Methanesulfonyl fluoride, an acetylcholinesterase inhibitor, attenuates simple learning and memory deficits in ischemic rats

Borlongan, Cesario V.; Sumaya, Isabel C.; Moss, Donald E.

doi:10.1016/j.brainres.2005.01.028

Cited by 30 publications

(18 citation statements)

References 52 publications

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“…Second, decreased ACh content and corresponding impairments in learning and memory were found in rats with 4-vessel occlusion [15] . Third, ChAT immunostaining was shown to be decreased in rats with transient occlusion of the middle cerebral artery (MCAO) [16][17][18] . Fourth, rats with multiple small embolizations have been shown to produce multiple infarctions and exhibit decreases in cholinergic markers [19] .…”

Section: Cholinergic Deficiency In Vad Animal Models and Vad Patientsmentioning

confidence: 99%

“…In fact, the effects of these AChE inhibitors have already been well evaluated in the treatment of VaD. Although the results were inconsistent, application of AChE inhibitors showed promising benefits in ameliorating the learning and memory impairments as well as other deficits found in VaD patients and VaD animal models [6,16,[70][71][72][73] .…”

Section: Acetylcholinesterase Inhibitorsmentioning

confidence: 99%

“…Methanesulfonyl fluoride (MSF), a highly selective CNS inhibitor of AChE, has recently been demonstrated to promote improvement in cognitive performance in patients with AD [124] , and it was also shown to attenuate simple learning and memory deficits in the MCAO rat model [16] . The seed extract of Cassia obtusifolia (COE), which has been found to inhibit AChE activity both in vitro and ex vivo, attenuated memory impairment induced by scopolamine or BCCAO in the passive-avoidance, Y-maze, and Morris water-maze tests in ICR mice [47] .…”

Section: Other Ache Inhibitorsmentioning

confidence: 99%

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Cholinergic deficiency involved in vascular dementia: possible mechanism and strategy of treatment

2009

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Vascular dementia (VaD) is a progressive neurodegenerative disease with a high prevalence. Several studies have recently reported that VaD patients present cholinergic deficits in the brain and cerebrospinal fluid (CSF) that may be closely related to the pathophysiology of cognitive impairment. Moreover, cholinergic therapies have shown promising effects on cognitive improvement in VaD patients. The precise mechanisms of these cholinergic agents are currently not fully understood; however, accumulating evidence indicates that these drugs may act through the cholinergic anti-inflammatory pathway, in which the efferent vagus nerve signals suppress pro-inflammatory cytokine release and inhibit inflammation, although regulation of oxidative stress and energy metabolism, alleviation of apoptosis may also be involved. In this paper, we provide a brief overview of the cholinergic treatment strategy for VaD and its relevant mechanisms of anti-inflammation.

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Section: Cholinergic Deficiency In Vad Animal Models and Vad Patientsmentioning

confidence: 99%

Section: Acetylcholinesterase Inhibitorsmentioning

confidence: 99%

Section: Other Ache Inhibitorsmentioning

confidence: 99%

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Cholinergic deficiency involved in vascular dementia: possible mechanism and strategy of treatment

2009

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“…It is known that ChAT levels are notably decreased in a number of pathologies, such as Alzheimer's disease, Huntington's disease, amyotrophic lateral sclerosis, schizophrenia and sudden infant death syndrome (Oda, 1999), but an increase of ChAT activity is not a consistent change connected to a particular physiologic state or pathology, although some reports mention that enhanced acetylcholine synthesis accompanies learning (Oh et al, 1996;Park et al, 1992). However it has been reported that MSF treatment -after experimentally induced stroke in rats-showed more intense staining of septal ChAT-immunoreactive neurons correlating with a better response in learning and memory tasks (Borlongan, Sumaya and Moss, 2005). These findings suggest that MSF, probably by cholinergic system's enhancement, lessened stroke-induced deficit in learning and memory.…”

Section: Discussionmentioning

confidence: 99%

In utero methanesulfonyl fluoride differentially affects learning and maze performance in the absence of long-lasting cholinergic changes in the adult rat

