How do sedatives work at the synaptic level?

Sedatives work by enhancing the effects of inhibitory neurotransmitters, reducing neuronal activity in the brain.

Sedatives, also known as tranquilisers, are a class of drugs that slow down brain activity. They achieve this by enhancing the effects of inhibitory neurotransmitters, which are chemicals that reduce the activity of neurons, the cells that transmit information in the brain. The primary inhibitory neurotransmitter in the human brain is gamma-aminobutyric acid (GABA).

GABA works by binding to specific receptors on the surface of neurons. When GABA binds to these receptors, it opens channels in the neuron's membrane that allow negatively charged chloride ions to flow into the cell. This influx of chloride ions makes the inside of the neuron more negatively charged, or hyperpolarised, which makes it less likely to fire and transmit information to other neurons. This reduces overall neuronal activity in the brain, leading to the calming effects associated with sedatives.

Many sedatives, including benzodiazepines and barbiturates, work by enhancing the effects of GABA. They do this by binding to specific sites on the GABA receptors, which makes the receptors more responsive to GABA. This means that more chloride ions flow into the neuron when GABA binds to the receptor, leading to a greater reduction in neuronal activity. Some sedatives can also increase the amount of time that the chloride channels stay open, further enhancing the inhibitory effects of GABA.

However, not all sedatives work in exactly the same way. Some, like alcohol, enhance the effects of GABA but also inhibit the effects of excitatory neurotransmitters, which increase neuronal activity. Others, like certain types of sleeping pills, work by mimicking the effects of GABA and binding directly to its receptors. Despite these differences, all sedatives work by reducing neuronal activity in the brain, leading to effects such as relaxation, drowsiness, and in higher doses, loss of consciousness.