PUBLICATION
Anaesthetic Tricaine Acts Preferentially on Neural Voltage-Gated Sodium Channels and Fails to Block Directly Evoked Muscle Contraction
- Authors
- Attili, S., Hughes, S.M.
- ID
- ZDB-PUB-140805-2
- Date
- 2014
- Source
- PLoS One 9: e103751 (Journal)
- Registered Authors
- Hughes, Simon M.
- Keywords
- none
- MeSH Terms
-
- Anesthetics/pharmacology*
- Voltage-Gated Sodium Channels/metabolism*
- Neurons/drug effects
- Neurons/physiology*
- Animals
- PubMed
- 25090007 Full text @ PLoS One
Abstract
Movements in animals arise through concerted action of neurons and skeletal muscle. General anaesthetics prevent movement and cause loss of consciousness by blocking neural function. Anaesthetics of the amino amide-class are thought to act by blockade of voltage-gated sodium channels. In fish, the commonly used anaesthetic tricaine methanesulphonate, also known as 3-aminobenzoic acid ethyl ester, metacaine or MS-222, causes loss of consciousness. However, its role in blocking action potentials in distinct excitable cells is unclear, raising the possibility that tricaine could act as a neuromuscular blocking agent directly causing paralysis. Here we use evoked electrical stimulation to show that tricaine efficiently blocks neural action potentials, but does not prevent directly evoked muscle contraction. Nifedipine-sensitive L-type Cav channels affecting movement are also primarily neural, suggesting that muscle Nav channels are relatively insensitive to tricaine. These findings show that tricaine used at standard concentrations in zebrafish larvae does not paralyse muscle, thereby diminishing concern that a direct action on muscle could mask a lack of general anaesthesia.
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