Agmatine protects against scopolamine-induced water maze performance impairment and hippocampal ERK and Akt inactivation

Moosavi, Maryam; Khales, Golnaz Yadollahi; Abbasi, Leila; Zarifkar, Asadollah; Rastegar, Karim

doi:10.1016/j.neuropharm.2011.12.031

Cited by 66 publications

(29 citation statements)

References 68 publications

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“…Whether the changes of Akt and GSK-3 may reduce memory retention in DM rat is not sure. Our results suggest that the increase of GSK-3 may be response for the impairment of step-down inhibitory avoidance task rather than Akt because the activities and the expression of Akt were not significantly different among DM group, DM + NaCl group, and DM + LiCl group, but other studies show that learning impairment and hippocampal ERK and Akt inactivation are induced by scopolamine in male Sprague-Dawley rats [29]. …”

Section: Discussionmentioning

confidence: 63%

Glycogen Synthase Kinase-3 Regulates Production of Amyloid-βPeptides and Tau Phosphorylation in Diabetic Rat Brain

Sun

et al. 2014

The Scientific World Journal

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The pathogenesis of diabetic neurological complications is not fully understood. Diabetes mellitus (DM) and Alzheimer's disease (AD) are characterized by amyloid deposits. Glycogen synthase kinase-3 (GSK-3) plays an important role in the pathogenesis of AD and DM. Here we tried to investigate the production of amyloid-β peptides (Aβ) and phosphorylation of microtubule-associated protein tau in DM rats and elucidate the role of GSK-3 and Akt (protein kinase B, PKB) in these processes. Streptozotocin injection-induced DM rats displayed an increased GSK-3 activity, decreased activity and expression of Akt. And Aβ40 and Aβ42 were found overproduced and the microtubule-associated protein tau was hyperphosphorylated in the hippocampus. Furthermore, selective inhibition of GSK-3 by lithium could attenuate the conditions of Aβ overproduction and tau hyperphosphorylation. Taken together, our studies suggest that GSK-3 regulates both the production of Aβ and the phosphorylation of tau in rat brain and may therefore contribute to DM caused AD-like neurological defects.

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Section: Discussionmentioning

confidence: 63%

Glycogen Synthase Kinase-3 Regulates Production of Amyloid-βPeptides and Tau Phosphorylation in Diabetic Rat Brain

Sun

et al. 2014

The Scientific World Journal

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“…Alzheimer’s disease (AD) is most common neurodegenerative disease and this disease induces progressive loss of learning ability and memory function (Moosavi et al, 2012). The degree of memory loss is correlated with the severity of AD (Howes et al, 2003).…”

Section: Introductionmentioning

confidence: 99%

Treadmill exercise ameliorates disturbance of spatial learning ability in scopolamine-induced amnesia rats

Heo¹,

Shin²,

Kim³

et al. 2014

J Exerc Rehabil

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Alzheimer’s disease is the most common neurodegenerative disease and this disease induces progressive loss of memory function Scopolamine is a non-selective muscarinic cholinergic receptor antagonist and it induces impairment of learning ability. Exercise is known to ameliorate memory deficits induced by various brain diseases. In the present study, we investigated the effect of treadmill exercise on spatial learning ability in relation with cell proliferation in the hippocampus using the scopolamine-induced amnesia mice. For the induction of amnesia, 1 mg/kg scopolamine hydrobromide was administered intraperitoneally once a day for 14 days. Morris water maze test for spatial learning ability was conducted. Immonofluorescence for 5-bromo-2-deoxyuri-dine (BrdU) and western blot for brain-derived neurotrophic factor (BDNF) and its receptor tyrosine kinase B (TrkB) were performed. In the present results, scopolamine-induced amnesia mice showed deterioration of spatial learning ability. Inhibition of cell proliferation and suppression of BDNF and TrkB expressions were observed in the scopolamine-induced amnesia mice. Treadmill exercise improved spatial learning ability and increased cell proliferation through activating of BDNF-TrkB pathway in the amnesia mice. These findings offer a possibility that treadmill exercise may provide preventive or therapeutic value for the memory loss induced by variable neurodegenerative diseases including Alzheimer’s disease.

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“…decreased ERK phosphorylation in the rat hippocampus [34], while the mAChR agonist carbachol increased ERK phosphorylation in rat hippocampal slices, which was blocked by the mAChR antagonist atropine [35]. The carbachol-stimulated ERK phosphorylation in the hippocampus is believed to be mediated by M 1 receptors because ERK responses to carbachol were blocked by knocking out M 1 but not M 2 /M 3 /M 4 receptors [36].…”

Section: Discussionmentioning

confidence: 99%

Antagonism of Muscarinic Acetylcholine Receptors Alters Synaptic ERK Phosphorylation in the Rat Forebrain

Mao

Wang

2016

Neurochem Res

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Acetylcholine (ACh) is a key transmitter in the mesocorticolimbic circuit. By interacting with muscarinic ACh receptors (mAChR) enriched in the circuit, ACh actively regulates various neuronal and synaptic activities. The extracellular signal-regulated kinase (ERK) is one of members of the mitogen-activated protein kinase family and is subject to the regulation by dopamine receptors, although the regulation of ERKs by limbic mAChRs is poorly understood. In this study, we investigated the role of mAChRs in the regulation of ERK phosphorylation (activation) in the mesocorticolimbic system of adult rat brains in vivo. We targeted a sub-pool of ERKs at synaptic sites. We found that a systemic injection of the mAChR antagonist scopolamine increased phosphorylation of synaptic ERKs in the striatum (caudate putamen and nucleus accumbens) and medial prefrontal cortex (mPFC). Increases in ERK phosphorylation in both forebrain regions were rapid and transient. Notably, pretreatment with a dopamine D1 receptor (D1R) antagonist SCH23390 blocked the scopolamine-stimulated ERK phosphorylation in these brain regions, while a dopamine D2 receptor antagonist eticlopride did not. Scopolamine and SCH23390 did not change the amount of total ERK proteins. These results demonstrate that mAChRs inhibit synaptic ERK phosphorylation in striatal and mPFC neurons under normal conditions. Blockade of this inhibitory mAChR tone leads to the upregulation of ERK phosphorylation likely through a mechanism involving the level of D1R activity.

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Agmatine protects against scopolamine-induced water maze performance impairment and hippocampal ERK and Akt inactivation

Cited by 66 publications

References 68 publications

Glycogen Synthase Kinase-3 Regulates Production of Amyloid-βPeptides and Tau Phosphorylation in Diabetic Rat Brain

Glycogen Synthase Kinase-3 Regulates Production of Amyloid-βPeptides and Tau Phosphorylation in Diabetic Rat Brain

Treadmill exercise ameliorates disturbance of spatial learning ability in scopolamine-induced amnesia rats

Antagonism of Muscarinic Acetylcholine Receptors Alters Synaptic ERK Phosphorylation in the Rat Forebrain

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