Frontal cortical α7 and α4β2 nicotinic acetylcholine receptors in working and reference memory

Chan, Wai Kit; Wong, Peter T.-H.; Sheu, Fwu‐Shan

doi:10.1016/j.neuropharm.2007.03.008

Cited by 65 publications

(59 citation statements)

References 31 publications

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“…Both ␤2-containing and ␣7 nAChRs have been implicated in different aspects of sustained attention and working or reference memory tasks (Hoyle et al, 2006;Chan et al, 2007;Young et al, 2007), and both subtypes have been shown to increase glutamate or excitatory amino acid release in rodent PFC (Gioanni et al, 1999;Lambe et al, 2003;Rousseau et al, 2005;Couey et al, 2007). Plastic changes at glutamatergic synapses in the PFC have been found to occur during working memory tasks (Laroche et al, 2000), and it is plausible that nicotine and other agonists exert their influence on attentional paradigms by contributing to synaptic plasticity.…”

Section: Discussionmentioning

confidence: 99%

“…nAChRs constitute a family of pentameric ligand-gated cation channels that are widely distributed in the brain (Gotti et al, 2006); both ␣7 and non-␣7 subtypes of nAChR in the prefrontal cortex (PFC) have been implicated in effects of nicotine on attentional processes and working memory (Hahn et al, 2003;Mansvelder et al, 2006;Chan et al, 2007;Young et al, 2007). Recently, nicotine was shown to increase the frequency and amplitude of spontaneous excitatory postsynaptic currents in pyramidal neurons in mouse PFC, consistent with the facilitation of glutamate release (Couey et al, 2007).…”

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confidence: 99%

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Presynaptic α7- and β2-Containing Nicotinic Acetylcholine Receptors Modulate Excitatory Amino Acid Release from Rat Prefrontal Cortex Nerve Terminals via Distinct Cellular Mechanisms

Dickinson

Kew²,

Wonnacott³

2008

Mol Pharmacol

149

120

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Nicotine can enhance working memory and attention. Activation of both ␣7 and ␤2* nicotinic acetylcholine receptors (nAChRs) in the prefrontal cortex (PFC) has been implicated in these processes. The ability of presynaptic nAChRs to modulate neurotransmitter release, notably glutamate release, is postulated to contribute to nicotine's effects. We have examined the cellular mechanisms underlying ␣7 and ␤2* nAChR-mediated ]D-aspartate release was also blocked by mitogen-activated protein kinase kinase 1 inhibitors, implicating extracellular signal-regulated kinase (ERK)1/2 in ␣7 nAChRevoked exocytosis. Western blotting confirmed that compound A, but not 5-iodo-A-85380, application increased ERK2 phosphorylation in PFC synaptosomes, and this was dependent on ryanodine-sensitive stores. Compound A also promoted synapsin-1 phosphorylation at ERK1/2-dependent sites, in a ryanodine-sensitive manner. Thus, ␤2* and ␣7 nAChR subtypes in the PFC mediate [3 H]D-aspartate release via distinct mechanisms as a result of their differential coupling to VOCCs and Ca 2ϩ -induced Ca 2ϩ release (CICR), respectively. The ability of ␣7 nAChRs to promote the phosphorylation of presynaptic ERK2 and synapsin-1, downstream of CICR, provides a potential mechanism for presynaptic facilitation in the PFC.

