Muscarinic acetylcholine neurotransmission enhances the late-phase of long-term potentiation in the hippocampal–prefrontal cortex pathway of rats in vivo: A possible involvement of monoaminergic systems

Lopes-Aguiar, Cleiton; Romcy-Pereira, Rodrigo Neves; Szawka, Raphael E.; Galvis-Alonso, Orfa Yineth; Anselmo-Franci, Janete Aparecida; Leite, João P.

doi:10.1016/j.neuroscience.2008.02.040

Cited by 38 publications

(49 citation statements)

References 82 publications

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“…It consisted of two series (10 min apart) of 10 trains (10 s apart), each train with 50 pulses at 250 Hz. LTP was evaluated in 10 min averaged fPSP amplitudes, which were plotted as ratios from the baseline mean amplitude (Lopes-Aguiar et al, 2008).…”

Section: Electrophysiologymentioning

confidence: 99%

“…Limbic-cortical synaptic plasticity can be dysfunctional in prodromal Alzheimer's disease, which could explain its mild cognitive alterations (Scheff et al, 2006;Arendt, 2009). In this context, the hippocampal CA1-medial prefrontal cortex (mPFC) communication is prone to long-term plasticity (Lopes-Aguiar et al, 2008Takita et al, 2013), is implicated in working memory (Spellman et al, 2015;Blot et al, 2015) and memory consolidation (Laroche et al, 2000;Taylor et al, 2016;Maingret et al, 2016;Jadhav et al, 2016;Barker et al, 2017). Thus, synaptic plasticity in this circuit could be increasingly altered as Alzheimer's disease develops, which can be experimentally studied using the icv-STZ model of sAD.…”

Section: Introductionmentioning

confidence: 99%

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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: Electrophysiologymentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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

et al. 2017

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“…Following HFS, single-pulse recording resumed for 90 minutes. 24 After LTP was recorded, the evoked responses of the last 20 minutes were normalized and used for the baseline of depotentiation (1 per minute), and then low frequency stimulation (LFS) containing two series of low-frequency stimulations (1 Hz, 10 minutes, total LFS 20 minutes) was applied. Following LFS, single-pulse recording resumed for 90 minutes.…”

Section: Ltp and Depotentiation Recordingmentioning

confidence: 99%

Nano-zinc oxide damages spatial cognition capability via over-enhanced long-term potentiation in hippocamus of Wistar rats

Han¹,

Tian²,

Zhang³

et al. 2011

IJN

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This study focused on the effects of zinc oxide nanoparticles (nano-ZnO) on spatial learning and memory and synaptic plasticity in the hippocampus of young rats, and tried to interpret the underlying mechanism. Rats were randomly divided into four groups. Nano-ZnO and phosphate-buffered saline were administered in 4-week-old rats for 8 weeks. Subsequently, performance in Morris water maze (MWM) was determined, and then long-term potentiation (LTP) and depotentiation were measured in the perforant pathway to dentate gyrus (DG) in anesthetized rats. The data showed that, (1) in MWM, the escape latency was prolonged in the nano-ZnO group and, (2) LTP was significantly enhanced in the nano-ZnO group, while depotentiation was barely influenced in the DG region of the nano-ZnO group. This bidirectional effect on long-term synaptic plasticity broke the balance between stability and flexibility of cognition. The spatial learning and memory ability was attenuated by the alteration of synaptic plasticity in nano-ZnO-treated rats.

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“…Many studies of functional pathways and neural networks, and a host of association studies demonstrate, on the one hand, the salience of such hypotheses, but on the other, their lack of full resolution (Abdolmaleky et al 2008;Bloom 1984;Haavik et al 2008;Jones and Craddock 2001;Lopes Aguiar et al 2008;Mokrovic et al 2008;Patrick 2000;Ressler and NemeroV 2000;Talkowski et al 2008;Vanyukov et al 2007). Early molecular hypotheses and investigations also suggested a potential role for proteins involved in ion transport, including ion channels, ATPases and other ion transporters in the etiology and/or pathophysiology of bipolar and related disorders (Akagawa et al 1980;Hokin-Neaverson and JeVerson 1989;Meyer et al 2005;Mynett-Johnson et al 1998;Wittekindt et al 1998).…”

Section: Ion Channels and Related Regulatory Proteinsmentioning

confidence: 99%

Pathways-based analyses of whole-genome association study data in bipolar disorder reveal genes mediating ion channel activity and synaptic neurotransmission

2008

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Despite known heritability, the complex genetic architecture of bipolar disorder (likely including trait, locus and allelic heterogeneity, as well as genetic interactions) has confounded genetic discovery for many years. Even modern day whole genome association studies (WGAS) using over half a million common SNPs have implicated only a handful of genes at the genomewide level. Temporally coincident with this series of WGAS, a host of pathways-based analyses (PBAs) have emerged as novel computational approaches in the examination of large-scale datasets, but thus far rarely have been applied to WGAS data in psychiatric disorders. Here, we report a series of PBAs conducted using exploratory visual analysis, an analytic and visualization software tool for examining genomic data, to examine results from the National Institutes of Mental Health and Wellcome-Trust Case Control Consortium WGAS in bipolar disorder. Consistent with a host of prior linkage findings, some candidate gene association studies, and recent WGAS, our strongest findings suggest involvement of ion channel structural and regulatory genes, including voltage-gated ion channels and the broader ion channel group that comprises both voltage- and ligand-gated channels. Moreover, we found only modest overlap in the particular genes driving the significance of these gene sets across the analyses. This observation strongly suggests that variation in ion channel genes, as a class of genes, may contribute to the susceptibility of bipolar disorder and that heterogeneity may figure prominently in the genetic architecture of this susceptibility.

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Muscarinic acetylcholine neurotransmission enhances the late-phase of long-term potentiation in the hippocampal–prefrontal cortex pathway of rats in vivo: A possible involvement of monoaminergic systems

Cited by 38 publications

References 82 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

Nano-zinc oxide damages spatial cognition capability via over-enhanced long-term potentiation in hippocamus of Wistar rats

Pathways-based analyses of whole-genome association study data in bipolar disorder reveal genes mediating ion channel activity and synaptic neurotransmission

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