Nicotinic actions on neuronal networks for cognition: General principles and long-term consequences

Poorthuis, Rogier B.; Goriounova, Natalia A.; Couey, Jonathan J.; Mansvelder, Huibert D.

doi:10.1016/j.bcp.2009.04.031

Cited by 91 publications

(77 citation statements)

References 131 publications

(173 reference statements)

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“…Saxena et al (2011) have shown that a 14-day chronic Nic treatment in icv-STZ-treated animals avoids mitochondrial dysfunctions and caspase-3 activity, evidencing the Nic protective influence against apoptosisrelated processes. Our findings, together with those from Srivareerat et al (2011), are in agreement with multiple reports on Nic neuroprotective roles (Fujii and Sumikawa, 2001;Picciotto and Zoli, 2002;Liu and Zhao, 2004;Unger et al, 2006;Poorthuis et al, 2009). In addition, it has been shown that neuroprotection is blocked by nAChR antagonists (Akaike et al, 2010), and that nicotinic receptors can modulate mnemonic processes involving ACh release and Ca 2+ homeostasis (Se´gue´la et al, 1993;McGehee et al, 1995).…”

Section: Discussionsupporting

confidence: 93%

Chronic nicotine attenuates behavioral and synaptic plasticity impairments in a streptozotocin model of Alzheimer’s disease

et al. 2017

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Abstract-Brain glucose metabolism is altered in sporadic Alzheimer's disease (sAD), whose pathologies are reproduced in rodents by intracerebroventricular (icv) infusion of streptozotocin (STZ) in subdiabetogenic doses. The icv-STZ model also culminates in central cholinergic dysfunctions, which in turn are known to underlie both the sAD cognitive decline, and synaptic plasticity impairments. Considering the cognitive-enhancing potential of chronic nicotine (Nic), we investigated whether it attenuates icv-STZ-induced impairments in recognition memory and synaptic plasticity in a cognition-relevant substrate: the hippocampal CA1-medial prefrontal cortex (mPFC) pathway. Rats treated with icv-STZ were submitted to a chronic Nic regime, and were evaluated for recognition memory. We then examined long-term potentiation (LTP), paired-pulse facilitation (PPF) under urethane anesthesia, and brains were also evaluated for hippocampus-mPFC cell density. We found that Nic treatment prevents icv-STZ-induced disruptions in recognition memory and LTP. STZ did not precipitate neuronal death, while Nic alone was associated with higher neuronal density in CA1 when compared to vehicle-injected animals. Through combining behavioral, neurophysiological, and neuropathological observations into the Nic-STZ interplay, our study reinforces that cholinergic treatments are of clinical importance against earlystage Alzheimer's disease and mild cognitive impairments.

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Section: Discussionsupporting

confidence: 93%

Chronic nicotine attenuates behavioral and synaptic plasticity impairments in a streptozotocin model of Alzheimer’s disease

et al. 2017

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“…Consequently this feature may alter the PFC's role in the ability to establish a rational evaluation of smoking even during adult age. We also observed that nicotine increased noradrenaline release in the PFC (Carboni et al, 2010) thus suggesting that this increase may have a role in the nicotine enhancement of cognition (see the review of Poorthuis et al, 2009). Furthermore local infusion of nicotine in the prelimbic mPFC can increase mPFC glutamate extracellular concentration supporting the role of nAChRs in modulating thalamocortical input to the PFC (Gioanni et al, 1999).…”

Section: Prefrontal Cortex Dopamine Transmission In Adolescence and Dsupporting

confidence: 61%

Role of Prefrontal Cortex Dopamine and Noradrenaline Circuitry in Addiction

Carboni¹,

Cadeddu²,

Carta³

2012

Addictions - From Pathophysiology to Treatment

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“…a4b2 receptors have a very high affinity for nicotine and desensitize at low concentrations of nicotine, corresponding to blood concentrations experienced by smokers. In contrast, a7 receptors have a low affinity for nicotine but do not desensitize at low nicotine concentrations (Poorthuis et al, 2009). In animal studies, local acute and chronic hippocampal infusion of a4b2 antagonists cause significant spatial working memory impairment (Arthur and Levin, 2002), while a4b2 receptor agonists significantly improve working memory and attention function .…”

Section: Introductionmentioning

confidence: 99%

Adjunctive Varenicline Treatment with Antipsychotic Medications for Cognitive Impairments in People with Schizophrenia: A Randomized Double-Blind Placebo-Controlled Trial

Shim

Jung

Jung³

et al. 2011

Neuropsychopharmacol

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The aim of this study is to examine the effects of treatment with varenicline, a partial agonist at the a4b2 and full agonist at the a7 nicotine acetylcholine receptor, on cognitive impairments in people with schizophrenia. In all, 120 clinically stable people with schizophrenia participated in randomized, double-blind, placebo-controlled 8-week trial. Antipsychotic and concomitant medication doses remained fixed throughout the study. Varenicline was titrated up to 1 mg twice daily for weeks 2-8. Neuropsychological, clinical, and safety assessments were administered at baseline and weeks 1, 2, 4, and 8. In the primary analyses of neurocognitive differences at week 8, no varenicline-placebo differences were significant. In secondary longitudinal analyses, varenicline improved compared with placebo on the Digital Symbol Substitution Test (p ¼ 0.013) and the Wisconsin Card Sorting Test non-perseverative errors (p ¼ 0.043). Some treatment effects were different between smokers and non-smokers. In smokers, Continuous Performance Test hit reaction time (p ¼ 0.008) and Stroop Interference (p ¼ 0.004) were reduced for varenicline compared with placebo, while there were no treatment differences in non-smokers. No significant treatment main effects or interactions were noted for total scores on the Positive and Negative Syndrome Scale or the Scale for the Assessment for Negative Symptoms. Our findings suggest beneficial effects of adjunctive varenicline treatment with antipsychotics for some cognitive impairments in people with schizophrenia. In some cases, effects of treatment varied between smokers and non-smokers. Further study is required to assess the functional significance of these changes.

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Nicotinic actions on neuronal networks for cognition: General principles and long-term consequences

Abstract: Nicotine enhances cognitive performance in humans and laboratory animals. The

Cited by 91 publications

References 131 publications

Chronic nicotine attenuates behavioral and synaptic plasticity impairments in a streptozotocin model of Alzheimer’s disease

Chronic nicotine attenuates behavioral and synaptic plasticity impairments in a streptozotocin model of Alzheimer’s disease

Role of Prefrontal Cortex Dopamine and Noradrenaline Circuitry in Addiction

Adjunctive Varenicline Treatment with Antipsychotic Medications for Cognitive Impairments in People with Schizophrenia: A Randomized Double-Blind Placebo-Controlled Trial

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