ArticleThe Journal of membrane biology2005
Block of a Ca(2+)-activated potassium channel by cocaine.
Article in The Journal of membrane biology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 20 citations in OpenAlex.
- The Critical Role of Peripheral Targets in Triggering Rapid Neural Effects of Intravenous Cocaine.Neuroscience · 2020Review
- Intravenous Cocaine Increases Oxygen Entry into Brain Tissue: Critical Role of Peripheral Drug Actions.ACS chemical neuroscience · 2019Article
- Central and peripheral contributions to dynamic changes in nucleus accumbens glucose induced by intravenous cocaine.Frontiers in neuroscience · 2015Article
- Cocaine Causes Apoptotic Death in Rat Mesencephalon and Striatum Primary Cultures.BioMed research international · 2015Article
- Effect of cocaine on ion channels and glutamatergic EPSCs in noradrenergic locus coeruleus neurons.Journal of molecular neuroscience : MN · 2014Article
- Ventral tegmental area neurons are either excited or inhibited by cocaine's actions in the peripheral nervous system.Neuroscience · 2012Article
- Differentiating the rapid actions of cocaine.Nature reviews. Neuroscience · 2011Article
- Rapid EEG desynchronization and EMG activation induced by intravenous cocaine in freely moving rats: a peripheral, nondopamine neural triggering.American journal of physiology. Regulatory, integrative and comparative physiology · 2010Article
- Article
- Cocaine serves as a peripheral interoceptive conditioned stimulus for central glutamate and dopamine release.PloS one · 2008Article
- Sensory effects of intravenous cocaine on dopamine and non-dopamine ventral tegmental area neurons.Brain research · 2008Article
- Article
- Investigating the Cocaine-induced Reduction of Potassium Current on the Generation of Action Potentials Using a Computational Model.Basic and clinical neuroscienceArticle
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The primary target for cocaine is believed to be monoamine transporters because of cocaine's high-affinity binding that prevents re-uptake of released neurotransmitter. However, direct interaction with ion channels has been shown to be important for certain pharmacological/toxicological effects of cocaine. Here I show that cocaine selectively blocks a calcium-dependent K(+) channel in hippocampal neurons grown in culture (IC(50)=approximately 30 microM). Single-channel recordings show that in the presence of cocaine, the channel openings are interrupted with brief closures (flicker block). As the concentration of cocaine is increased the open-time is reduced, whereas the duration of brief closures is independent of concentration. The association and dissociation rate constants of cocaine for the neuronal Ca(2+)-activated K(+ )channels are 261+/-37 microM: (-1)s(-1) and 11451+/-1467 s(-1). The equilibrium dissociation constant (K(B)) for cocaine, determined from single-channel parameters, is 43 microM. The lack of voltage dependence of block suggests that cocaine probably binds to a site at the mouth of the pore. Block of Ca(2+)-dependent K(+) channels by cocaine may be involved in functions that include broadening of the action potential, which would facilitate transmitter release, enhancement of smooth muscle contraction particularly in blood vessels, and modulation of repetitive neuronal firing by altering the repolarization and afterhyperpolarization phases of the action potential.
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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.