In pharmacology,<unk> s are<unk>  allosteric<unk>  (PAM) molecules that increase the activity of the GABAA<unk>  protein in the vertebrate central nervous system. GABA is a major inhibitory neurotransmitter in the central nervous system. Upon binding, it triggers the GABAA<unk>  to open its chloride channel to allow chloride ions into the neuron, making the cell hyperpolarized and less likely to fire. GABAA PAMs increase the effect of GABA by making the channel open more frequently or for longer periods. However, they have no effect if GABA or another agonist is not present. Unlike GABAA<unk>  agonists, GABAA PAMs do not bind at the same active site as the γ-Aminobutyric acid (GABA) neurotransmitter molecule: they affect the<unk>  by binding at a different site on the protein. This is called allosteric modulation. In psychopharmacology, GABAA<unk>  PAMs used as drugs have mainly sedative and anxiolytic effects. Examples of GABAA PAMs include alcohol (ethanol), benzodiazepines such as diazepam (Valium) and alprazolam (Xanax), Z-drugs such as zolpidem (Ambien) and the barbiturate drugs.
GABAA receptor positive allosteric modulator
GABAA receptor negative allosteric modulator
Norepinephrine–dopamine disinhibitor
Adenosine receptor antagonist
NMDA receptor antagonist
GABA analogue
Chloride channel opener
Serotonin receptor agonist