Activation of nicotinic α7 acetylcholine receptor enhances long term potentation in wild type mice but not in APPswe/PS1ΔE9 mice

Søderman, Andreas; Mikkelsen, Jens D.; West, Mark J.; Christensen, Ditte Z.; Jensen, Morten Skovgaard

doi:10.1016/j.neulet.2010.10.049

Cited by 26 publications

(17 citation statements)

References 26 publications

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Section: Aβ and Excitatory Neurotransmissionmentioning

confidence: 99%

“…On the other hand, it has been proposed that α7-nAChR is functionally blocked in hippocampal CA1 neurons due to an interaction between the receptor and Aβ (Soderman et al, 2011). The functional consequences of such interaction may lead to impairments in both cognitive function (Soderman et al, 2008) and synaptic plasticity (Soderman et al, 2011). α 7-nAChR inhibition has also been explained by sustained increase in presynaptic Ca 2 + evoked by Aβ which may underlie disruption of neuronal signaling via nAChRs in the early stages of AD (Dougherty et al, 2003).…”

Section: Aβ and Excitatory Neurotransmissionmentioning

confidence: 99%

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GABAergic neurotransmission and new strategies of neuromodulation to compensate synaptic dysfunction in early stages of Alzheimerâ€™s disease

Nava-Mesa¹,

Jiménez‐Díaz²,

Yajeya³

et al. 2014

Front. Cell. Neurosci.

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Alzheimer’s disease (AD) is a progressive neurodegenerative disease characterized by cognitive decline, brain atrophy due to neuronal and synapse loss, and formation of two pathological lesions: extracellular amyloid plaques, composed largely of amyloid-beta peptide (Aβ), and neurofibrillary tangles formed by intracellular aggregates of hyperphosphorylated tau protein. Lesions mainly accumulate in brain regions that modulate cognitive functions such as the hippocampus, septum or amygdala. These brain structures have dense reciprocal glutamatergic, cholinergic, and GABAergic connections and their relationships directly affect learning and memory processes, so they have been proposed as highly susceptible regions to suffer damage by Aβ during AD course. Last findings support the emerging concept that soluble Aβ peptides, inducing an initial stage of synaptic dysfunction which probably starts 20–30 years before the clinical onset of AD, can perturb the excitatory–inhibitory balance of neural circuitries. In turn, neurotransmission imbalance will result in altered network activity that might be responsible of cognitive deficits in AD. Therefore, Aβ interactions on neurotransmission systems in memory-related brain regions such as amygdaloid complex, medial septum or hippocampus are critical in cognitive functions and appear as a pivotal target for drug design to improve learning and dysfunctions that manifest with age. Since treatments based on glutamatergic and cholinergic pharmacology in AD have shown limited success, therapies combining modulators of different neurotransmission systems including recent findings regarding the GABAergic system, emerge as a more useful tool for the treatment, and overall prevention, of this dementia. In this review, focused on inhibitory systems, we will analyze pharmacological strategies to compensate neurotransmission imbalance that might be considered as potential therapeutic interventions in AD.

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Section: Aβ and Excitatory Neurotransmissionmentioning

confidence: 99%

Section: Aβ and Excitatory Neurotransmissionmentioning

confidence: 99%

GABAergic neurotransmission and new strategies of neuromodulation to compensate synaptic dysfunction in early stages of Alzheimerâ€™s disease

Nava-Mesa¹,

Jiménez‐Díaz²,

Yajeya³

et al. 2014

Front. Cell. Neurosci.

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“…However, although selective for ␣7 nAChRs at low nanomolar concentrations, it interacts with other nAChR subtypes, notably ␣6␤2* nAChRs, at higher concentrations (Mogg et al, 2002). Small-molecular-weight ␣7 nAChR agonists include 3- (Levin et al, 1999;Simosky et al, 2002;Martin et al, 2004;Hansen et al, 2007;Söderman et al, 2011). Choline, the breakdown product of ACh, is also found to selectively activate ␣7 nAChRs at millimolar concentrations (Alkondon et al, 1997).…”

Section: Pharmacological Tools To Study Nicotinic Acetylcholine Recepmentioning

confidence: 99%

α6β2* and α4β2* Nicotinic Acetylcholine Receptors As Drug Targets for Parkinson's Disease

Quik

Wonnacott²

2011

Pharmacol Rev

175

185

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“…They are objects of pharmacologists’ interest as they are suitable for cognitive function amelioration in patients suffering from Alzheimer’s disease and schizophrenia [46]. Moreover, amyloid β released in Alzheimer’s disease patients also extensively binds to the brain α7 nAChR and prevents its natural function [47]. As acetylcholine level is limited in Alzheimer’s disease damaged brain agonizing α7 nAChR is considered as a promising way to enhance cognitive functions [48].…”

Section: α7 Nicotinic Acetylcholine Receptor In Brainmentioning

confidence: 99%

Alpha7 Nicotinic Acetylcholine Receptor Is a Target in Pharmacology and Toxicology

Pohanka

2012

IJMS

152

106

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Alpha7 nicotinic acetylcholine receptor (α7 nAChR) is an important part of the cholinergic nerve system in the brain. Moreover, it is associated with a cholinergic anti-inflammatory pathway in the termination of the parasympathetic nervous system. Antagonists of α7 nAChR are a wide group represented by conotoxin and bungarotoxin. Even Alzheimer’s disease drug memantine acting as an antagonist in its side pathway belongs in this group. Agonists of α7 nAChR are suitable for treatment of multiple cognitive dysfunctions such as Alzheimer’s disease or schizophrenia. Inflammation or even sepsis can be ameliorated by the agonistic acting compounds. Preparations RG3487, SEN34625/WYE-103914, SEN12333, ABT-107, Clozapine, GTS-21, CNI-1493, and AR-R17779 are representative examples of the novel compounds with affinity toward the α7 nAChR. Pharmacological, toxicological, and medicinal significance of α7 nAChR are discussed throughout this paper.

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Activation of nicotinic α7 acetylcholine receptor enhances long term potentation in wild type mice but not in APPswe/PS1ΔE9 mice

Cited by 26 publications

References 26 publications

GABAergic neurotransmission and new strategies of neuromodulation to compensate synaptic dysfunction in early stages of Alzheimerâ€™s disease

GABAergic neurotransmission and new strategies of neuromodulation to compensate synaptic dysfunction in early stages of Alzheimerâ€™s disease

α6β2* and α4β2* Nicotinic Acetylcholine Receptors As Drug Targets for Parkinson's Disease

Alpha7 Nicotinic Acetylcholine Receptor Is a Target in Pharmacology and Toxicology

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