Nicotine imptoves cognitive disturbance in senescence-accelerated mice

Meguro, Kenichi; Yamaguchi, Satoshi; Arai, Hiroyuki; Nakagawa, Toshiaki; Doi, C.; Yamada, Munekazu; Ikarashi, Yasushi; Maruyama, Yūji; Sasaki, Hidetada

doi:10.1016/0091-3057(94)90100-7

Cited by 23 publications

(10 citation statements)

References 21 publications

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“…Thus, this study should be considered inconclusive. In contrast with these findings, nicotine and nicotinic agonist ABT-418 have been shown to improve memory in both young (Buccafusco and Jackson 1991;Buccafusco et al 1995;Elrod et al 1988;Jackson et al 1989;Rupniak and Iversen 1989) and aged monkeys (Buccafusco and Jackson 1991;Jackson et al 1989) and in senescence-accelerated mice (Meguro et al 1994) and aged rats (Levin and Torry 1996;Socci et al 1995). However, chronic nicotine administration fails to improve working memory in aged rats, possibly due to the decrease in functional nicotinic receptors in aged animals (Levin and Torry 1996).…”

Section: Animal Studiesmentioning

confidence: 82%

Nicotinic effects on cognitive function: behavioral characterization, pharmacological specification, and anatomic localization

2005

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Discovery of the behavioral, pharmacological, and anatomic specificity of nicotinic effects on learning, memory, and attention not only aids the understanding of nicotinic involvement in the basis of cognitive function, but also helps in the development of novel nicotinic treatments for cognitive dysfunction. Nicotinic treatments directed at specific receptor subtypes and nicotinic cotreatments with drugs affecting interacting transmitter systems may provide cognitive benefits most relevant to different syndromes of cognitive impairment such as Alzheimer's disease, schizophrenia, and attention deficit hyperactivity disorder. Further research is necessary in order to determine the efficacy and safety of nicotinic treatments of these cognitive disorders.

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Section: Animal Studiesmentioning

confidence: 82%

Nicotinic effects on cognitive function: behavioral characterization, pharmacological specification, and anatomic localization

2005

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“…24], Although this is the first known human study to examine acute nicotine effects with respect to aging, the attenuated frequency response to acute smok ing seen in elderly smokers parallels animal evidence of reduced neurochemical (i.e. dopamine) responsivity to acute nicotine challenges in aged rats, presumably result ing from a decline in the number of nicotinic receptors associated with the aged brain [57], Nicotine however has been shown to improve cognitive disturbance in senes cence-accelerated mice [58] and in rats it has been shown to reverse performance impairments induced by musca rinic cholinergic blockade [59] and to attenuate the memory/cognitive impairments induced by lesions of the cho linergically rich nucleus basalis [60] and associated cho linergic projections, including the septohippocampal and the basolocortical projections [61,62], Nicotine's amelio rative effects in these infrahuman investigations may well reflect the central arousing properties exerted by this sub stance which, as exhibited by the equivalent smokinginduced power shifts in young and elderly smokers, are capable of alerting young and aged brains alike.…”

Section: Discussionmentioning

confidence: 99%

Assessing the Topographic EEG Changes Associated with Aging and Acute/Long-Term Effects of Smoking

Knott¹,

Harr²

1996

Neuropsychobiology

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As neuroelectric research into the smoking/nicotine habit has focused exclusively on young and middle-aged adults, this electroencephalographic (EEG) study was conducted to determine whether a long-term smoking history alters the aging brain and/or whether the aging brain demonstrates an altered sensitivity to acute smoking/nicotine. Forty healthy adults, 20 young, aged 18-39 years, and 20 elderly, aged 64–81 years, volunteered for participation. Half of the young and elderly were nonsmokers with no previous smoking history and the remaining half of the young and elderly were current smokers with average smoking histories of 9.3 and 52.0 years, respectively. Smokers attended the laboratory for two randomized test sessions during which multisite EEG recordings were collected pre and post sham and cigarette smoking. Nonsmokers attended the laboratory for one nonsmoking EEG recording session. Spectral power indices showed aging to be associated with significant reductions in absolute delta and theta power and increases in relative beta power and faster mean total band frequency. Aging effects varied with recording region but not with smoker versus nonsmoker status. Smokers did exhibit a faster mean beta frequency. Acute cigarette smoking decreased absolute delta power in young smokers and increased relative alpha2, beta power and mean alpha frequency in both young and elderly smokers. Only the young smokers showed increase in mean theta and total frequency. The results are discussed in relation to cognition in normal and pathological aging.

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“…Accelerated senescence-prone (SAM-P/8) mice that were selectively bred for age-related impairment in cognitive function had lower levels of ACh in the thalamus and hypothalamus than accelerated senescence-resistant mice, and acute nicotine treatment improved passive avoidance learning in SAM-P/8 mice (Meguro et al, 1994). In addition, chronic nicotine treatment could not improve working memory performance in aged rats but did improve performance of young adult rats, whereas the nAChR blocker mecamylamine impaired memory performance in the young adult but not in aged rats (Levin and Torry, 1996).…”

Section: Effects Of Nicotine On Learning and Memory In Aged Or Dementmentioning

confidence: 99%

Nicotinic receptors in aging and dementia

2002

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Activation of neuronal nicotinic acetylcholine receptors (nAChRs) has been shown to maintain cognitive function following aging or the development of dementia. Nicotine and nicotinic agonists have been shown to improve cognitive function in aged or impaired subjects. Smoking has also been shown in some epidemiological studies to be protective against the development of neurodegenerative diseases. This is supported by animal studies that have shown nicotine to be neuroprotective both in vivo and in vitro. Treatment with nicotinic agonists may therefore be useful in both slowing the progression of neurodegenerative illnesses, and improving function in patients with the disease. While increased nicotinic function has been shown to be beneficial, loss of cholinergic markers is often seen in patients with dementia, suggesting that decreased cholinergic function could contribute to both the cognitive deficits, and perhaps the neuronal degeneration, associated with dementia. In this article we will review the literature on each of these areas. We will also present hypotheses that might address the mechanisms underlying the ability of nAChR function to protect against neurodegeneration or improve cognition, two potentially distinct actions of nicotine.

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Nicotine imptoves cognitive disturbance in senescence-accelerated mice

Cited by 23 publications

References 21 publications

Nicotinic effects on cognitive function: behavioral characterization, pharmacological specification, and anatomic localization

Nicotinic effects on cognitive function: behavioral characterization, pharmacological specification, and anatomic localization

Assessing the Topographic EEG Changes Associated with Aging and Acute/Long-Term Effects of Smoking

Nicotinic receptors in aging and dementia

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