Start Valium less sedating than klonopin

Valium less sedating than klonopin

Benzodiazepine receptors are ubiquitous throughout the central nervous system.

Caution must be used when prescribing benzodiazepines to patients with a current or remote history of substance abuse.

Benzodiazepines enhance the affinity of the recognition site for GABA by inducing conformational changes that make GABA binding more efficacious.

Activation of the benzodiazepine-GABA-chloride ionophor complex is responsible for producing the therapeutic anxiolytic effects of benzodiazepines and for mediating many of the side effects and, possibly, dependence and withdrawal from these drugs.6Similarly, other sites for drug and neurotransmitter binding are associated with the GABA receptor complex, which serves as a primary site of action of benzodiazepines, barbiturates and other sedative-hypnotics, such as alcohol.6 Benzodiazepines and barbiturates act at separate binding sites on the receptor to potentiate the inhibitory action of GABA.

With long-term high-dose use of benzodiazepines (or ethanol), there is an apparent decrease in the efficacy of GABA-A receptors, presumably a mechanism of tolerance.67 When high-dose benzodiazepines or ethanol are abruptly discontinued, this “down-regulated” state of inhibitory transmission is unmasked, leading to characteristic withdrawal symptoms such as anxiety, insomnia, autonomic hyperactivity and, possibly, seizures.

With the introduction of chlordiazepoxide (Librium) in 1960, and because of the relative safety of benzodiazepines, these agents rapidly replaced barbiturates as sedative-hypnotics.

Benzodiazepines are widely prescribed for a variety of conditions, particularly anxiety and insomnia.

They are relatively safe and, with overdose, rarely result in death.

They do so by allosterically altering the receptor (changing its conformation) so that it has a greater binding affinity for GABA.