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Presynaptic α7- and β2-Containing Nicotinic Acetylcholine Receptors Modulate Excitatory Amino Acid Release from Rat Prefrontal Cortex Nerve Terminals via Distinct Cellular Mechanisms

Dickinson

Kew²,

Wonnacott³

2008

Mol Pharmacol

149

120

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“…Of the nicotinic acetylcholine receptors (nAChRs), the most prevalent subtypes in the brain are comprised of α4β2 and α7 subunits (Paterson and Nordberg, 2000;Dani and Bertrand, 2007) and it has been suggested that they play an important role in cognition (Chan et al, 2007;Gray and Roth, 2007;Schreiber et al, 2002). These receptors are highly expressed in the hippocampus, cortex, striatum, thalamus and ventral tegmentum (Breese et al, 2000;Freedman et al, 1995;Gotti et al, 2006).…”

Section: Introductionmentioning

confidence: 99%

Nicotinic α7 and α4β2 agonists enhance the formation and retrieval of recognition memory: Potential mechanisms for cognitive performance enhancement in neurological and psychiatric disorders

McLean

Grayson

Marsh

et al. 2016

Behavioural Brain Research

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In the current study we investigated the efficacy of donepezil, risperidone and selective nicotinic α7 and α4β2 receptor agonists to reverse a delay-induced deficit in recognition memory. Adult female hooded-Lister rats received drug treatments and were tested in the novel object recognition (NOR) task following a 6 hour inter-trial interval (ITI). In all treatment groups there was no preference for the left or right identical objects in the acquisition trial. In the retention trial vehicle, risperidone (0.16mg/kg), PNU-282987, an α7 agonist (5mg/kg) and RJR-2403, an α4β2 agonist (1mg/kg) treated rats were unable to discriminate between the novel and familiar objects following a 6 hour ITI. In contrast, donepezil (1.0mg/kg), PNU-282987 (10mg/kg) and RJR-2403 (0.1mg/kg) treated rats spent significantly more time exploring the novel compared to the familiar object following the 6 hour ITI, indicative of enhanced cognitive performance (P<0.05-P<0.01). Interestingly, these compounds were efficacious when administered either before the acquisition or the retention trial of the task, suggesting an important role for nicotinic receptor subtypes in the formation and retrieval of recognition memory.

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“…Both of these receptor subtypes play a role in cognitive processing (Chan et al, 2007;Gray and Roth, 2007;Schreiber et al, 2002).…”

mentioning

confidence: 99%

PNU-120596, a positive allosteric modulator of α7 nicotinic acetylcholine receptors, reverses a sub-chronic phencyclidine-induced cognitive deficit in the attentional set-shifting task in female rats

et al. 2011

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The α7 nicotinic acetylcholine receptors (nAChRs) have been highlighted as a target for cognitive enhancement in schizophrenia. Adult female hooded-Lister rats received sub-chronic PCP (2 mg/kg) or vehicle i.p. twice daily for seven days, followed by 7-days washout. PCP-treated rats then received PNU-120596 (10 mg/kg; s.c.) or saline and were tested in the attentional set-shifting task. Sub-chronic PCP produced a significant cognitive deficit in the extra-dimensional shift (EDS) phase of the task (P<0.001, compared with vehicle). PNU-120596 significantly improved performance of PCP-treated rats in the EDS phase of the attentional set-shifting task (P<0.001). In conclusion, these data demonstrate that PNU-120596 improves cognitive dysfunction in our animal model of cognitive dysfunction in schizophrenia, most likely via modulation of α7 nACh receptors.

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Frontal cortical α7 and α4β2 nicotinic acetylcholine receptors in working and reference memory

Cited by 65 publications

References 31 publications

Presynaptic α7- and β2-Containing Nicotinic Acetylcholine Receptors Modulate Excitatory Amino Acid Release from Rat Prefrontal Cortex Nerve Terminals via Distinct Cellular Mechanisms

Presynaptic α7- and β2-Containing Nicotinic Acetylcholine Receptors Modulate Excitatory Amino Acid Release from Rat Prefrontal Cortex Nerve Terminals via Distinct Cellular Mechanisms

Nicotinic α7 and α4β2 agonists enhance the formation and retrieval of recognition memory: Potential mechanisms for cognitive performance enhancement in neurological and psychiatric disorders

PNU-120596, a positive allosteric modulator of α7 nicotinic acetylcholine receptors, reverses a sub-chronic phencyclidine-induced cognitive deficit in the attentional set-shifting task in female rats

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