How do barbiturates affect neural signalling?

Barbiturates affect neural signalling by enhancing the inhibitory effects of the neurotransmitter gamma-aminobutyric acid (GABA).

Barbiturates are a class of drugs that are commonly used as sedatives and anaesthetics. They work by interacting with the central nervous system, specifically by affecting the neurotransmitter gamma-aminobutyric acid (GABA). GABA is the primary inhibitory neurotransmitter in the brain, meaning it reduces neuronal excitability and slows down brain activity.

When barbiturates enter the body, they bind to the GABA receptors on the neurons. This binding enhances the inhibitory effects of GABA, causing an influx of chloride ions into the neuron. The influx of chloride ions hyperpolarises the neuron, making it less likely to fire an action potential. This results in a decrease in neural signalling, leading to the calming and sedative effects associated with barbiturates.

Furthermore, at higher doses, barbiturates can directly inhibit the action of excitatory neurotransmitters, such as glutamate, by blocking their receptors. This further reduces neural signalling and can lead to a state of deep sedation or even unconsciousness.

However, it's important to note that prolonged use of barbiturates can lead to tolerance and dependence. The brain may adapt to the presence of the drug by reducing the number of GABA receptors or by decreasing the sensitivity of these receptors to GABA. This means that over time, higher doses of the drug are needed to achieve the same effect, increasing the risk of overdose and other harmful effects.

In summary, barbiturates affect neural signalling by enhancing the inhibitory effects of GABA and, at higher doses, by inhibiting the action of excitatory neurotransmitters. This results in a decrease in neural signalling, producing calming and sedative effects.