Nicotine Enhances Stimulus Detection Performance of Middle- and Old-Aged Rats

Grilly, David M.; Simon, Barbara B.; Levin, Edward D.

doi:10.1016/s0091-3057(99)00259-2

Cited by 34 publications

(21 citation statements)

References 58 publications

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“…Administration of nicotine enhances cognition (Warburton 1992;Levin and Simon 1998;Grilly et al 2000;Levin and Rezvani 2002), whereas nicotinic antagonists impair it (Levin et al 2006). …”

Section: Neuronal Nachrs Are Involved In Normal Mammalian Cognitive Pmentioning

confidence: 99%

Cognitive Deficits in Schizophrenia: Focus on Neuronal Nicotinic Acetylcholine Receptors and Smoking

Ochoa

Lasalde‐Dominicci

2007

Cell Mol Neurobiol

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Patients with schizophrenia present with deficits in specific areas of cognition. These are quantifiable by neuropsychological testing and can be clinically observable as negative signs. Concomitantly, they self-administer nicotine in the form of cigarette smoking. Nicotine dependence is more prevalent in this patient population when compared to other psychiatric conditions or to non-mentally ill people. The target for nicotine is the neuronal nicotinic acetylcholine receptor (nAChR). There is ample evidence that these receptors are involved in normal cognitive operations within the brain. This review describes neuronal nAChR structure and function, focusing on both cholinergic agonist-induced nAChR desensitization and nAChR upregulation. The several mechanisms proposed for the nAChR up-regulation are examined in detail. Desensitization and up-regulation of nAChRs may be relevant to the physiopathology of schizophrenia. The participation of several subtypes of neuronal nAChRs in the cognitive processing of non-mentally ill persons and schizophrenic patients is reviewed. The role of smoking is then examined as a possible cognitive remediator in this psychiatric condition. Finally, pharmacological strategies focused on neuronal nAChRs are discussed as possible therapeutic avenues that may ameliorate the cognitive deficits of schizophrenia.

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“…Administration of nicotine enhances cognition (Warburton 1992;Levin and Simon 1998;Grilly et al 2000;Levin and Rezvani 2002), whereas nicotinic antagonists impair it (Levin et al 2006). …”

Section: Neuronal Nachrs Are Involved In Normal Mammalian Cognitive Pmentioning

confidence: 99%

Cognitive Deficits in Schizophrenia: Focus on Neuronal Nicotinic Acetylcholine Receptors and Smoking

Ochoa

Lasalde‐Dominicci

2007

Cell Mol Neurobiol

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“…Nicotine improved the performance of aged animals in several other tests of cognitive function. In a twochoice, stimulus detection task a significant doserelated improvement in percent correct choices and decrease in choice response times was found at both 24 -25 and 34 -35 months of age (Grilly et al, 2000). Acute treatment of aged rats (22-24 month old) with either nicotine or the partial ␣7-type nAChR agonist GTS-21 enhanced acquisition of one-way active avoidance and Lashley III maze performance (Arendash et al, 1995a,b).…”

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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“…Tasks designed to tax the selectivity component of attention such as the Stroop paradigm have been less successful in showing performance enhancement (Parrott and Craig, 1992;Foulds et al, 1996;Poltavski and Petros, 2006). Similarly, animal studies support enhancement of simple stimulus detection (Grilly et al, 2000;Hahn et al, 2002Hahn et al, , 2003, but not of discriminatory processes (Turchi et al, 1995;Bushnell et al, 1997), after nicotinic agonist administration. Thus, improved stimulus detection by nicotine does not reflect an enhanced ability to actively direct attention to selected stimulus aspects.…”

Section: Introductionmentioning

confidence: 99%

Nicotine Enhances Visuospatial Attention by Deactivating Areas of the Resting Brain Default Network

Hahn¹,

Ross²,

Yang³

et al. 2007

J. Neurosci.

187

165

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Nicotine-induced attentional enhancement is of potential therapeutic value. To investigate the precise attentional function(s) affected and their neuronal mechanisms, the current functional magnetic resonance imaging (fMRI) study used an attention task in which subjects responded to stimuli of high (INT high ) or low intensity presented randomly in one of four peripheral locations. Central cues of varying precision predicted the target location. In some trials, the cue was not followed by a target, allowing separate analysis of blood oxygenation level-dependent (BOLD) responses to cue. Minimally deprived smokers underwent fast event-related fMRI twice: once with a nicotine patch (21 mg) and once with a placebo patch. Matched nonsmokers were scanned twice without a patch. Behaviorally, nicotine reduced omission errors and reaction time (RT) of valid and invalid cue trials and intra-individual variability of RT and did so preferentially in trials with INT high . The BOLD signal related to cue-only trials, regardless of cue precision, demonstrated nicotine-induced deactivation in anterior and posterior cingulate, angular gyrus, middle frontal gyrus, and cuneus. These regions overlapped with the so-called "default network," which activates during rest and deactivates with attention-demanding activities. Partial correlations controlling for nicotine plasma levels indicated associations of deactivation by nicotine in posterior cingulate and angular gyrus with performance improvements under INT high . Performance and regional activity in the absence of nicotine never differed between smokers and nonsmokers, ruling out a simple reversal of a deprivation-induced state. These findings suggest that nicotine improved attentional performance by downregulating resting brain function in response to task-related cues. Together with the selectivity of effects for INT high , this suggests a nicotine-induced potentiation of the alerting properties of external stimuli.

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Nicotine Enhances Stimulus Detection Performance of Middle- and Old-Aged Rats

Cited by 34 publications

References 58 publications

Cognitive Deficits in Schizophrenia: Focus on Neuronal Nicotinic Acetylcholine Receptors and Smoking

Cognitive Deficits in Schizophrenia: Focus on Neuronal Nicotinic Acetylcholine Receptors and Smoking

Nicotinic receptors in aging and dementia

Nicotine Enhances Visuospatial Attention by Deactivating Areas of the Resting Brain Default Network

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