The effects of nicotine upon memory and problem solving performance

doi:10.1016/S0031-9384(86)80003-8

Physiology & Behavior

Volume 37, Issue 6, 1986, Pages 849-854

https://doi.org/10.1016/S0031-9384(86)80003-8 Get rights and content

This study examined the effects of 4 mg nicotine and placebo upon problem solving performance in word and number tasks, and subsequent recall and recognition of the answers to these problems. The results demonstrated that the drug had no effect upon the subject's ability to generate the correct answers to the problems, but that immediate and delayed recall and recognition were significantly impaired. These data clearly do not support the view that nicotine, without exception, enhances information processing, and it was suggested that the effects of nicotine upon information retrieval may be specific to tasks which assess episodic memory in the absence of retrieval cues or a problem solving context.

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Rapid eye movement sleep deprivation (REM-SD) is associated with spatial learning and memory impairment. During REM-SD, an increase in nicotine consumption among habitual smokers and initiation of tobacco use by non-smokers have been reported. We have shown recently that nicotine treatment prevented learning and memory impairments associated with REM-SD. We now report the interactive effects of post-learning REM-SD and/or nicotine. The animals were first trained on the radial arm water maze (RAWM) task, then they were REM-sleep deprived using the modified multiple platform paradigm for 24 h. During REM-SD period, the rats were injected with saline or nicotine (1 mg/kg s.c. every 12 h: a total of 3 injections). The animals were tested for long-term memory in the RAWM at the end of the REM-SD period. The 24 h post-learning REM-SD significantly impaired long-term memory. However, nicotine treatment reversed the post-learning REM-SD-induced impairment of long-term memory. On the other hand, post-learning treatment of normal rats with nicotine for 24 h enhanced long-term memory. These results indicate that post-learning acute nicotine treatment prevented the deleterious effect of REM-SD on cognitive abilities.
Chronic nicotine restores normal Aβ levels and prevents short-term memory and E-LTP impairment in Aβ rat model of Alzheimer's disease
2011, Neurobiology of Aging
Citation Excerpt :
Accordingly, these data suggest that BDNF is involved in the regulation of nicotine-mediated neuroprotection in AD. In accordance with previous reports from this and other laboratories, the present study shows that chronic nicotine treatment prevents Aβ-induced impairments of short-term memory, without affecting memory in normal rats (Dunne et al., 1986; Parrott and Winder, 1989; Aleisa et al., 2006a). The concentration of nicotine used in the present study is comparable to the low dose achieved by smoking (Lee, 1994; Newhouse et al., 2001; Rezvani and Levin, 2001).
Alzheimer's disease (AD) is a devastating neurodegenerative disorder characterized by increased deposition of beta-amyloid (Aβ) peptides and progressive cholinergic dysfunction in regions of the brain involved in learning and memory processing. In AD, progressive accumulation of Aβ peptide impairs nicotinic acetylcholine receptor (nAChR) function by an unknown mechanism believed to involve α₇- and α₄β₂-nAChR blockade. The three approaches of the current study evaluated the effects of chronic nicotine treatment in the prevention of Aβ-induced impairment of learning and short-term memory. Rat AD model was induced by 14-day i.c.v. osmotic pump infusion of a 1:1 mixture of 300 pmol/day Aβ_1–40/Aβ_1–42 or Aβ_40–1 (inactive peptide, control). The effect of nicotine (2 mg/(kg day)) on Aβ-induced spatial learning and memory impairments was assessed by evaluation of performance in the radial arm water maze (RAWM), in vivo electrophysiological recordings of early-phase long-term potentiation (E-LTP) in urethane-anesthetized rats, and immunoblot analysis to determine changes in the levels of beta-site amyloid precursor protein (APP)-cleaving enzyme (BACE), Aβ and memory-related proteins. The results indicate that 6 weeks of nicotine treatment reduced the levels of Aβ_1–40 and BACE1 peptides in hippocampal area CA1 and prevented Aβ-induced impairment of learning and short-term memory. Chronic nicotine also prevented the Aβ-induced inhibition of basal synaptic transmission and LTP in hippocampal area CA1. Furthermore, chronic nicotine treatment prevented the Aβ-induced reduction of α₇- and α₄-nAChR. These effects of nicotine may be due, at least in part, to upregulation of brain derived neurotropic factor (BDNF).
Absence of α7-containing neuronal nicotinic acetylcholine receptors does not prevent nicotine-induced seizures
2002, Molecular Brain Research
Nicotine is the primary addictive component in tobacco, and at relatively low doses it affects cardiovascular responses, locomotor activity, thermoregulation, learning, memory, and attention. At higher doses nicotine produces seizures. The mechanisms underlying the convulsive effects of nicotine are not known, but studies conducted on a number of inbred strains of mice have indicated a positive correlation between the number of α-bungarotoxin (α-BTX) binding sites in the hippocampus and the sensitivity to nicotine-induced seizures. Because α7-containing neuronal nicotinic acetylcholine receptors (nAChRs) represent the major binding site for α-BTX, mice lacking the α7 nAChR subunit were predicted to be less sensitive to the convulsive effects of nicotine. To test this hypothesis, we injected nicotine intraperitoneally in α7 mutant mice and found that the dose–response curve for nicotine-induced seizures was similar in the α7 +/+, α7 +/− and α7 −/− mice. The retained sensitivity to the convulsant effects of nicotine could not be explained by the presence of cholinergic compensatory mechanisms such as increases in mRNA levels for other nAChR subunits, or changes in binding levels or affinity for nicotinic ligands such as epibatidine and nicotine. These findings indicate that α7 may not be necessary for the mechanisms underlying nicotine-induced seizures.
