Cholinergic Neurotransmission Is Essential for Perirhinal Cortical Plasticity and Recognition Memory

Warburton, E. Clea; Koder, Tim; Cho, Kwangwook; Massey, Peter V.; Duguid, Gail; Barker, Gareth R I; Aggleton, John Patrick; Bashir, Zafar I.; Brown, Malcolm W.

doi:10.1016/s0896-6273(03)00358-1

Cited by 206 publications

(270 citation statements)

References 53 publications

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“…Moreover, perirhinal muscarinic receptor antagonism by scopolamine can block LTD while sparing LTP (Warburton et al, 2003). It is worth noting that in the developing rat brain, there is a visual experience-dependent switch from mGlu receptor-dependent to muscarinic receptor-dependent LTD which indicates not only that LTD might play a functional role in the perirhinal cortex but also that the forms of LTD expressed in the area are not set in stone and could be further modified with behavioural experience.…”

Section: Synaptic Plasticity In the Perirhinal Cortexmentioning

confidence: 99%

“…The bulk of research on synaptic plasticity within the perirhinal cortex has focussed on long-term depression (LTD) due to its possible role in recognition memory (see below and Jerusalinsky et al, 1997;Warburton et al, 2003;Wan et al, 2004;Barker et al, 2006a;Griffiths et al, 2008;Seoane et al, 2009). Ziakopoulos et al (1999) demonstrated that the perirhinal cortex could also undergo depressive synaptic plasticity; short-term depression in the form of paired-pulse depression (PPD) could be induced with a 200 ms IPI and this PPD was GABA B -dependent (Ziakopoulos et al, 2000).…”

Section: Synaptic Plasticity In the Perirhinal Cortexmentioning

confidence: 99%

“…Furthermore, transgenic overexpression of the NR2B subunit in hippocampal and cortical neurons enhances performance in an object recognition task yet does not promote LTD in the area CA1 (Wang et al, 2009) which is a conflicting finding compared to the majority of research in this area. There are a large number of molecular mechanisms involved in object recognition memory that are correlated with LTD including L-type voltage-dependent Ca 2+ channels (Seoane et al, 2009), CREB (Warburton et al, 2005), muscarinic cholinergic receptors (Warburton et al, 2003;Massey et al, 2008), GABA receptors (Wan et al, 2004) mGlu receptors (Barker et al, 2006a;Moult et al, 2006), NMDA receptors (Cho et al, 2000Roberts et al, 2009;, kainate receptors (Barker et al, 2006a;Park et al, 2006;Holman et al, 2007) and AMPA receptor internalisation (Griffiths et al, 2008). Therefore, although both LTP and LTDlike processes might be involved in object recognition memory, it would appear that an LTD-like process is the principle physiological mechanism underlying recognition memory.…”

Section: Object Recognition Memorymentioning

confidence: 99%

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The rat perirhinal cortex: A review of anatomy, physiology, plasticity, and function

Kealy

Commins

2011

Progress in Neurobiology

103

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Section: Synaptic Plasticity In the Perirhinal Cortexmentioning

confidence: 99%

Section: Synaptic Plasticity In the Perirhinal Cortexmentioning

confidence: 99%

Section: Object Recognition Memorymentioning

confidence: 99%

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The rat perirhinal cortex: A review of anatomy, physiology, plasticity, and function

Kealy

Commins

2011

Progress in Neurobiology

103

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“…The doses of scopolamine were based on similar behavioral studies that used scopolamine infusion into cortical and/or hippocampal formation regions (Barros et al, 2001;Herremans et al, 1996;Warburton et al, 2003;Winters et al, 2006). Importantly, these doses were lower than the doses shown before to impair classical conditioning when infused to BLA (See et al, 2003), because impairment of conditioning per se (impaired conditioning in the NPE groups) masks the effects of experimental manipulations on LI.…”

Section: Drugs and Infusionsmentioning

confidence: 99%

Differential Role of Muscarinic Transmission within the Entorhinal Cortex and Basolateral Amygdala in the Processing of Irrelevant Stimuli

