Neuronal Nicotinic Receptor and Psychiatric Disorders: Functional and Behavioral Effects of Nicotine

Araki, Hiroaki; Suemaru, Katsuya; Gomita, Yutaka

doi:10.1254/jjp.88.133

Cited by 41 publications

(21 citation statements)

References 34 publications

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“…6, bottom). Jonnala and Buccafusco, 2001;Shimohama and Kihara, 2001), and to serve as a potential drug target in disease states such as schizophrenia (Marutle et al, 2001;Araki et al, 2002), epilepsy (Gil et al, 2002), Alzheimer's disease (Briggs et al, 1997;Meyer et al, 1997;Kem, 2000), and Parkinson's disease (Burghaus et al, 2003). As new ␣7nAChR compounds become available it would be advantageous to have an efficient, objective, and experimentally simple model for drug efficacy.…”

Section: Resultsmentioning

confidence: 99%

Role of α7 Nicotinic Acetylcholine Receptors in the Pressor Response to Intracerebroventricular Injection of Choline: Blockade by Amyloid Peptide Aβ1-42

Li¹,

Buccafusco²

2004

J Pharmacol Exp Ther

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Systemic blood pressure and cardiac function have long been known to be under the control of central autonomic and hormonal pathways that, in part, use cholinergic neural systems. Recently choline, a precursor and product of acetylcholine metabolism, has been shown to serve as a selective endogenous agonist for the ␣7 subtype of the nicotinic acetylcholine receptor (␣7nAChR). This receptor subtype mediates several responses to nicotine in animals, most notably, neuroprotection and enhanced cognition. The purpose of this study was to determine whether the cardiovascular changes induced by central injection of choline in rats also were mediated by ␣7nAChRs. Moreover, we sought to determine whether these cardiovascular changes to choline could be blocked by central pretreatment with amyloid ␤ peptide (1-42) (A␤1-42), a neurotoxic component of cerebral amyloid that is known to bind with high affinity to ␣7nAChRs. Central, i.c.v. injection of choline (50, 100, or 150 g) produced dose-dependent (10 -15-min duration) pressor response of up to about 20 mm Hg. The most consistent change in heart rate included a brief increase (up to 40 beats/min) that lasted 2 to 3 min, followed by a prolonged decrease averaging 50 beats/min that lasted up to 30 min. Pretreatment (i.c.v.) with the selective ␣7nAChR antagonists ␣-bungarotoxin and methyllycaconitine significantly inhibited the pressor and heart rate responses to subsequent injection of choline. Pretreatment with the non-␣7-preferring antagonist dihydro-␤-erythroidin was not effective. These findings suggested that the cardiovascular response to i.c.v. injection of choline was mediated at least in part through ␣7nAChRs. Pretreatment (30 min) with low doses (1-100 pmol) of amyloid peptide A␤1-42 (but not with A␤40-1) administered by the i.c.v. route significantly inhibited the choline-induced blood pressure increase as well as the choline-induced decrease in heart rate.One of the most prominent pathological changes associated with the Alzheimer's disease (AD) is the loss of cholinergic innervation of the cortex and hippocampus. This neuronal loss is accompanied by a decrease in the brain density of the ␣7 subtype of the nicotinic acetylcholine receptor (␣7nAChR). The ␣7nAChR is a unique member of the nicotinic receptor family that in recent years has been shown to enjoy significant physiological importance. In particular, this receptor subtype is known to mediate several responses to nicotine administration in animals, including neuroprotection and cognitive enhancement. For example, ␣7nAChR-preferring agonists, such as anabaseine and GTS-21, were shown to improve working memory in rats (Meyer et al., 1994;Arendash et al., 1995;Briggs et al., 1997). Another ␣7nAChR agonist, ARR 17779 [(Ϫ)-spiro[azabicyclo[2.2.2]octane-3,5Ј-oxazolidin-2Ј-one (4a)], was shown to reverse the working memory deficits induced by fimbria-fornix lesions (Levin et al., 1999). However, other than procedures that estimate aspects of behavior, no objective measure of central ␣7nAChR activation i...

