Search research articles

ABOUT JoVE

Overview Leadership Blog JoVE Help Center

AUTHORS

Publishing Process Editorial Board Scope & Policies Peer Review FAQ Submit

LIBRARIANS

Testimonials Subscriptions Access Resources Library Advisory Board FAQ

RESEARCH

JoVE Journal Methods Collections JoVE Encyclopedia of Experiments Archive

EDUCATION

JoVE Core JoVE Business JoVE Science Education JoVE Lab Manual Faculty Resource Center Faculty Site

Terms & Conditions of Use

Related Concept Videos

Local Anesthetics: Mechanism of Action

Local Anesthetics: Mechanism of Action

Local anesthetics (LAs) block sensory and motor impulses by inhibiting the sodium channels on the nerve cell membranes. This induces temporary loss of sensation, relieving pain in a specific body area.
Local anesthetics are amphiphilic molecules consisting of a hydrophobic aromatic part linked to a hydrophilic group by an ester or amide linkage. They are weak bases and are usually available as salts, which increases their solubility and stability. Once administered, LAs exist in the body either...

Local Anesthetics: Chemistry and Structure-Activity Relationship

Local Anesthetics: Chemistry and Structure-Activity Relationship

Local anesthetics (LAs) are drugs that induce a temporary loss of sensation in a limited body area, preventing pain. Cocaine was the first local anesthetic discovered in the late 19th century. Cocaine is a benzoic acid ester obtained from the leaves of coca shrubs and was often used for its psychotropic effects. Cocaine was first isolated in 1860 by Albert Niemann. Sigmund Freud studied the physiological actions of cocaine. Carl Koller later introduced it into clinical practice in 1884 as a...

Local Anesthetics: Differential Sensitivity of Nerve Fibers

Local Anesthetics: Differential Sensitivity of Nerve Fibers

Local anesthetics (LAs) block the sodium channels of nerve trunks, sensory nerve endings, and neuromuscular junctions. Although LAs can block all kinds of nerves, the sensitivity of nerve fibers differs according to nerve types and structures. LAs are known to block myelinated fibers faster than unmyelinated ones. Also, they block pain or sensory neurons at low concentrations without affecting the motor neurons involved in muscle contractions. This helps relieve labor pain without affecting the...

Local Anesthetics: Common Agents and Their Applications

Local Anesthetics: Common Agents and Their Applications

Local anesthetics (LAs) are commonly used for various applications in medical and dental procedures. Some of the common agents used are cocaine, lidocaine, and bupivacaine.
Cocaine is an ester of benzoic acid and methylecgogine. It is used to anesthetize and vasoconstrict locally. Currently, it is used primarily for topical applications. It is beneficial for surgeries on the upper respiratory tract, providing anesthesia and shrinking the mucosa. Cocaine in the form of cocaine hydrochloride is...

Local Anesthetics: Clinical Application as Surface, Infiltration, and Conduction Block Anesthesia

Local Anesthetics: Clinical Application as Surface, Infiltration, and Conduction Block Anesthesia

Depending on the target organ, local anesthetics (LAs) can be administered via various routes. In surface anesthesia, LAs are applied directly to the surface of the skin or mucous membranes. It is widely used for topical skin numbing before venipuncture or minor surgical procedures. Commonly used surface local anesthetics are lidocaine or benzocaine sprays or creams. Surface anesthesia occurs within 5 minutes and lasts for about 60 minutes. One of the main disadvantages of topical anesthesia is...

Local Anesthetics: Clinical Application as Spinal Anesthesia

Local Anesthetics: Clinical Application as Spinal Anesthesia

Spinal anesthetics are given during lower abdomen and limb surgeries to block sensory and motor neurons. They are administered in the mid to low lumbar regions, primarily acting on the cauda equina's nerve roots. The blockade level depends on the local anesthetic (LA) concentration. Usually, low LA concentrations are sufficient to block sensory fibers, while only high LA concentrations block motor fibers. Other factors like injection volume and speed, the patient's posture, and the drug...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by

Same author

Distinct properties and activation of hexameric and heptameric Pannexin 1 channel concatemers.

The Journal of general physiology·2024

Same author

Novel Pannexin 1 isoform is increased in cancer.

bioRxiv : the preprint server for biology·2024

Same author

Intrinsic Molecular Proton Sensitivity Underlies GPR4 Effects on Retrotrapezoid Nucleus Neuronal Activation and CO<sub>2</sub>-Stimulated Breathing.

