagonist, was exploited as a parmarcological model for AD in rats. Scopolamine interfere with central cholinergic functions and memory circuits, leading to decreased Ach release and subsequent memory, attention, and executive function-related deficits that are seen in aging and dementia [14]. Due to this, scopolamine-induced cognitive dysfunction is extensively used to probe potential therapeutic agents attenuating cognitive deficits [15].…”
AMP-activated protein kinase (AMPK), an important regulator of energy metabolism, is activated in response to cellular stress when intracellular levels of AMP increase. We investigated the neuroprotective effects of AMPK against scopolamine-induced memory impairment in vivo and glutamate-induced cytotoxicity in vitro. An adenovirus expressing AMPK wild type alpha subunit (WT) or a dominant negative form (DN) was injected into the hippocampus of rats using a stereotaxic apparatus. The AMPK WT-injected rats showed significant reversal of the scopolamine induced cognitive deficit as evaluated by escape latency in the Morris water maze. In addition, they showed enhanced acetylcholinesterase (AChE)-reactive neurons in the hippocampus, implying increased cholinergic activity in response to AMPK. We also studied the cellular mechanism by which AMPK protects against glutamate-induced cell death in primary cultured rat hippocampal neurons. We further demonstrated that AMPK WT-infected cells increased cell viability and reduced Annexin V positive hippocampal neurons. Western blot analysis indicated that AMPK WT-infected cells reduced the expression of Bax and had no effects on Bcl-2, which resulted in a decreased Bax/Bcl-2 ratio. These data suggest that AMPK is a useful cognitive impairment treatment target, and that its beneficial effects are mediated via the protective capacity of hippocampal neurons.
“…injection of scopolamine causes memory impairment, in accordance with previous investigations [4,18]. Scopolamine is a tropane alkaloid drug that exhibits competitive antagonism at muscarinic acetylcholine receptors (mAChRs) by interfering with cholinergic transmission in the central nervous system (CNS) [16,17]. Moreover, scopolamine administration to animals is used as an experimental model of the cognitive deterioration and memory disturbances in AD.…”
“…Scopolamine (hyoscine) is an anticholinergic drug that causes dementia by interfering with LTP. It can be used to induce memory impairment in animal models (31). It has been reported that scopolamine causes memory impairment in Morris water maze test through down regulation of protein kinase C and iNOS (32).…”
Background: Crocus sativus L., (Iridaceace), known as saffron, is used in traditional medicine for different purposes such as memory improvment. Crocin is one of the pharmacologically active constituents responsible for many medicinal properties of saffron. Objectives: In this study, the effects of crocin, an active saffron constituent, on hyoscine induced memory impairment and its effect on protein and mRNA transcript levels of CREB (cAMP response element binding protein), BDNF (brain-derived neurotrophic factor), and phospho-CREB (p-CREB) were investigated in rat hippocampus. Methods: Rats were intraperitoneally treated with crocin (10, 20, and 40 mg/kg), normal saline (1 mL/kg), and rivastigmine (1.5 mg/kg) 30 minutes prior to hyoscine (1 mg/kg) for five days. The effects were studied on spacial learning and memory using Morris water maze. Protein and transcript levels of CREB and BDNF were analyzed using western blotting and qRT PCR methods, respectively. Results: Five days treatment with crocin (20 and 40 mg/kg) and rivastigmine significantly increased the presence of animals in target quadrant in probe trial on the 8th day compared to hyoscine. Crocin (20 mg/Kg) increased significantly BDNF and CREB protein and transcript levels compared to hyoscine. Conclusions: Crocin improved memory impairment induced by hyoscine through reduction of the latency to find the platform in the probe trial in Morris water maze test. Crocin improved memory probably due to the increase of BDNF and CREB protein and transcript levels.
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