Mediaspace scheduled maintenance: Aug 25, 2026 07:00 - 12:00 AM. During this time, videos will be temporarily unavailable. Check status updates.

Lecture

Benzodiazepines

Description

This lecture covers the structure and amino acid sequences of GABA receptors, the effects of benzodiazepines on specific subunits, point mutations in GABA receptors, and genome editing to mutate GABA receptors in mice.

In MOOC

Cellular Mechanisms of Brain Function

Official source

Quiz

Related concepts (24)

Benzodiazepine

Benzodiazepines (BZD, BDZ, BZs), colloquially called "benzos", are a class of depressant drugs whose core chemical structure is the fusion of a benzene ring and a diazepine ring. They are prescribed to treat conditions such as anxiety disorders, insomnia, and seizures. The first benzodiazepine, chlordiazepoxide (Librium), was discovered accidentally by Leo Sternbach in 1955 and was made available in 1960 by Hoffmann–La Roche, who soon followed with diazepam (Valium) in 1963.

Benzodiazepine withdrawal syndrome

Benzodiazepine withdrawal syndrome, often abbreviated to benzo withdrawal or BZD withdrawal, is the cluster of signs and symptoms that may emerge when a person who has been taking benzodiazepines as prescribed develops a physical dependence on them and then reduces the dose or stops taking them without a safe taper schedule.

GABAA receptor

DISPLAYTITLE:GABAA receptor The GABAA receptor (GABAAR) is an ionotropic receptor and ligand-gated ion channel. Its endogenous ligand is γ-aminobutyric acid (GABA), the major inhibitory neurotransmitter in the central nervous system. Upon opening, the GABAA receptor on the postsynaptic cell is selectively permeable to chloride ions (Cl−) and, to a lesser extent, bicarbonate ions (HCO3−). Depending on the membrane potential and the ionic concentration difference, this can result in ionic fluxes across the pore.

Point mutation

A point mutation is a genetic mutation where a single nucleotide base is changed, inserted or deleted from a DNA or RNA sequence of an organism's genome. Point mutations have a variety of effects on the downstream protein product—consequences that are moderately predictable based upon the specifics of the mutation. These consequences can range from no effect (e.g. synonymous mutations) to deleterious effects (e.g. frameshift mutations), with regard to protein production, composition, and function.

Effects of long-term benzodiazepine use

The effects of long-term benzodiazepine use include drug dependence as well as the possibility of adverse effects on cognitive function, physical health, and mental health. Long-term use is sometimes described as use not shorter than three months. Benzodiazepines are generally effective when used therapeutically in the short term, but even then the risk of dependency can be significantly high. There are significant physical, mental and social risks associated with the long-term use of benzodiazepines.

Related lectures (32)

Neurotransmitters: GABA and Glycine

Explores the classification and effects of GABA and Glycine neurotransmitters, including drug interactions.

Drug Targets: ligand-gated ion channels and kinase-linked receptors

Explores drug targets in ligand-gated ion channels and kinase-linked receptors, focusing on GABAA receptors, benzodiazepines, and insulin therapy.

Molecules of Life: Understanding Translation and Protein Synthesis

Provides an overview of translation and protein synthesis, covering the genetic code, tRNA, and the steps involved in protein formation.

Mutations and Cancer: The Role of P53 and HPV

Covers mutations, the role of P53 in cancer, and HPV's impact on tumorigenesis.

Genomic Alterations in Cancer