Barak

Weiner

2010

Neuropsychopharmacol

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Cholinergic projections to the entorhinal cortex (EC) and basolateral amygdala (BLA) mediate distinct cognitive processes through muscarinic acetylcholine receptors (mAChRs). In this study, we sought to further differentiate the role of muscarinic transmission in these regions in cognition, using the latent inhibition (LI) phenomenon. LI is a cross-species phenomenon manifested as poorer conditioning to a stimulus experienced as irrelevant during an earlier stage of repeated non-reinforced pre-exposure to that stimulus, and is considered to index the ability to ignore, or to in-attend to, irrelevant stimuli. Given our recent findings that systemic administration of the mAChR antagonist scopolamine can produce two contrasting LI abnormalities in rats, ie, abolish LI under conditions yielding LI in non-treated controls, or produce abnormally persistent LI under conditions preventing its expression in non-treated controls, we tested whether mAChR blockade in the EC and BLA would induce LI abolition and persistence, respectively. We found that intra-EC scopolamine infusion (1, 10 mg per hemisphere) abolished LI when infused in pre-exposure or both pre-exposure and conditioning, but not in conditioning alone, whereas intra-BLA scopolamine infusion led to persistent LI when infused in conditioning or both stages, but not in pre-exposure alone. Although cholinergic innervation of the EC and BLA has long been implicated in attention to novel stimuli and in processing of motivationally significant stimuli, respectively, our results provide evidence that EC mAChRs also have a role in the development of inattention to stimuli, whereas BLA mAChRs have a role in re-attending to previously irrelevant stimuli that became motivationally relevant.

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“…Basalis of Meynert, NBM) (Mesulam, 2004a). A number of pharmacological and lesion studies in humans and animals show that cholinergic neuromodulation is critical for learning and memory (Chudasama et al, 2004;Drachman and Leavitt, 1974;Sarter et al, 2005;Tang et al, 1997;Turchi et al, 2005;Warburton et al, 2003) and for regulating and maintaining attention possibly by enhancing the response to sensory input (Hasselmo and Giocomo, 2006;Mesulam, 2004a). Also, cholinergic neuromodulation is implicated in the ability to maintain stimulus information online in working memory (Hasselmo and Stern, 2006).…”

Section: Introductionmentioning

confidence: 99%

Basal forebrain integrity and cognitive memory profile in healthy aging

Düzel¹,

Münte²,

Lindenberger³

et al. 2010

Brain Research

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Age-related dysfunctions in cholinergic and dopaminergic neuromodulation are assumed to contribute to age-associated impairment of explicit memory. Both neurotransmitters also modulate attention, working memory, and processing speed. To date, in vivo evidence linking structural age-related changes in these neuromodulatory systems to dysfunction within or across these cognitive domains remains scarce. Using a factor analytical approach in a cross-sectional study including 86 healthy older (aged 55 to 83 years) and 24 young (aged 18 to 30 years) adults, we assessed the relationship between structural integrity-as measured by magnetization transfer ratio (MTR)-of the substantia nigra/ventral tegmental area (SN/VTA), main origin of dopaminergic projections, basal forebrain (major origin of cortical cholinergic projections), frontal white matter (FWM), and hippocampus to neuropsychological and psychosocial scores. Basal forebrain MTR and FWM changes correlated with a factor combining verbal learning and memory and working memory and, as indicated by measures of diffusion, were most likely due to vascular pathology. These findings suggest that frontal white matter integrity and cholinergic neuromodulation provide clues as to why age-related cognitive decline is often correlated across cognitive domains. IntroductionAge-related decline in learning and memory, often termed age-associated memory impairment (AAMI) (Crook et al., 1986), is a well-documented finding in healthy older adults (Balota et al., 2000;Cabeza et al., 2000;Craik, 1994;Salthouse, 2003), but the neurobiological correlates of this decline are still under debate. A consistent pattern of AAMI is a decrement in declarative memory (Tulving, 1985) most clearly apparent in impaired free recall and recollection (Buckner, 2004;Craik, 2006;Hedden and Gabrieli, 2004;Nilsson, 2003). Evidence from lesion studies in humans and animals indicates that

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Cholinergic Neurotransmission Is Essential for Perirhinal Cortical Plasticity and Recognition Memory

Cited by 206 publications

References 53 publications

The rat perirhinal cortex: A review of anatomy, physiology, plasticity, and function

The rat perirhinal cortex: A review of anatomy, physiology, plasticity, and function

Differential Role of Muscarinic Transmission within the Entorhinal Cortex and Basolateral Amygdala in the Processing of Irrelevant Stimuli

Basal forebrain integrity and cognitive memory profile in healthy aging

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