Radial-arm maze deficits produced by colchicine administered into the area of the nucleus basalis are ameliorated by cholinergic agents

Tilson, Hugh A.; McLamb, Ronnie L.; Shaw, Stevan; Rogers, Ben; Pediaditakis, Peter; Cook, Larry L.

doi:10.1016/0006-8993(88)91326-1

Cited by 77 publications

(15 citation statements)

References 66 publications

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“…Further, bilateral intracerebral injection of colchicine into the area of the nucleus basalis impaired learning and, concomitantly, decreased ChAT activity and levels of biogenic amines in the neocortex (108). These effects resemble the results produced by ibotenic and kainic acid except that, unlike these two agents, colchicine did not produce cell loss.…”

Section: Introductionsupporting

confidence: 51%

Hypothesis: microtubules, a key to Alzheimer disease.

Matsuyama¹,

Jarvik²

1989

Proc. Natl. Acad. Sci. U.S.A.

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Alzheimer disease (AD) is a clinicopathologic syndrome of unknown etiology with numerous abnormalities in neuronal and nonneuronal cells. A review of the literature suggests that a common basic intracellular defect may underlie many of the reported abnormalities. We hypothesize impairment of the microtubule (MT) system as one explanation for the pathogenesis of AD. Evidence in support of the hypothesis includes the following: MTs are ubiquitous and vital cell components, unequally distributed, with the highest concentration in the brain; various abnormalities, including the key neuropathologic lesions, can be explained by impairments of the MT system; and experiments utilizing pharmacologic agents known to disrupt MTs have reproduced certain abnormalities observed in AD. The hypothesis provides a framework for systematic investigations of MTs at the cellular and molecular levels as well as the basis for in vivo diagnostic tests for AD.

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Section: Introductionsupporting

confidence: 51%

Hypothesis: microtubules, a key to Alzheimer disease.

Matsuyama¹,

Jarvik²

1989

Proc. Natl. Acad. Sci. U.S.A.

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“…1988;Foster et al 1989). Previously reported beneficial effects of muscarinic agonists in basal forebrain lesioned animals (Murray and Fibiger 1986;Ridley et al 1986;Tilson et al 1988) may reflect improvements in performance rather than in memory processes (Robbins et al 1989). Given the evidence on widely unchanged density and function of muscarinic receptors in SDAT (see above), and the ineffectiveness of muscarinic agonists, it seems most likely that the nature of the cholinergic denervation-induced cognitive impairments require treatment strategies other than transmitter replacement and tonic postsynaptic receptor stimulation (Crews et at.…”

Section: Effects Of Muscarinic Agonistsmentioning

confidence: 94%

Activating the damaged basal forebrain cholinergic system: tonic stimulation versus signal amplification

1990

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The hypothesis that the cognitive decline in senile dementia is related to the loss of cortical cholinergic afferent projections predicts that pharmacological manipulations of the remaining cholinergic neurons will have therapeutic effects. However, treatment with cholinesterase inhibitors or muscarinic agonists has been, for the most part, largely unproductive. These drugs seem to disrupt the normal patterning of cholinergic transmission and thus may block proper signal processing. An alternative pharmacological strategy which focuses on the amplification of presynaptic activity without disrupting the normal patterning of cholinergic transmission appears to be more promising. Such a strategy may make use of the normal GABAergic innervation of basal forebrain cholinergic neurons in general, and in particular of the inhibitory hyperinnervation of remaining cholinergic neurons which may develop under pathological conditions. Disinhibition of the GABAergic control of cholinergic activity is assumed to intensify presynaptic cortical cholinergic activity and to enhance cognitive processing. Although the extent to which compounds such as the benzodiazepine receptor antagonist beta-carboline ZK 93,426 act via the basal forebrain GABA-cholinergic link is not yet clear, the available data suggest that the beneficial behavioral effects of this compound established in animals and humans are based on indirect cholinomimetic mechanisms. It is proposed that an activation of residual basal forebrain cholinergic neurons can be achieved most physiologically via inhibitory modulation of afferent GABAergic transmission. This modulation may have a therapeutic value in treating behavioral syndromes associated with cortical cholinergic denervation.

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“…Nicotine has been found to effectively reverse the effects of some types of brain damage in experimental animals. The working memory impairment in the radial-arm maze caused by colchicine lesions of the nucleus basalis is ameliorated by a high dose of 1.5 mg/ kg nicotine tartrate (Tilson et al 1988). Nicotine is also effective in reversing the learning deficits seen in the Morris water maze after septal lesions in rats (Decker and Majchrzak 1991).…”

Section: Nicotine-induced Reversal Of Cognitive Deficits In Animalsmentioning

confidence: 98%

Nicotinic systems and cognitive function

1992

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Nicotinic acetylcholine receptors have been found to be important for maintaining optimal performance on a variety of cognitive tasks. In humans, nicotine-induced improvement of rapid information processing is particularly well documented. In experimental animals nicotine has been found to improve learning and memory on a variety of tasks, while the nicotinic antagonist mecamylamine has been found to impair memory performance. Nicotine has been found to be effective in attenuating memory deficits resulting from lesions of the septohippocampal pathway or aging in experimental animals. Nicotinic receptors are decreased in the cortex of patients with Alzheimer's disease. Preliminary studies have found that some aspects of the cognitive deficit in Alzheimer's disease can be attenuated by nicotine. Nicotine may prove to be useful therapeutic treatment for this and other types of dementia.

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Radial-arm maze deficits produced by colchicine administered into the area of the nucleus basalis are ameliorated by cholinergic agents

Cited by 77 publications

References 66 publications

Hypothesis: microtubules, a key to Alzheimer disease.

Hypothesis: microtubules, a key to Alzheimer disease.

Activating the damaged basal forebrain cholinergic system: tonic stimulation versus signal amplification

Nicotinic systems and cognitive function

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