Attentional functions of cortical cholinergic inputs: What does it mean for learning and memory?

Sarter, Martin; Bruno, John P.; Givens, Bennet

doi:10.1016/s1074-7427(03)00070-4

Cited by 251 publications

(151 citation statements)

References 137 publications

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“…Our data confirm the disruptive effects of scopolamine on object recognition and a dose of 0.1 mg/ kg was selected for reversal studies with Ro4368554 and metrifonate. Although reversal effects of a scopolamineinduced deficit is typically interpreted in terms of an effect on cognitive function, it has been suggested that scopolamine may primarily affect sensory/attention processes rather than inducing a direct and selective effect on learning and memory processes (Blokland, 1995;Sarter et al, 2003). Since the present study did not address attentional or motivational functions, the possibility of attentional or sensorimotor effects cannot be completely ruled out.…”

Section: Impairment In Object Recognitionmentioning

confidence: 72%

The Selective 5-HT6 Receptor Antagonist Ro4368554 Restores Memory Performance in Cholinergic and Serotonergic Models of Memory Deficiency in the Rat

Lieben

Blokland

Şık

et al. 2005

Neuropsychopharmacol

134

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Antagonists at serotonin type 6 (5-HT 6 ) receptors show activity in models of learning and memory. Although the underlying mechanism(s) are not well understood, these effects may involve an increase in acetylcholine (ACh) levels. The present study sought to characterize the cognitive-enhancing effects of the 5-HT 6 antagonist Ro4368554 (3-benzenesulfonyl-7-(4-methyl-piperazin-1-yl)1H-indole) in a rat object recognition task employing a cholinergic (scopolamine pretreatment) and a serotonergic-(tryptophan (TRP) depletion) deficient model, and compared its pattern of action with that of the acetylcholinesterase inhibitor metrifonate. Initial testing in a time-dependent forgetting task employing a 24-h delay between training and testing showed that metrifonate improved object recognition (at 10 and 30 mg/kg, p.o.), whereas Ro4368554 was inactive. Both, Ro4368554 (3 and 10 mg/kg, intraperitoneally (i.p.)) and metrifonate (10 mg/kg, p.o., respectively) reversed memory deficits induced by scopolamine and TRP depletion (10 mg/kg, i.p., and 3 mg/kg, p.o., respectively). In conclusion, although Ro4368554 did not improve a time-related retention deficit, it reversed a cholinergic and a serotonergic memory deficit, suggesting that both mechanisms may be involved in the facilitation of object memory by Ro4368554 and, possibly, other 5-HT 6 receptor antagonists.

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Section: Impairment In Object Recognitionmentioning

confidence: 72%

The Selective 5-HT6 Receptor Antagonist Ro4368554 Restores Memory Performance in Cholinergic and Serotonergic Models of Memory Deficiency in the Rat

Lieben

Blokland

Şık

et al. 2005

Neuropsychopharmacol

134

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“…As a result, relative to the SRT, Paragraph Recall may be an easier task. There is much evidence from the animal literature that describes the increasing involvement of the cholinergic system with increasing task difficulty (Sarter et al 2003). Thus, the differential task difficulty in the SRT and Paragraph Recall tests may explain their differential sensitivity to the E2-cholinergic interaction.…”

Section: Discussionmentioning

confidence: 99%

Estradiol interacts with the cholinergic system to affect verbal memory in postmenopausal women: Evidence for the critical period hypothesis

Dumas

Hancur-Bucci

Naylor

et al. 2008

Hormones and Behavior

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Estradiol has been shown to interact with the cholinergic system to affect cognition in postmenopausal women. This study further investigated the interaction of estradiol and cholinergic system functioning on verbal memory and attention in two groups of healthy younger (ages 50-62) and older (ages 70-80) postmenopausal women. Twenty-two postmenopausal women were randomly and blindly placed on 1 mg of 17-beta estradiol orally for one month then 2 mg for two months or matching placebo pills after which they participated in three anticholinergic challenge sessions when verbal memory performance was assessed. Subjects were administered either the antimuscarinic drug scopolamine (SCOP), the antinicotinic drug mecamylamine (MECA) or placebo. After the first challenge phase, they were crossed over to the other hormone treatment for another three months and repeated the challenges. Results showed that estradiol pretreatment significantly attenuated the anticholinergic drug-induced impairments on a test of episodic memory (the Buschke Selective Reminding test) for the younger group only, while estradiol treatment impaired performance of the older group. The results suggest that younger subjects may experience more cholinergic benefit from estradiol treatment than older subjects, supporting the concept of a critical period for postmenopausal estrogen use.