The Journal of neuroscience : the official journal of the Society for Neuroscience·2024

Same author

Expression of Endogenous Epitope-Tagged GPR4 in the Mouse Brain.

eNeuro·2024

Same author

Liver-Selective Imidazolopyrazine Mitochondrial Uncoupler SHD865 Reverses Adiposity and Glucose Intolerance in Mice.

Diabetes·2023

Same author

Criteria for central respiratory chemoreceptors: experimental evidence supporting current candidate cell groups.

Frontiers in physiology·2023

Search research articles

Related Experiment Video

Updated: Jun 4, 2026

One-channel Cell-attached Patch-clamp Recording

One-channel Cell-attached Patch-clamp Recording

Published on: June 9, 2014

Local anesthetic inhibits hyperpolarization-activated cationic currents.

Qing-Tao Meng¹, Zhong-Yuan Xia, Jin Liu

¹Laboratory of Anesthesia and Critical Care Medicine, West China Hospital of Sichuan University, Chengdu, China.

Molecular Pharmacology

|February 10, 2011

Summary

Lidocaine, a local anesthetic, inhibits hyperpolarization-activated and cyclic nucleotide-gated (HCN) channels, impacting heart rhythm and central nervous system function. This study clarifies mechanisms behind its perioperative benefits and potential toxicity.

More Related Videos

Microelectrode Impalement Method to Record Membrane Potential from a Cannulated Middle Cerebral Artery

Microelectrode Impalement Method to Record Membrane Potential from a Cannulated Middle Cerebral Artery

Published on: July 2, 2019

Optogenetic Activation of Afferent Pathways in Brain Slices and Modulation of Responses by Volatile Anesthetics

Optogenetic Activation of Afferent Pathways in Brain Slices and Modulation of Responses by Volatile Anesthetics

Published on: July 23, 2020

Related Experiment Videos

Last Updated: Jun 4, 2026

One-channel Cell-attached Patch-clamp Recording

One-channel Cell-attached Patch-clamp Recording

Published on: June 9, 2014

Microelectrode Impalement Method to Record Membrane Potential from a Cannulated Middle Cerebral Artery

Microelectrode Impalement Method to Record Membrane Potential from a Cannulated Middle Cerebral Artery

Published on: July 2, 2019

Optogenetic Activation of Afferent Pathways in Brain Slices and Modulation of Responses by Volatile Anesthetics

Optogenetic Activation of Afferent Pathways in Brain Slices and Modulation of Responses by Volatile Anesthetics

Published on: July 23, 2020

Area of Science:

Pharmacology
Neuroscience
Cardiology

Background:

Systemic local anesthetics offer perioperative benefits, including anesthetic-sparing and antiarrhythmic effects.
The precise mechanisms underlying these beneficial actions remain incompletely understood.

Purpose of the Study:

To investigate the effects of the local anesthetic lidocaine on hyperpolarization-activated and cyclic nucleotide-gated (HCN) channels.
To elucidate the role of HCN channel modulation in the physiological and toxicological effects of lidocaine.

Main Methods:

Utilized voltage-clamp recordings to study cloned HCN subunit currents in Xenopus laevis oocytes and human embryonic kidney (HEK) 293 cells.
Administered lidocaine and its metabolite monoethylglycinexylidide to assess effects on current amplitude, activation kinetics, and voltage-dependence.

Main Results:

Lidocaine inhibited HCN1, HCN2, HCN1-HCN2, and HCN4 channel currents, reducing both tonic and maximal current by 30-50% and slowing activation.
A hyperpolarizing shift in half-activation voltage was observed for HCN1 and HCN1-HCN2 channels.
Lidocaine exhibited dose-dependent inhibition with EC50 values ranging from 30-70 μM, and its metabolite showed similar inhibitory effects.

Conclusions:

Lidocaine potently inhibits HCN channel subunits in a dose-dependent manner within a clinically relevant concentration range.
Modulation of cardiac I(f) by lidocaine may contribute to antiarrhythmic effects or cardiovascular toxicity.
Inhibition of neuronal I(h) by lidocaine could underlie central nervous system depression observed during systemic administration.