Chronic nicotic agonist and antagonist effects on T-maze alternation
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Levin, E. D., N. C. Christopher and S. J. Briggs. Chronic nicotinic agonist and antagonist effects on T-maze alternation. Physiol Behav 61(6) 863–866, 1997.—A variety of studies have found that nicotine improves working memory function. However, other studies have either not found improvements or have found nicotine-induced deficits. The demands of the particular memory test may be critical for the expression of the nicotine effects. In several studies, we have found that chronic nicotine administration improves working memory performance in the radial arm maze. Chronic mecamylamine coadministration reversed this effect. The current study was conducted to determine the effects of chronic nicotine and mecamylamine on choice accuracy in a T-maze spatial alternation task. The same dose and duration of nicotine administration that we have previously found to significantly improve choice accuracy in the radial-arm maze was not effective in altering T-maze spatial alternation. The critical difference in task demands may be the presence with T-maze alternation of proactive interference. During a session, a choice alternative repeatedly changes valence from correct to incorrect and back again. In contrast, with the radial-arm maze as run in our studies, in a session the valence of an arm only changes once from correct to incorrect. Previous work with nicotine effects on spatial alternation in an operant task found evidence that nicotine increased the negative effect of proactive interference on performance. In the current study, chronic mecamylamine caused a significant deficit in T-maze spatial alternation. This same dose did not produce a deficit in the radial-arm maze and, in fact, caused an improvement during the first week of administration.
Acetylcholine, aging, and Alzheimer's disease
1997, Pharmacology Biochemistry and Behavior
A substantial body of literature has suggested that the memory and learning deficits associated with Alzheimer's disease and aging are attributable to degeneration of the cholinergic magnocellular neurons of the nucleus basalis of Meynert (nbM). Subsequently, lesion-induced damage to the cholinergic projections from the nbM to the neocortex has been utilized extensively as an animal model of dementia. In addition, the effect of the normal aging process on deterioration of these neurons and on cognitive function has also been examined. Such studies have revealed, for example, that many of the learning and memory impairments traditionally attributed to the cholinergic corticopetal system are not due to degeneration of the cholinergic neurons of the nbM, but instead may be due to damage of more rostral elements of the cholinergic basal forebrain system. This review will examine the contribution of behavioural animal and human studies to our understanding of the role of the basal forebrain cholinergic neurons in age-related cognitive impairments.
Effects of nicotinic dimethylaminoethyl esters on working memory performance of rats in the radial-arm maze
1995, Pharmacology, Biochemistry and Behavior
Nicotine has been found to improve memory performance in a variety of tests, including the radial-arm maze. This improvement, together with the consistent finding of a decline in cortical nicotinic receptor concentration in Alzheimer's patients, has fueled the search for novel nicotinic ligands with therapeutic potential. In the current studies, a series of nicotinic compounds was tested for effects on working memory performance in the radial-arm maze. One of the three compounds tested, DMAE II (dimethylaminoethanol cyclohexyl carboxylate fumurate), produced significant improvements in working memory performance. In the first experiment, this drug produced a biphasic dose-response curve with improved performance at the 20-mg/kg dose but not at 10 or 40 mg/kg. In a second round of DMAE II administration, the same rats showed a significant improvement with the 40-mg/kg dose. In the second experiment, a new set of rats also showed a biphasic dose-response to DMAE II. The 20-mg/ kg dose caused a significant improvement whereas the 40-mg/kg dose did not. Interactions of DMAE II with nicotine and mecamylamine were also studied. Nicotine (0.2 mg/kg) by itself caused a significant improvement in working memory performance. No additive effects of DMAE II with nicotine were seen. In fact, some attenuation of response was seen with the combination. Choice accuracy data for mecamylamine could not be analyzed because of excessive sedation and nonresponding. These studies show that, like nicotine, the nicotinic ligand DMAE II causes an improvement in radial-arm mace choice accuracy. The lack of additivity with nicotine may have been due to the partial agonist effects of DMAE II.

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View full text

The effects of nicotine upon memory and problem solving performance

Cogn Sci

Pharmacol Ther

Effects of cigarette smoking on verbal rote learning and physiological arousal

The cue-dependent nature of state-dependent retrieval

Mem Cogn

Note on selective effects of short-term tobaccoabstinence on complex versus simple mental tasks

Percept Mot Skills

A generation effect with numbers rather than words

Mem Cogn

Paradoxical tranquilizing and emotion-reducing effects of nicotine

Psychol Bull

Cigarette smoking and stimulus selection

Br J Psychol

Effects of smoking on free recall and organisation

Am J Psychiatry