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“…Striatal ACh increase associated with cocaine acquisition Crespo et al, 2006;Mark et al, 1999) Striatal ACh alters cocaine-induced locomotor sensitization Hikida et al, 2001Hikida et al, , 2003 mACh receptors decrease after chronic cocaine (Lipton et al, 1995;Macedo et al, 2004;Wilson et al, 1994;Zeigler et al, 1991) Amygdala mAChR may facilitate acquisition of associative learning underlying context-dependent sensitization Itzhak and Martin, 2000) Explicit memory Hippocampus ACh involved in the encoding of new information (Hasselmo and Fehlau, 2001;Hasselmo et al, 2002) Hippocampal ACh increases following cocaine use (Imperato et al, 1993a(Imperato et al, , b, 1996Smith et al, 2004a, b) Conditioned learning VTA VTA ACh involved in conditioned learning (Bechara and van der Kooy, 1989;Museo and Wise, 1994;Olmstead and Franklin, 1993) M 5 -deficient rats decrease cocaine-induced CPP (Fink-Jensen et al, 2003) Striatum Striatal ACh involved in conditioned learning (Legault et al, 2006) NAc ACh inhibits cocaine-induced CPP (Hikida et al, 2001 ACh antagonist blocks induction of locomotor sensitization to cocaine-induced CPP (Itzhak and Martin, 2000) Amygdala Amygdalar ACh facilitates conditioned learning (McIntyre et al, 1998;Power et al, 2003) Amygdalar ACh alters cocaine-induced conditioned learning (See et al, 2003;Zeigler et al, 1991) Attention PFC Elevated ACh may focus attentional resources toward salient stimuli (Baxter and Chiba, 1999;Robbins, 2002;Sarter et al, 2003) Cocaine-addicted subjects show impaired attention (Horner et al, 1996;Jovanovski et al, 2005) Set shifting PFC ACh involved in set shifting (Ragozzino and Choi...…”

Section: Overview Of Animal Models Of Addictionmentioning

confidence: 99%

“…Within the CNS, ACh is involved in motor behaviors, modulating the behavioral states associated with incoming information such as emotional tone, motivation, and arousal (Mesulam, 1996), as well as complex cognitive processes such as attention, learning, and memory (Sarter et al, 2003). Limbic and paralimbic regions of the CNS contain the highest density of ACh innervations in the brain (Mesulam, 1996) and are thought to be most relevant to the process of addiction (Bonson et al, 2002;Childress et al, 1999;Goldstein and Volkow, 2002).…”

Section: Overview Of the Central Cholinergic Systemmentioning

confidence: 99%

“…Attention refers to the different capacities or processes that relate to how an organism becomes receptive to stimuli and how it begins to process incoming or attended-to (internal or external) excitation (Parasuraman, 1998). ACh is strongly linked to these attentional processes (Baxter and Chiba, 1999;Robbins, 2002;Sarter et al, 2003). ACh efflux, for example, is increased into the medial frontal cortex during a five-choice serial reaction time task (5-CSRTT)Fa measure of visual attention.…”

Section: Acetylcholine and Prefrontal Cortical Cognitionmentioning

confidence: 99%

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The Role of Acetylcholine in Cocaine Addiction

Williams

Adinoff²

2007

Neuropsychopharmacol

160

138

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Central nervous system cholinergic neurons arise from several discrete sources, project to multiple brain regions, and exert specific effects on reward, learning, and memory. These processes are critical for the development and persistence of addictive disorders. Although other neurotransmitters, including dopamine, glutamate, and serotonin, have been the primary focus of drug research to date, a growing preclinical literature reveals a critical role of acetylcholine (ACh) in the experience and progression of drug use. This review will present and integrate the findings regarding the role of ACh in drug dependence, with a primary focus on cocaine and the muscarinic ACh system. Mesostriatal ACh appears to mediate reinforcement through its effect on reward, satiation, and aversion, and chronic cocaine administration produces neuroadaptive changes in the striatum. ACh is further involved in the acquisition of conditional associations that underlie cocaine self-administration and context-dependent sensitization, the acquisition of associations in conditioned learning, and drug procurement through its effects on arousal and attention. Long-term cocaine use may induce neuronal alterations in the brain that affect the ACh system and impair executive function, possibly contributing to the disruptions in decision making that characterize this population. These primarily preclinical studies suggest that ACh exerts a myriad of effects on the addictive process and that persistent changes to the ACh system following chronic drug use may exacerbate the risk of relapse during recovery. Ultimately, ACh modulation may be a potential target for pharmacological treatment interventions in cocaine-addicted subjects. However, the complicated neurocircuitry of the cholinergic system, the multiple ACh receptor subtypes, the confluence of excitatory and inhibitory ACh inputs, and the unique properties of the striatal cholinergic interneurons suggest that a precise target of cholinergic manipulation will be required to impact substance use in the clinical population.

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Attentional functions of cortical cholinergic inputs: What does it mean for learning and memory?

Cited by 251 publications

References 137 publications

The Selective 5-HT6 Receptor Antagonist Ro4368554 Restores Memory Performance in Cholinergic and Serotonergic Models of Memory Deficiency in the Rat

The Selective 5-HT6 Receptor Antagonist Ro4368554 Restores Memory Performance in Cholinergic and Serotonergic Models of Memory Deficiency in the Rat

Estradiol interacts with the cholinergic system to affect verbal memory in postmenopausal women: Evidence for the critical period hypothesis

The Role of Acetylcholine in Cocaine Addiction

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