ArticlePflugers Archiv : European journal of physiology2012
Identification of the muscarinic pathway underlying cessation of sleep-related burst activity in rat thalamocortical relay neurons.
Article in Pflugers Archiv : European journal of physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 33 citations in OpenAlex.
- Awake alpha bursting emerges as the dynamic working state in a lateral geniculate thalamocortical cell model.PLoS computational biology · 2026Article
- TREK1 Channels Shape Spindle-Like Oscillations, Neuronal Activity, and Short-Term Synaptic Plasticity in Thalamocortical Circuits.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Article
- A mechanism for deviance detection and contextual routing in the thalamus: a review and theoretical proposal.Frontiers in neuroscience · 2024Article
- Thalamocortical circuits in generalized epilepsy: Pathophysiologic mechanisms and therapeutic targets.Neurobiology of disease · 2023Review
- Tandem pore TWIK-related potassium channels and neuroprotection.Neural regeneration research · 2019Review
- The Involvement of Sortilin/NTSR3 in Depression as the Progenitor of Spadin and Its Role in the Membrane Expression of TREK-1.Frontiers in pharmacology · 2018Article
- GABAChannels (Austin, Tex.) · 2017Article
- Acetylcholine-dependent upregulation of TASK-1 channels in thalamic interneurons by a smooth muscle-like signalling pathway.The Journal of physiology · 2017Article
- Pedunculopontine arousal system physiology-Effects of psychostimulant abuse.Sleep science (Sao Paulo, Brazil) · 2015Review
- Thalamic Kv 7 channels: pharmacological properties and activity control during noxious signal processing.British journal of pharmacology · 2015Article
- The role of K₂p channels in anaesthesia and sleep.Pflugers Archiv : European journal of physiology · 2015Review
- The CNS under pathophysiologic attack--examining the role of K₂p channels.Pflugers Archiv : European journal of physiology · 2015Review
- Much more than a leak: structure and function of K₂p-channels.Pflugers Archiv : European journal of physiology · 2015Review
- The role of two-pore-domain background K⁺ (K₂p) channels in the thalamus.Pflugers Archiv : European journal of physiology · 2015Review
- Differential phospholipase C-dependent modulation of TASK and TREK two-pore domain K+ channels in rat thalamocortical relay neurons.The Journal of physiology · 2015Article
- Synaptic mechanisms underlying cholinergic control of thalamic reticular nucleus neurons.The Journal of physiology · 2014Review
- Article
- Ca(2+)-dependent large conductance K(+) currents in thalamocortical relay neurons of different rat strains.Pflugers Archiv : European journal of physiology · 2013Article
- Article
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12 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Modulation of the standing outward current (I (SO)) by muscarinic acetylcholine (ACh) receptor (MAChR) stimulation is fundamental for the state-dependent change in activity mode of thalamocortical relay (TC) neurons. Here, we probe the contribution of MAChR subtypes, G proteins, phospholipase C (PLC), and two pore domain K(+) (K(2P)) channels to this signaling cascade. By the use of spadin and A293 as specific blockers, we identify TWIK-related K(+) (TREK)-1 channel as new targets and confirm TWIK-related acid-sensitve K(+) (TASK)-1 channels as known effectors of muscarinic signaling in TC neurons. These findings were confirmed using a high affinity blocker of TASK-3 and TREK-1, namely, tetrahexylammonium chloride. It was found that the effect of muscarinic stimulation was inhibited by M(1)AChR-(pirenzepine, MT-7) and M(3)AChR-specific (4-DAMP) antagonists, phosphoinositide-specific PLCβ (PI-PLC) inhibitors (U73122, ET-18-OCH(3)), but not the phosphatidylcholine-specific PLC (PC-PLC) blocker D609. By comparison, depleting guanosine-5'-triphosphate (GTP) in the intracellular milieu nearly completely abolished the effect of MAChR stimulation. The block of TASK and TREK channels was accompanied by a reduction of the muscarinic effect on I (SO). Current-clamp recordings revealed a membrane depolarization following MAChR stimulation, which was sufficient to switch TC neurons from burst to tonic firing under control conditions but not during block of M(1)AChR/M(3)AChR and in the absence of intracellular GTP. These findings point to a critical role of G proteins and PLC as well as TASK and TREK channels in the muscarinic modulation of thalamic activity modes.
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