ArticleBMC neuroscience2012
Distinct muscarinic acetylcholine receptor subtypes mediate pre- and postsynaptic effects in rat neocortex.
Article in BMC neuroscience, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 19 citations in OpenAlex.
- Transcriptional and functional profiles of muscarinic receptor-expressing neurons in primate lateral prefrontal and anterior cingulate cortices.Communications biology · 2026Article
- Multiple cholinergic receptor subtypes coordinate dual modulation of acetylcholine on anterior and posterior paraventricular thalamic neurons.Journal of neurochemistry · 2024Article
- Prefrontal cortical distribution of muscarinic M2 and cannabinoid-1 (CB1) receptors in adult male mice with or without chronic adolescent exposure to Δ9-tetrahydrocannabinol.Cerebral cortex (New York, N.Y. : 1991) · 2022Article
- Perisomatic Inhibition and Its Relation to Epilepsy and to Synchrony Generation in the Human Neocortex.International journal of molecular sciences · 2021Article
- Immunolocalization of muscarinic M1 receptor in the rat medial prefrontal cortex.The Journal of comparative neurology · 2018Article
- Muscarinic Receptors Are Responsible for the Cholinergic Modulation of Projection Neurons in the Song Production Brain Nucleus RA of Zebra Finches.Frontiers in cellular neuroscience · 2017Article
- Muscarinic acetylcholine receptors act in synergy to facilitate learning and memory.Learning & memory (Cold Spring Harbor, N.Y.) · 2016Article
- Different pharmacology of N-desmethylclozapine at human and rat M2 and M 4 mAChRs in neocortex.Naunyn-Schmiedeberg's archives of pharmacology · 2015Article
- Acetylcholine functionally reorganizes neocortical microcircuits.Journal of neurophysiology · 2014Article
- Reverse translation of the rodent 5C-CPT reveals that the impaired attention of people with schizophrenia is similar to scopolamine-induced deficits in mice.Translational psychiatry · 2013Article
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundCholinergic transmission has been implicated in learning, memory and cognition. However, the cellular effects induced by muscarinic acetylcholine receptors (mAChRs) activation are poorly understood in the neocortex. We investigated the effects of the cholinergic agonist carbachol (CCh) and various agonists and antagonists on neuronal activity in rat neocortical slices using intracellular (sharp microelectrode) and field potential recordings.
resultsCCh increased neuronal firing but reduced synaptic transmission. The increase of neuronal firing was antagonized by pirenzepine (M₁/M₄ mAChRs antagonist) but not by AF-DX 116 (M₂/M₄ mAChRs antagonist). Pirenzepine reversed the depressant effect of CCh on excitatory postsynaptic potential (EPSP) but had marginal effects when applied before CCh. AF-DX 116 antagonized the depression of EPSP when applied before or during CCh. CCh also decreased the paired-pulse inhibition of field potentials and the inhibitory conductances mediated by GABA(A) and GABA(B) receptors. The depression of paired-pulse inhibition was antagonized or prevented by AF-DX 116 or atropine but only marginally by pirenzepine. The inhibitory conductances were unaltered by xanomeline (M₁/M₄ mAChRs agonist), yet the CCh-induced depression was antagonized by AF-DX 116. Linopirdine, a selective M-current blocker, mimicked the effect of CCh on neuronal firing. However, linopirdine had no effect on the amplitude of EPSP or on the paired-pulse inhibition, indicating that M-current is involved in the increase of neuronal excitability but neither in the depression of EPSP nor paired-pulse inhibition.
conclusionsThese data indicate that the three effects are mediated by different mAChRs, the increase in firing being mediated by M₁ mAChR, decrease of inhibition by M₂ mAChR and depression of excitatory transmission by M₄ mAChR. The depression of EPSP and increase of neuronal firing might enhance the signal-to-noise ratio, whereas the concomitant depression of inhibition would facilitate long-term potentiation. Thus, this triade of effects may represent a "neuronal correlate" of attention and learning.
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