ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2000
Cannabinoids decrease the K(+) M-current in hippocampal CA1 neurons.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.
What it found
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The trial behind it
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Who cites it
50 citing papers in PubMed, 127 citations in OpenAlex.
- Neuroinflammation in the Central Nervous System: Exploring the Evolving Influence of Endocannabinoid System.Biomedicines · 2023Review
- A critical review of cannabis in medicine and dentistry: A look back and the path forward.Clinical and experimental dental research · 2022Review
- Cannabidiol activates neuronal Kv7 channels.eLife · 2022Article
- The Synaptic Interactions of Alcohol and the Endogenous Cannabinoid System.Alcohol research : current reviews · 2022Review
- CRISPR knockdown of Kcnq3 attenuates the M-current and increases excitability of NPY/AgRP neurons to alter energy balance.Molecular metabolism · 2021Article
- Targeting Cannabinoid Receptors: Current Status and Prospects of Natural Products.International journal of molecular sciences · 2020Review
- Monoacylglycerol lipase alpha inhibition alters prefrontal cortex excitability and blunts the consequences of traumatic stress in rat.Neuropharmacology · 2020Article
- 17β-Estradiol Increases Arcuate KNDy Neuronal Sensitivity to Ghrelin Inhibition of the M-Current in Female Mice.Neuroendocrinology · 2020Article
- Mechanisms of cannabinoid CBEBioMedicine · 2019Article
- Endogenous dopamine and endocannabinoid signaling mediate cocaine-induced reversal of AMPAR synaptic potentiation in the nucleus accumbens shell.Neuropharmacology · 2018Article
- CBNeuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2018Review
- Competition between Persistent NaFrontiers in cellular neuroscience · 2017Article
- CB2 and GPR55 Receptors as Therapeutic Targets for Systemic Immune Dysregulation.Frontiers in pharmacology · 2016Review
- The endocannabinoid 2-AG controls skeletal muscle cell differentiation via CB1 receptor-dependent inhibition of Kv7 channels.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- Alterations in the intrinsic burst activity of Purkinje neurons in offspring maternally exposed to the CB1 cannabinoid agonist WIN 55212-2.The Journal of membrane biology · 2014Article
- Synaptic targets of Δ9-tetrahydrocannabinol in the central nervous system.Cold Spring Harbor perspectives in medicine · 2013Review
- Marijuana, endocannabinoids, and epilepsy: potential and challenges for improved therapeutic intervention.Experimental neurology · 2013Review
- New insights on endocannabinoid transmission in psychomotor disorders.Progress in neuro-psychopharmacology & biological psychiatry · 2012Review
- Serotonin 5-HT2C receptor-mediated inhibition of the M-current in hypothalamic POMC neurons.American journal of physiology. Endocrinology and metabolism · 2012Article
- Contributions of Kv7-mediated potassium current to sub- and suprathreshold responses of rat layer II/III neocortical pyramidal neurons.Journal of neurophysiology · 2011Article
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
Cannabinoid effects on sustained conductances that control neuronal excitability have not been investigated in brain. Here, intracellular voltage-clamp recordings were performed using the rat hippocampal slice preparation to study the postsynaptic effect of cannabinoid agonists on CA1 pyramidal neurons. Superfusion of the cannabimimetics WIN55212-2 or methanandamide onto CA1 neurons elicited an inward steady-state current that reversed near the equilibrium potential for K(+) and voltage-dependently activated from a threshold of approximately -70 mV. The cannabinoid receptor (CB1) antagonist SR141716 did not alter membrane properties but prevented this effect. Further investigation revealed that the inward current elicited by cannabinoids was caused by a decrease of the noninactivating voltage-dependent K(+) M-current (I(M)). Cannabinoids had no effect in slices pretreated with the M-channel blocker linopirdine. Assessment of the I(M) relaxation indicated that cannabinoids decreased I(M) in a concentration-dependent manner, with a maximum inhibition of 45 +/- 3% with WIN55212-2 (EC(50) of 0. 6 microM) and 41 +/- 5% with methanandamide (EC(50) of 1 microM). Cannabinoids did not affect the inwardly rectifying cationic h-current (I(h)). The cannabinoid-induced I(M) decrease was prevented by SR141716 but remained unaffected by the muscarinic receptor antagonist atropine. Conversely, the cholinergic agonist carbamylcholine decreased I(M) in the presence of SR141716, indicating that cannabinoid and muscarinic receptor activation independently diminish I(M). It is concluded that cannabinoids may postsynaptically augment the excitability of CA1 pyramidal neurons by specifically decreasing the persistent voltage-dependent I(M).
Indexed as
Identifiers
10627580PMC6774097W1556249553What 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.