ArticleThe Journal of physiology2018
Preferential cholinergic excitation of corticopontine neurons.
Article in The Journal of physiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 45 citations in OpenAlex.
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- Afferent-specific modulation of excitatory synaptic transmission by acetylcholine and serotonin in the prelimbic cortex.bioRxiv : the preprint server for biology · 2025Article
- Cell-type-specific cholinergic control of granular retrosplenial cortex with implications for angular velocity coding across brain states.Progress in neurobiology · 2025Article
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- Cholinergic Neuromodulation of Prefrontal Attractor Dynamics Controls Performance in Spatial Working Memory.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- Cholinergic Activation of Corticofugal Circuits in the Adult Mouse Prefrontal Cortex.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- Variation and convergence in the morpho-functional properties of the mammalian neocortex.Frontiers in systems neuroscience · 2024Review
- Neuromodulatory control of complex adaptive dynamics in the brain.Interface focus · 2023Review
- Cholinergic depolarization recruits a persistent CaJournal of neurophysiology · 2023Article
- Xanomeline restores endogenous nicotinic acetylcholine receptor signaling in mouse prefrontal cortex.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2023Article
- Differential Regulation of Prelimbic and Thalamic Transmission to the Basolateral Amygdala by Acetylcholine Receptors.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
- Targeting 5-HTNeuroscience letters · 2022Article
- Spike Afterhyperpolarizations Govern Persistent Firing Dynamics in Rat Neocortical and Hippocampal Pyramidal Cells.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022Article
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3 authors at 1 institution in 1 country.
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Abstract
key pointsPhasic activation of M1 muscarinic receptors generates transient inhibition followed by longer lasting excitation in neocortical pyramidal neurons. Corticopontine neurons in the mouse prefrontal cortex exhibit weaker cholinergic inhibition, but more robust and longer lasting excitation, than neighbouring callosal projection neurons. Optogenetic release of endogenous ACh in response to single flashes of light (5 ms) preferentially enhances the excitability of corticopontine neurons for many tens of seconds. Cholinergic excitation of corticopontine neurons involves at least three ionic mechanisms: suppression of K ABSTRACT: Pyramidal neurons in layer 5 of the neocortex comprise two broad classes of projection neurons: corticofugal neurons, including corticopontine (CPn) neurons, and intratelencephalic neurons, including commissural/callosal (COM) neurons. These non-overlapping neuron subpopulations represent discrete cortical output channels contributing to perception, decision making and behaviour. CPn and COM neurons have distinct morphological and physiological characteristics, and divergent responses to modulatory transmitters such as serotonin and acetylcholine (ACh). To better understand how ACh regulates cortical output, in slices of mouse prefrontal cortex (PFC) we compared the responsivity of CPn and COM neurons to transient exposure to exogenous or endogenous ACh. In both neuron subtypes, exogenous ACh generated qualitatively similar biphasic responses in which brief hyperpolarization was followed by longer lasting enhancement of excitability. However, cholinergic inhibition was more pronounced in COM neurons, while excitatory responses were larger and longer lasting in CPn neurons. Similarly, optically triggered release of endogenous ACh from cholinergic terminals preferentially and persistently (for ∼40 s) enhanced the excitability of CPn neurons, but had little impact on COM neurons. Cholinergic excitation of CPn neurons involved at least three distinct ionic mechanisms: suppression of K
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