Cholinergic function and intellectual decline in Alzheimer's disease

Collerton, Daniel

doi:10.1016/0306-4522(86)90002-3

Cited by 589 publications

(186 citation statements)

References 169 publications

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“…p< 05). 8 Visible platform loops and passes In the visible platform task the Naive PCPA+SCO group had more loops and passes than the remaining groups. which did not differ (F(6,69)=7.08, p<.000i; Naive PCPA+SCO vs. each other goup.…”

Section: 1 7 Visible Platform Search Timementioning

confidence: 95%

The effect of nonspatial water maze pretraining in rats subjected to serotonin depletion and muscarinic receptor antagonism: a detailed behavioural assessment of spatial performance

Beiko

Candusso

Cain

1997

Behavioural Brain Research

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Section: 1 7 Visible Platform Search Timementioning

confidence: 95%

The effect of nonspatial water maze pretraining in rats subjected to serotonin depletion and muscarinic receptor antagonism: a detailed behavioural assessment of spatial performance

Beiko

Candusso

Cain

1997

Behavioural Brain Research

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“…1) Alzheimer's disease (AD) is a progressive neurodegenerative disorder characterized by the depletion of high affinity nicotinic acetylcholine receptors (nAChR) and marked loss of cholinergic neurons. 2,3) Selective depletion of cholinergic neurons in the basalis of Meynert, decreased choline acetyltransferase and acetylcholinesterase activity, or down-regulation of neuronal nicotinic acetylcholine receptors suggest the roles of cholinergic deficits in Alzheimer's disease. [3][4][5][6][7][8][9][10] Donepezil, galantamine and tacrine are acetylcholinesterase inhibitors (AChEI) that have been developed for the treatment of AD under the presumption that increasing cholinergic transmission through inhibition of acetylcholinesterase will enhance cognitive function.…”

Section: Introductionmentioning

confidence: 99%

Roles of Nicotinic Receptors in Acetylcholinesterase Inhibitor-Induced Neuroprotection and Nicotinic Receptor Up-Regulation

Takada‐Takatori

Kume

Izumi

et al. 2009

Biological & Pharmaceutical Bulletin

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Protection of neurons from neuronal damage and cell death in neurodegenerative disease is a major challenge in neuroscience research. Donepezil, galantamine and tacrine are acetylcholinesterase inhibitors used for the treatment of Alzheimer's disease, and were believed to be symptomatic drugs whose therapeutic effects are achieved by slowing the hydrolysis of acetylcholine at synaptic termini. However, recent accumulated evidence strongly suggests that these acetylcholinesterase inhibitors also possess neuroprotective properties whose mechanism is independent of acetylcholinesterase inhibition. We have shown that acetylcholinesterase inhibitors protect neurons from glutamate-induced neurotoxicity in the primary culture of rat cortical neurons. It was also found that acetylcholinesterase inhibitor treatment induces up-regulation of nicotinic receptor expression levels, a property which may also have some bearing on their therapeutic effects. We next showed that a a4 and a a7-nicotinic receptors play important roles in acetylcholinesterase inhibitor-induced neuroprotection and nicotinic receptor up-regulation. Our results also demonstrate the important roles of the phosphatidylinositol 3-kinase pathway downstream of nicotinic receptors in protecting neurons from death and up-regulating nicotinic receptors. This review summarizes recent findings on the roles of the nicotinic receptor in acetylcholinesterase inhibitor-induced neuroprotection and nicotinic receptor up-regulation.

