Acetylcholinesterase inhibitors block acetylcholine-evoked release of dopamine in rat striatum, in vivo

Dajas-Bailador, Federico; Costa, Gustavo; Emmett, Stevan R.; Bonilla, Carolina; Dajas, Federico

doi:10.1016/0006-8993(96)00133-3

Cited by 14 publications

(5 citation statements)

References 29 publications

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“…Donepezil, a piperidine derivative that inhibits the degradation of Ach, or an acetylcholinesterase inhibitor, can preserve Ach and DA levels in the AD model. Not all acetylcholinesterase inhibitors can modulate DA release (Dajas-Bailador et al, 1996, Francis et al, 1999, Zhang et al, 2004). Donepezil treatment rescued deficits in memory in in vivo AD models (Kim et al, 2014).…”

Section: Discussionmentioning

confidence: 99%

Oxidative and nitrative stress in neurodegeneration

Cobb

Cole

2015

Neurobiology of Disease

241

180

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Aerobes require oxygen for metabolism and normal free radical formation. As a result, maintaining the redox homeostasis is essential for brain cell survival due to their high metabolic energy requirement to sustain electrochemical gradients, neurotransmitter release, and membrane lipid stability. Further, brain antioxidant levels are limited compared to other organs and less able to compensate for reactive oxygen and nitrogen species (ROS/RNS) generation which contribute oxidative/nitrative stress (OS/NS). Antioxidant treatments such as vitamin E, minocycline, and resveratrol mediate neuroprotection by prolonging the incidence of or reversing OS and NS conditions. Redox imbalance occurs when the antioxidant capacity is overwhelmed, consequently leading to activation of alternate pathways that remain quiescent under normal conditions. If OS/NS fails to lead to adaptation, tissue damage and injury ensue, resulting in cell death and/or disease. The progression of OS/NS-mediated neurodegeneration along with contributions from microglial activation, dopamine metabolism, and diabetes comprise a detailed interconnected pathway. This review proposes a significant role for OS/NS and more specifically, lipid peroxidation (LPO) and other lipid modifications, by triggering microglial activation to elicit a neuroinflammatory state potentiated by diabetes or abnormal dopamine metabolism. Subsequently, sustained stress in the neuroinflammatory state overwhelms cellular defenses and prompts neurotoxicity resulting in the onset or amplification of brain damage.

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Section: Discussionmentioning

confidence: 99%

Oxidative and nitrative stress in neurodegeneration

Cobb

Cole

2015

Neurobiology of Disease

241

180

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“…It was found that unilateral microinfusion of fasciculin did not change the level of dopamine and its metabolites in the rat substantia nigra [34]. Application of fasciculin through push-pull cannula to the striatum of rats alone or with acetylcholine indicated that this polypeptide acetylcholiesterase inhibitor blocked acetylcholine-evoked release of dopamine in rat striatum in vivo [35]. Furthermore, these studies revealed the possible existence of at least two distinctive pools of acetylcholinesterases with, respectively, non-cholinergic and cholinergic actions.…”

Section: B) Effects Of Polypeptides Being Injected Directly Into the mentioning

confidence: 93%

“…Several studies was done using fasciculins, potent acetycholinesterase inhibitors from venom of mambas (genus Dendroaspis) [34][35][36][37]. It was found that unilateral microinfusion of fasciculin did not change the level of dopamine and its metabolites in the rat substantia nigra [34].…”

Section: B) Effects Of Polypeptides Being Injected Directly Into the mentioning

confidence: 99%

Effects of Snake Venom Polypeptides on Central Nervous System

Osipov¹,

Utkin²

2012

CNSAMC

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The nervous system is a primary target for animal venoms as the impairment of its function results in the fast and efficient immobilization or death of a prey. There are numerous evidences about effects of crude snake venoms or isolated toxins on peripheral nervous system. However, the data on their interactions with the central nervous system (CNS) are not abundant, as the blood-brain barrier (BBB) impedes penetration of these compounds into brain. This updated review presents the data about interaction of snake venom polypeptides with CNS. Such data will be described according to three main modes of interactions: - Direct in vivo interaction of CNS with venom polypeptides either capable to penetrate BBB or injected into the brain. - In vitro interactions of cell or sub-cellular fractions of CNS with crude venoms or purified toxins. - Indirect effects of snake venoms or their components on functioning of CNS under different conditions. Although the venom components penetrating BBB are not numerous, they seem to be the most suitable candidates for the leads in drug design. The compounds with other modes of action are more abundant and better studied, but the lack of the data about their ability to penetrate BBB may substantially aggravate the potentials for their medical perspectives. Nevertheless, many such compounds are used for research of CNS in vitro. These investigations may give invaluable information for understanding the molecular basis of CNS diseases and thus lay the basis for targeted drug design. This aspect also will be outlined in the review.

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“…5). Previous findings have demonstrated that AChEIs-induced stimulation of cholinergic activity induces an increase in DA levels (25,64), while other studies have shown no significant effect (10,65). However, interactions between cholinergic and dopaminergic systems seem to play a role in the modulation of memory processes.…”

Section: Effects On Monoaminergic Systemsmentioning

confidence: 96%

CHF2819: Pharmacological Profile of a Novel Acetylcholinesterase Inhibitor

et al. 2002

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CHF2819 is a novel orally active acetylcholinesterase inhibitor (AChEI) developed for the treatment of Alzheimer's disease (AD). CHF2819 is a selective inhibitor of AChE, it is 115 times more potent against this enzyme than against butyrylcholinesterase (BuChE). Moreover, CHF2819 is more selective for inhibition of central (brain) AChE than peripheral (heart) AChE. In vivo CHF2819, 0.5, 1.5, and 4.5 mg/kg p.o., significantly and in dose-dependent manner increased acetylcholine (ACh) levels in hippocampus of young adult rats. Moreover, aging animals, with lower basal ACh levels than young adult rats, also exhibit a marked increase in hippocampal levels of this neurotransmitter after administration of CHF2819. At 1.5 mg/kg p.o. CHF2819 attenuated scopolamine-induced amnesia in a passive avoidance task. Furthermore, it decreased dopamine (DA) levels and increased extracellular levels of 5-hydroxytryptamine (5-HT) in the hippocampus, without modifying norepinephrine (NE) levels. By oral administration to young adult rats CHF2819 did not affect extracellular hippocampal levels of glutamate (Glu), aspartate (Asp), ã-aminobutyric acid (GABA), taurine (Tau), arginine (Arg) or citrulline (Cit).Functional observational battery (FOB) screening demonstrated that CHF2819 (1.5 and 4.5 mg/kg p.o.) does not affect activity, excitability, autonomic, neuromuscular, and sensorimotor domains, as well as physiological endpoints (body weight and temperature). CHF2819 induced, however, involuntary motor movements (ranging from mild tremors to myoclonic jerks) in a dose-dependent manner.The neurochemical and behavioral profiles of CHF2819 suggest that this orally active novel AChEI could be of clinical interest for the treatment of Alzheimer-type dementia as-53

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Acetylcholinesterase inhibitors block acetylcholine-evoked release of dopamine in rat striatum, in vivo

Cited by 14 publications

References 29 publications

Oxidative and nitrative stress in neurodegeneration

Oxidative and nitrative stress in neurodegeneration

Effects of Snake Venom Polypeptides on Central Nervous System

CHF2819: Pharmacological Profile of a Novel Acetylcholinesterase Inhibitor

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