Barbiturates prolong the duration of Cl- channel opening and increase Cl- ion influx. They also have additional inhibitory abilities related and unrelated to the Cl- channel
Benzodiazepines increase the activity of GABA by increasing the frequency of Cl- channel opening
Barbiturates are derived from barbituric acid
At higher doses, all barbiturates can produce general anesthesia due to their CNS depressing effects.
The DMMS in the liver is what's responsible for metabolizing barbiturates
Adverse effects of barbiturates are CNS depressant effects such as: drowsiness, dry mouth, lethargy and incoordination. The elderly are especially susceptible to these
Withdrawal symptoms of barbiturates are: anxiety, insomnia, cramping, tremors, delirium and convulsions.
Barbiturate ODs cause extensive extensive depression to the vital centers in the medulla oblongata.
There is no antidote for barbiturate overdose
Benzos are commonly referred to as antianxiety drugs
Benzos are lipid soluble drugs that are metabolized by the DMMS.
Benzos don't cause enzyme induction so withdrawal symptoms are much more reduced than something like barbiturates
Benzos potentiate the actions of other CNS depressants such as alcohol and barbiturates.
The neurotransmitter dopamine contributes a lot to psychosis
Typical antipsychotics are phenothiazines, butyrophenones and thioxanthines