Final answer:
Ethanol inactivates the enzyme acetylcholinesterase, which is responsible for breaking down the neurotransmitter acetylcholine (ACh). This leads to increased levels of ACh in synapses and prolonged activation of ACh receptors, resulting in enhanced muscarinic and nicotinic effects within the autonomic nervous system.
Step-by-step explanation:
When ethanol is introduced to the body, it has an impact on the release of the neurotransmitter acetylcholine (ACh). Acetylcholine is crucial for transmitting signals in the nervous system. Normally, the enzyme acetylcholinesterase (AChE) actively breaks down ACh. However, ethanol can inactivate acetylcholinesterase, leading to increased levels of ACh in synapses. This increased presence of ACh can cause enhanced muscarinic and nicotinic effects due to prolonged activation of ACh receptors.
Specifically, the presence of ethanol prevents the breakdown of ACh, meaning that ACh continues to bind to receptors on postganglionic fibers in the autonomic nervous system, leading to prolonged depolarization and the potential for continuous activation of the target organ. This effect can be compared to the action of nicotine, which also binds to ACh receptors, mimicking the action of ACh at preganglionic synapses and causing similar activation.
ACh typically binds to receptors, opening sodium ion channels and leading to an action potential in the sarcolemma. However, if the enzyme acetylcholinesterase is inactivated, the breakdown of ACh does not occur as efficiently, which can lead to the various physiological effects associated with altered ACh levels, including effects on muscle action, heart rate, and other bodily functions regulated by the autonomic nervous system.