Final answer:
GABA neurotransmitters' activity is increased by substances like ethanol, barbiturates, and benzodiazepines, leading to a hyperpolarized state in neurons and resulting in sedative effects.
Step-by-step explanation:
Let's consider the neurotransmitter GABA (Gamma-Aminobutyric Acid), which is predominantly inhibitory in the brain. Drugs such as ethanol, barbiturates, and benzodiazepines affect GABA by increasing its activity. These substances are classified as GABA agonists because they enhance the effect of GABA on its receptors. The activation of GABA receptors by these drugs results in an increased influx of chloride ions into the neuron, Hyperpolarizing it, and thus making it less likely to fire an action potential. This action is primarily responsible for their sedative and anxiolytic effects.
The effect of a neurotransmitter on the postsynaptic element is entirely dependent on the receptor protein. When acetylcholine binds to the nicotinic receptor, the postsynaptic cell is depolarized because the receptor is a cation channel and positively charged Nat will rush into the cell. However, when acetylcholine binds to the muscarinic receptor, it might cause depolarization or hyperpolarization of the target cell.