Propofol is sedative-hypnotic agent injected intravenously to induce and maintain general anaesthesia causing unconsciousness in order to preform surgery. The injection of Propofol produces hypnosis rapidly within 40 seconds from the start of the injection. The rapid rate of induction is caused by the speed in which Propofol can travel through the blood plasma to the CNS. Recovery from Propofol induced anaesthesia is also rapid, with few side-effects. In the CNS Propofol inhibits voltage-gated sodium channels in the axon of neurons. This sodium ions from entering the neuron, and therefore prevents depolarization. The prevention of depolarization means the neuron cannot fire, which means it cannot send an action potential to the presynapse, which then cannot release neurotransmitters to signal the next neuron to fire. Propofol further ensures no action potential can occur by activating GABA A receptors. Propofol attaches to subunit beta-2 and subunit beta-3 of the GABA A receptors. GABA A receptors increase the amount of chloride ions entering the postsynaptic neuron which causes hyperpolarization. Hyperpolarization is when the potential is a negative value, which makes depolarization more difficult to achieve, further preventing neurons from firing action potentials. This inactivity in the brain causes a sedative-hypnotic effect. Propofol also travels to skeletal muscles where it inhibits a voltage-gated sodium channel with protein type 4 subunit alpha. This specific voltage-gated sodium channel is only present in skeletal muscles. Voltage-gated sodium channels in skeletal muscles perpetuate action potentials in the tubule from the depolarization caused by nicotinic Acetylcholine receptors (nAchR). The prevention of action potential in the muscle cell prevents the muscle from contracting.

Propofol Pathway References