Hippocampal Injections of Amyloid β-Peptide 1-40 Impair Subsequent One-Trial/Day Reward Learning

Malin, David H.; Crothers, Marie K.; Lake, John R.; Goyarzu, Pilar; Plotner, Robert E.; Garcia, Sergio A.; Spell, Stacy H.; Tomsic, Beverly J.; Giordano, Tony; Kowall, Neil W.

doi:10.1006/nlme.2000.3991

Cited by 25 publications

(10 citation statements)

References 46 publications

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“…Numerous animal models have been until now generated to reproduce, at least partly, the neural and behavioural characteristics of AD patients. Among those, both the acute or continuous administration of various fragments of Ab either in situ (nucleus basalis [1], hippocampus [2], amygdala [3]) or in the lateral cerebral ventricle [4][5][6] have been reported to cause behavioural alterations mainly reflecting defects in temporal lobe depending memory [1,[4][5][6][7]. Demonstration that infusion of Ab into the lateral cerebral ventricle blocks hippocampal LTP in vivo [8] was in agreement with these behavioural findings.…”

Section: Introductionsupporting

confidence: 66%

Enhanced procedural learning following beta-amyloid protein (1-42) infusion in the rat

Ammassari–Teule¹,

Middei²,

Passino³

et al. 2002

NeuroReport

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Wistar rats receiving intracerebroventricular infusion of the beta-amyloid protein (Abeta1-42) or of the inactive fragment (Abeta1-42) were subjected to the cross-maze task. According to the standard protocol, rats were released from the south arm and trained to collect food at the end of the east arm. After a 5-day training period, they were given a probe trial during which they were released from the north arm and allowed to choose either the east arm (place learning) or the west arm (response learning). Control rats showed predominant place learning whereas all rats receiving (Abeta1-42) showed response learning. These data indicate that exposure to (Abeta1-42) does not only impair cognitive responding but elicits strong procedural (motor-based) responding.

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Section: Introductionsupporting

confidence: 66%

Enhanced procedural learning following beta-amyloid protein (1-42) infusion in the rat

Ammassari–Teule¹,

Middei²,

Passino³

et al. 2002

NeuroReport

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show abstract

“…1 A) (99.48 Ϯ 1.43% of baseline slope at 120 min after tetanus, n ϭ 5; F (1, 7) ϭ 1.003, p Ͼ 0.1 compared with control slices, n ϭ 4). As a control for nonspecific effects of the peptide, we tested A␤ 1-42 with a scrambled sequence (Malin et al, 2001), which did not affect the amount of potentiation (supplemental Fig. 9, available at www.jneurosci.org as supplemental material).…”

Section: Dea/no An No Donor Protects Against A␤-induced Impairment mentioning

confidence: 99%

Amyloid-β Peptide Inhibits Activation of the Nitric Oxide/cGMP/cAMP-Responsive Element-Binding Protein Pathway during Hippocampal Synaptic Plasticity

Puzzo¹,

Vitolo²,

Trinchese³

et al. 2005

J. Neurosci.

226

219

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“…Furthermore, P2X7R activation by ATP or the high affinity P2X7R agonist BzATP (3'-O-(4-benzoyl)benzoyl-ATP) (Erb et al, 1990) significantly enhanced ROS production in primary rat microglia, and P2X7R–expressing microglia in APPswe/PS1dE9 mice exhibited significant ROS production that colocalized with decreased expression of the synapse protein postsynaptic density-95 (PSD-95), suggesting that P2X7R–mediated ROS production by microglia cells contributes to synaptic loss in this mouse model of AD (Parvathenani et al, 2003; Lee et al, 2011). Microglial P2X7R upregulation was also observed in a rat model where Aβ 1-42 was directly injected into the hippocampus, which lead to memory deficits and degeneration of hippocampal neurons within 7 days (Kowall et al, 1991; Malin et al, 2001; McLarnon et al, 2006). Administration of the selective P2X7R antagonist Brilliant Blue G (BBG) (Jiang et al, 2000) following hippocampal Aβ 1-42 injection was shown to confer neuroprotection and reduce inflammatory responses, reactive gliosis and neuronal loss in the hippocampus (Ryu and McLarnon, 2008).…”

Section: P2 Receptors In Alzheimer’s Diseasementioning

confidence: 87%

Purinergic receptors as potential therapeutic targets in Alzheimer's disease

et al. 2016

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Alzheimer’s disease (AD) is a neurodegenerative disorder characterized by a progressive loss of memory and cognitive ability and is a serious cause of mortality. Many of the pathological characteristics associated with AD are revealed post-mortem, including amyloid-β plaque deposition, neurofibrillary tangles containing hyperphosphorylated tau proteins and neuronal loss in the hippocampus and cortex. Although several genetic mutations and risk factors have been associated with the disease, the causes remain poorly understood. Study of disease-initiating mechanisms and AD progression in humans is inherently difficult as most available tissue specimens are from late-stages of disease. Therefore, AD researchers rely on in vitro studies and the use of AD animal models where neuroinflammation has been shown to be a major characteristic of AD. Purinergic receptors are a diverse family of proteins consisting of P1 adenosine receptors and P2 nucleotide receptors for ATP, UTP and their metabolites. This family of receptors has been shown to regulate a wide range of physiological and pathophysiological processes, including neuroinflammation, and may contribute to the pathogenesis of neurodegenerative diseases like Parkinson’s disease, multiple sclerosis and AD. Experimental evidence from human AD tissue has suggested that purinergic receptors may play a role in AD progression and studies using selective purinergic receptor agonists and antagonists in vitro and in AD animal models have demonstrated that purinergic receptors represent novel therapeutic targets for the treatment of AD.

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Hippocampal Injections of Amyloid β-Peptide 1-40 Impair Subsequent One-Trial/Day Reward Learning

Cited by 25 publications

References 46 publications

Enhanced procedural learning following beta-amyloid protein (1-42) infusion in the rat

Enhanced procedural learning following beta-amyloid protein (1-42) infusion in the rat

Amyloid-β Peptide Inhibits Activation of the Nitric Oxide/cGMP/cAMP-Responsive Element-Binding Protein Pathway during Hippocampal Synaptic Plasticity

Purinergic receptors as potential therapeutic targets in Alzheimer's disease

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