Carcoba

Santiago

Moss

et al. 2008

Pharmacology Biochemistry and Behavior

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There is increasing evidence that acetylcholinesterase (AChE) may have various specific developmental roles in brain development. Nevertheless, specific effects of AChE inhibition during early brain development have not been adequately described. Therefore, methanesulfonyl fluoride (MSF), an irreversible AChE inhibitor that shows high selectivity for the CNS was used to produce AChE inhibition in utero to study subsequent adult behaviors, sleep, and cholinergic markers. Rats exposed to MSF in utero showed a deficit in spatial learning tasks using appetitive motivation but, surprisingly, they performed equally well or better than controls when aversive motivation was used. One hypothesis was that MSF treatment in utero affected the response to stress. Tests of anxiety however showed no differences in basal levels of anxiety. Studies of sleep behavior, however, indicated a higher level of REM sleep which is only seen during the light phase of male rats exposed to MSF in utero as compared to controls. No differences in cholinergic markers in the brains of adults were found except that females exposed to MSF in utero had a higher level of ChAT activity in the synaptosomal fraction of the hippocampus. Even so, whether cholinergic alterations accompany the in utero MSF exposure remains to be determined. The failure to find widespread changes in cholinergic markers in the adult brains suggests changes in behaviors should be further investigated by testing the participation of postsynaptic mechanisms, measuring of cholinergic markers during earlier development periods and the possible participation of other neurotransmitter systems to clearly reveal the role of the cholinergic system following in utero MSF exposure.

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“…Deleterious infarctions of the middle cerebral artery (MCA) are at risk of developing massive edema because of the necrosis of cells located in the primary zone (Borlongan et al, 2005). The most effective drug, tissue plasminogen activator, the only Food and Drug Administration-approved thrombolytic drug used in ischemia, is widely employed in clinic.…”

Section: Introductionmentioning

confidence: 99%

Involvement of Multitargets in Paeoniflorin-Induced Preconditioning

Chen¹,

Liang²,

Cai³

et al. 2006

J Pharmacol Exp Ther

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Paeoniflorin (PF) is the principal component of Paeoniae radix prescribed in traditional Chinese medicine. The delayed neuroprotection induced by PF preconditioning and its underlying mechanisms were investigated in rat middle cerebral artery occlusion (MCAO) and reperfusion model. At a dosage of 20 or 40 mg/kg, PF preconditioning 48 h before MCAO followed by 24-h reperfusion significantly reduced the mortality and infarct volume and reversed the neurological deficits caused by ischemia. Likewise, the ameliorative effects on mortality, infarct size, and neurological impairment induced by MCAO emerged as well when PF was administered 24 h, 48 h, or 5 days before MCAO at the dose of 20 mg/kg. Furthermore, comparative proteomics analysis was adopted to identify the differentially expressed proteins induced by PF preconditioning itself. The relative levels of 42 proteins were altered after PF preconditioning, among which 20 were elevated and 22 reduced. In summary, A 1 receptor-regulator of G protein signaling-K ATP signaling, arachidonic acid cascade, nitric oxide system, markers of neuronal damage, mitochondrial damage-related molecules, and the mitogen-activated protein kinase and nuclear factor-B pathway are associated with the mechanisms of PF preconditioning.Ischemic stroke is the second leading cause of death in China, leaving survivors burdened with severe disabilities. Deleterious infarctions of the middle cerebral artery (MCA) are at risk of developing massive edema because of the necrosis of cells located in the primary zone (Borlongan et al., 2005). The most effective drug, tissue plasminogen activator, the only Food and Drug Administration-approved thrombolytic drug used in ischemia, is widely employed in clinic. However, it has a very narrow therapeutic time window of 3 h, and only 1 to 3% of ischemic stroke patients have been benefited (Pulsinelli et al., 1997). Therefore, the current focus of stroke research requires investigation of novel neuroprotective agents and strategies, which could prolong the therapeutic window.Paeoniflorn (PF), the principal component of Paeoniae radix ("Shaoyao" in Chinese), has been widely investigated as antioxidant, cognitive enhancer, and endothelium-dependent vasodilator Ryu et al., 2001;Tabata et al., 2001). Recently, our laboratory found that PF could produce a dose-dependent decrease in both neurological impairment and infarct volume in acute transient cerebral ischemia through activating adenosine A 1 receptor in a manner different from its classic agonists (Liang et al., 2005;Liu et al., 2005b).Ischemic preconditioning (IPC) is an endogenous mechanism by which brief episodes of a sublethal insult induce a robust protection against the deleterious effects of subsequent, prolonged lethal ischemia. There are two kinds of protection: "classic IPC" and "delayed IPC." Various drugs ABBREVIATIONS: MCA, middle cerebral artery; PF, paeoniflorn; IPC, ischemic preconditioning; PPC, pharmacological preconditioning; DPCPX, 8-cyclopentyl-1,3-dipropylxanthine; TTC, 2,3,...

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Methanesulfonyl fluoride, an acetylcholinesterase inhibitor, attenuates simple learning and memory deficits in ischemic rats

Cited by 30 publications

References 52 publications

Cholinergic deficiency involved in vascular dementia: possible mechanism and strategy of treatment

Cholinergic deficiency involved in vascular dementia: possible mechanism and strategy of treatment

In utero methanesulfonyl fluoride differentially affects learning and maze performance in the absence of long-lasting cholinergic changes in the adult rat

Involvement of Multitargets in Paeoniflorin-Induced Preconditioning

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