Benzodiazepines are often utilized for the management of anxiety symptoms and disorders. They bind to the post-synaptic GABA-A receptors and enhance the effects of GABA. Benzodiazepine binding decreases the reactivity of the post-synaptic neurons to stimulation. Their specific activity on the GABA-A receptor is shown in the graphic. Commonly used benzodiazepines are diazepam, oxazepam, lorazepam, temazepam, and alprazolam. Many clinicians avoid prescribing benzodiazepines out of fear of physiologic dependence.
This occurs when the post-synaptic receptors upregulate to the point that more benzodiazepines are needed to achieve the therapeutic effect. The result can be that the patient feels dependent on the benzodiazepines because if he/she misses a dose, withdrawal symptoms can occur. If several doses are missed the patient can experience benzodiazepine withdrawal syndrome which includes anxiety, insomnia, tachycardia, and tremor and this can lead to altered mental status, convulsions and death.
The projections from the raphe nuclei to the locus coeruleus are inhibitory, thus decrease the effects of NE.
Extra info: When benzodiazepine bind with the post-synaptic GABA-A receptor, the membrane threshold is relatively increased.
Benzodiazepines require the presence of GABA to be effective.
Extra info: Without GABA, the effect of benzodiazepines would be undeterminable.
Of the many benzodiazepines available on the market, they all have the same general pharmacological mechanism of action, but differ in terms of pharmacokinetic profile.
Extra info: This statement appears to be true at this time, as no true variation in pharmacological effect can be seen between the benzodiazepines.
Aside for use in anxiety disorders, benzodiazepines are also used for anesthesia, insomnia, and status epilepticus.
Extra info: The decrease in the membrane potential renders these agents useful for disorders where a decrease in neuronal stimulation is desired.