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Section: Resultsmentioning

confidence: 99%

Role of α7 Nicotinic Acetylcholine Receptors in the Pressor Response to Intracerebroventricular Injection of Choline: Blockade by Amyloid Peptide Aβ1-42

Li¹,

Buccafusco²

2004

J Pharmacol Exp Ther

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“…Depending on the concentration and task, an increase in cholinergic transmission, for example via smoking, produces improvements of cognitive functions like memory and attention [2,7,14,37,58,67], whereas blocking cholinergic transmission impairs cognition [15,32,35,43,51,65,73].…”

Section: Introductionmentioning

confidence: 99%

Cholinergic blockade under working memory demands encountered by increased rehearsal strategies: evidence from fMRI in healthy subjects

Voß

Thienel

Reske

et al. 2011

Eur Arch Psychiatry Clin Neurosci

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The connection between cholinergic transmission and cognitive performance has been established in behavioural studies. The specific contribution of the muscarinic receptor system on cognitive performance and brain activation, however, has not been evaluated satisfyingly. To investigate the specific contribution of the muscarinic transmission on neural correlates of working memory, we examined the effects of scopolamine, an antagonist of the muscarinic receptors, using functional magnetic resonance imaging (fMRI). Fifteen healthy male, non-smoking subjects performed a fMRI scanning session following the application of scopolamine (0.4 mg, i.v.) or saline in a placebo-controlled, repeated measure, pseudo-randomized, single-blind design. Working memory was probed using an n-back task. Compared to placebo, challenging the cholinergic transmission with scopolamine resulted in hypoactivations in parietal, occipital and cerebellar areas and hyperactivations in frontal and prefrontal areas. These alterations are interpreted as compensatory strategies used to account for downregulation due to muscarinic acetylcholine blockade in parietal and cerebral storage systems by increased activation in frontal and prefrontal areas related to working memory rehearsal. Our results further underline the importance of cholinergic transmission to working memory performance and determine the specific contribution of muscarinic transmission on cerebral activation associated with executive functioning.

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“…Various studies indicated that tobacco smoking may represent a form of self-medication in some psychiatric diseases [5][6][7][8]. However, the use of nicotine in therapy is severely limited by its carcinogenic and cardiovascular side effects.…”

Section: Introductionmentioning

confidence: 99%

Nicotine-induced memory impairment by increasing brain oxidative stress

Hrițcu

Ciobîcă²,

Gorgan

2009

Open Life Sciences

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Male Wistar rats were subjected to chronic nicotine treatment (0.3 mg/kg; 7 continuous days) and their memory performance was studied by means of Y-maze and multi-trial passive avoidance tasks. Nicotine significantly decreased spontaneous alternation in Y-maze task and step-through-latency in the multi-trial passive avoidance task, suggesting effects on both short-term memory and long-term memory, respectively. In addition, nicotine induced neuronal apoptosis, DNA fragmentation, reduced antioxidant enzymes activity, and increased production of lipid peroxidation and reactive oxygen species, suggesting pro-oxidant activity. Our results provide further support that nicotine-induced memory impairment is due to an increase in brain oxidative stress in rats.

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Neuronal Nicotinic Receptor and Psychiatric Disorders: Functional and Behavioral Effects of Nicotine

Cited by 41 publications

References 34 publications

Role of α7 Nicotinic Acetylcholine Receptors in the Pressor Response to Intracerebroventricular Injection of Choline: Blockade by Amyloid Peptide Aβ1-42

Role of α7 Nicotinic Acetylcholine Receptors in the Pressor Response to Intracerebroventricular Injection of Choline: Blockade by Amyloid Peptide Aβ1-42

Cholinergic blockade under working memory demands encountered by increased rehearsal strategies: evidence from fMRI in healthy subjects

Nicotine-induced memory impairment by increasing brain oxidative stress

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