ArticleMolecular neurodegeneration2013
Aβ impairs nicotinic regulation of inhibitory synaptic transmission and interneuron excitability in prefrontal cortex.
Article in Molecular neurodegeneration, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
17 citing papers in PubMed, 29 citations in OpenAlex.
- Lamotrigine Restores Impairments in Theta Rhythms and LTP as Early Biomarkers of AβAging and disease · 2025Article
- The interaction between neurotransmitter receptor activity and amyloid-β pathology in Alzheimer's disease.Journal of Alzheimer's disease : JAD · 2025Review
- Acetylcholine deficiency disrupts extratelencephalic projection neurons in the prefrontal cortex in a mouse model of Alzheimer's disease.Nature communications · 2022Article
- Relevance of 5-HTCNS drugs · 2021Review
- Changes in neuronal excitability and synaptic transmission in nucleus accumbens in a transgenic Alzheimer's disease mouse model.Scientific reports · 2020Article
- Impact of Sleep and Circadian Rhythms on Addiction Vulnerability in Adolescents.Biological psychiatry · 2018Review
- Chronic nicotine differentially affects murine transcriptome profiling in isolated cortical interneurons and pyramidal neurons.BMC genomics · 2017Article
- AmyloidInternational journal of peptides · 2017Article
- Cannabinoid CB2 Receptor Mediates Nicotine-Induced Anti-Inflammation in N9 Microglial Cells Exposed to β Amyloid via Protein Kinase C.Mediators of inflammation · 2016Article
- Modulation of AMPA receptor mediated current by nicotinic acetylcholine receptor in layer I neurons of rat prefrontal cortex.Scientific reports · 2015Article
- Cannabinoid receptor CB1 is involved in nicotine-induced protection against Aβ1-42 neurotoxicity in HT22 cells.Journal of molecular neuroscience : MN · 2015Article
- M1 muscarinic acetylcholine receptor in Alzheimer's disease.Neuroscience bulletin · 2014Review
- The γ-secretase complex: from structure to function.Frontiers in cellular neuroscience · 2014Review
- Article
- Forebrain deletion of the vesicular acetylcholine transporter results in deficits in executive function, metabolic, and RNA splicing abnormalities in the prefrontal cortex.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013Article
- A rapid facilitation of acid-sensing ion channels current by corticosterone in cultured hippocampal neurons.Neurochemical research · 2013Article
- Amyloid Beta peptides differentially affect hippocampal theta rhythms in vitro.International journal of peptides · 2013Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
Abstract
backgroundAccumulation of β-amyloid (Aβ) and cholinergic deficiency are two prominent features of Alzheimer's disease (AD). To understand how Aβ-induced dysfunction of the nicotinic system may contribute to cognitive impairment in AD, we examined the effect of Aβ on nicotinic regulation of synaptic transmission and neuronal excitability in prefrontal cortex (PFC), a brain region critical for cognitive processes.
resultsWe found that activation of nicotinic acetylcholine receptors (nAChRs) with nicotine increased the inhibitory postsynaptic currents recorded in PFC pyramidal neurons, which was associated with the nicotine-induced increase in the excitability of PFC layer I GABAergic interneurons. Both effects of nicotine were disrupted by Aβ. However, Aβ did not impair nicotinic regulation of excitatory neurotransmission in PFC interneurons. The nicotinic effect on synaptic inhibition was also lost in transgenic mice with five familial Alzheimer's disease mutations. Inhibiting PKC attenuated nicotinic regulation of inhibitory, but not excitatory, neurotransmission.
conclusionsOur study suggests that Aβ selectively impairs nicotinic regulation of inhibitory inputs to PFC pyramidal neurons, which might be due to its interference with PKC activation. Thus, in the PFC circuits of AD, the balance between inhibition and excitation under the control of nAChRs may be disturbed by Aβ.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.