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“…For example, ACh and NE levels fluctuate across the sleep-wake cycle, as hippocampal function alternates between memory encoding during wakefulness and consolidation during sleep (Hobson et al, 1975;Kafka et al, 1986;Aston-Jones et al, 1991;Hasselmo, 1999). Cholinergic and/or noradrenergic signaling can also be reduced in hippocampus during aging and neurodegenerative diseases (Carlsson et al, 1980;Tomlinson et al, 1981;Collerton, 1986;Springer et al, 1987;Bickford-Wimer et al, 1988;ChanPalay and Asan, 1989;German et al, 1992;Kasa et al, 1997). Therefore, that ACh and NE can share signaling mechanisms depending on the receptors activated raises the possibility that increased activity of one neurotransmitter may be able to compensate for loss of the other.…”

Section: Introductionmentioning

confidence: 99%

Coactivation of M₁Muscarinic and α1 Adrenergic Receptors Stimulates Extracellular Signal-Regulated Protein Kinase and Induces Long-Term Depression at CA3–CA1 Synapses in Rat Hippocampus

et al. 2008

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Intact cholinergic innervation from the medial septum and noradrenergic innervation from the locus ceruleus are required for hippocampal-dependent learning and memory. However, much remains unclear about the precise roles of acetylcholine (ACh) and norepinephrine (NE) in hippocampal function, particularly in terms of how interactions between these two transmitter systems might play an important role in synaptic plasticity. Previously, we reported that activation of either muscarinic M 1 or adrenergic ␣1 receptors induces activity-and NMDA receptor-dependent long-term depression (LTD) at CA3-CA1 synapses in acute hippocampal slices, referred to as muscarinic LTD (mLTD) and norepinephrine LTD (NE LTD), respectively. In this study, we tested the hypothesis that mLTD and NE LTD are independent forms of LTD, yet require activation of a common G␣q-coupled signaling pathway for their induction, and investigated the net effect of coactivation of M 1 and ␣1 receptors on the magnitude of LTD induced. We find that neither mLTD nor NE LTD requires phospholipase C activation, but both plasticities are prevented by inhibiting the Src kinase family and extracellular signalregulated protein kinase (ERK) activation. Interestingly, LTD can be induced when M 1 and ␣1 agonists are coapplied at concentrations too low to induce LTD when applied separately, via a summed increase in ERK activation. Thus, because ACh and NE levels in vivo covary, especially during periods of memory encoding and consolidation, cooperative signaling through M 1 and ␣1 receptors could function to induce long-term changes in synaptic function important for cognition.

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Cholinergic function and intellectual decline in Alzheimer's disease

Cited by 589 publications

References 169 publications

The effect of nonspatial water maze pretraining in rats subjected to serotonin depletion and muscarinic receptor antagonism: a detailed behavioural assessment of spatial performance

The effect of nonspatial water maze pretraining in rats subjected to serotonin depletion and muscarinic receptor antagonism: a detailed behavioural assessment of spatial performance

Roles of Nicotinic Receptors in Acetylcholinesterase Inhibitor-Induced Neuroprotection and Nicotinic Receptor Up-Regulation

Coactivation of M₁Muscarinic and α1 Adrenergic Receptors Stimulates Extracellular Signal-Regulated Protein Kinase and Induces Long-Term Depression at CA3–CA1 Synapses in Rat Hippocampus

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Cholinergic function and intellectual decline in Alzheimer's disease

Cited by 589 publications

References 169 publications

The effect of nonspatial water maze pretraining in rats subjected to serotonin depletion and muscarinic receptor antagonism: a detailed behavioural assessment of spatial performance

The effect of nonspatial water maze pretraining in rats subjected to serotonin depletion and muscarinic receptor antagonism: a detailed behavioural assessment of spatial performance

Roles of Nicotinic Receptors in Acetylcholinesterase Inhibitor-Induced Neuroprotection and Nicotinic Receptor Up-Regulation

Coactivation of M1Muscarinic and α1 Adrenergic Receptors Stimulates Extracellular Signal-Regulated Protein Kinase and Induces Long-Term Depression at CA3–CA1 Synapses in Rat Hippocampus

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Coactivation of M₁Muscarinic and α1 Adrenergic Receptors Stimulates Extracellular Signal-Regulated Protein Kinase and Induces Long-Term Depression at CA3–CA1 Synapses in Rat Hippocampus