A gardener was accidentally poisoned by a weed killer that inhibits acetylcholinesterase. Which of the following alterations in neurochemical transmission at brain cholinergic synapses is the most likely result of this poisoning?
**Core Concept**
The poisoning described involves inhibition of acetylcholinesterase, the enzyme responsible for breaking down acetylcholine (ACh) into choline and acetic acid at the synapse. This leads to an accumulation of ACh in the synaptic cleft, resulting in overstimulation of nicotinic and muscarinic receptors.
**Why the Correct Answer is Right**
Inhibition of acetylcholinesterase causes an excessive release of acetylcholine, leading to overstimulation of nicotinic and muscarinic receptors. This results in an increase in excitatory neurotransmission, manifesting as overactivity of the parasympathetic nervous system. The symptoms of poisoning would include excessive salivation, lacrimation, urination, and defecation, as well as muscle weakness and respiratory failure.
**Why Each Wrong Option is Incorrect**
**Option A:** This option is incorrect because the poisoning would lead to an increase in acetylcholine levels, not a decrease.
**Option B:** This option is incorrect because the poisoning would lead to overstimulation of nicotinic and muscarinic receptors, not decreased receptor activity.
**Option C:** This option is incorrect because the poisoning would lead to an increase in excitatory neurotransmission, not decreased neurotransmission.
**Clinical Pearl / High-Yield Fact**
In cases of organophosphate poisoning, the use of pralidoxime (2-PAM) can help restore acetylcholinesterase activity by reactivating the enzyme and reducing the accumulation of acetylcholine.
**Correct Answer: C. Excessive release of acetylcholine, leading to overstimulation of nicotinic and muscarinic receptors.**