### Experiment Overview: Impact of Various Drugs on Synaptic Transmission in Cholinergic Neurons You are performing experiments on **cholinergic neurons** in mutant vs. WT *C. elegans* looking for mutants that are drug resistant. Your experiments involve using various drugs (listed below) that impact different steps in chemical neurotransmission. Forget what might be going on in the mutants. Let's just focus on the predicted responses of the WT neurons. For each drug, describe which step in synaptic transmission would be impacted and how. #### Drugs and Their Impact on Synaptic Transmission: **Drug 1: Aldicarb, an acetylcholinesterase inhibitor** - **Impact:** Aldicarb inhibits the enzyme acetylcholinesterase, which is responsible for breaking down the neurotransmitter acetylcholine in the synaptic cleft. Inhibition of this enzyme results in an accumulation of acetylcholine, leading to prolonged activation of acetylcholine receptors on the postsynaptic neuron. **Drug 2: Dyhydropyridine, a calcium channel blocker** - **Impact:** Dyhydropyridine blocks voltage-gated calcium channels on the presynaptic neuron. This prevents the influx of calcium ions, which is necessary for vesicle fusion and release of neurotransmitters into the synaptic cleft. Consequently, neurotransmitter release is reduced or inhibited. **Drug 3: Levamisole, an acetylcholine receptor agonist (activator)** - **Impact:** Levamisole acts as an agonist at acetylcholine receptors, meaning it binds to these receptors and activates them in a manner similar to acetylcholine. This leads to increased activation of the postsynaptic neuron. **Drug 4: Botulism toxin, a drug that cleaves and deactivates SNARE proteins** - **Impact:** Botulism toxin cleaves SNARE proteins, which are critical for the fusion of synaptic vesicles with the presynaptic membrane. By deactivating these proteins, the toxin prevents the release of acetylcholine into the synaptic cleft, thus inhibiting synaptic transmission. **Drug 5: Dynasore, a drug that inhibits dynamin** - **Impact:** Dynasore inhibits dynamin, a GTPase required for the endocytosis of synaptic vesicles. Inhibition of dynamin disrupts the recycling of synaptic vesicles, leading to a depletion of vesicles ready for neurotransmitter release.
### Experiment Overview: Impact of Various Drugs on Synaptic Transmission in Cholinergic Neurons You are performing experiments on **cholinergic neurons** in mutant vs. WT *C. elegans* looking for mutants that are drug resistant. Your experiments involve using various drugs (listed below) that impact different steps in chemical neurotransmission. Forget what might be going on in the mutants. Let's just focus on the predicted responses of the WT neurons. For each drug, describe which step in synaptic transmission would be impacted and how. #### Drugs and Their Impact on Synaptic Transmission: **Drug 1: Aldicarb, an acetylcholinesterase inhibitor** - **Impact:** Aldicarb inhibits the enzyme acetylcholinesterase, which is responsible for breaking down the neurotransmitter acetylcholine in the synaptic cleft. Inhibition of this enzyme results in an accumulation of acetylcholine, leading to prolonged activation of acetylcholine receptors on the postsynaptic neuron. **Drug 2: Dyhydropyridine, a calcium channel blocker** - **Impact:** Dyhydropyridine blocks voltage-gated calcium channels on the presynaptic neuron. This prevents the influx of calcium ions, which is necessary for vesicle fusion and release of neurotransmitters into the synaptic cleft. Consequently, neurotransmitter release is reduced or inhibited. **Drug 3: Levamisole, an acetylcholine receptor agonist (activator)** - **Impact:** Levamisole acts as an agonist at acetylcholine receptors, meaning it binds to these receptors and activates them in a manner similar to acetylcholine. This leads to increased activation of the postsynaptic neuron. **Drug 4: Botulism toxin, a drug that cleaves and deactivates SNARE proteins** - **Impact:** Botulism toxin cleaves SNARE proteins, which are critical for the fusion of synaptic vesicles with the presynaptic membrane. By deactivating these proteins, the toxin prevents the release of acetylcholine into the synaptic cleft, thus inhibiting synaptic transmission. **Drug 5: Dynasore, a drug that inhibits dynamin** - **Impact:** Dynasore inhibits dynamin, a GTPase required for the endocytosis of synaptic vesicles. Inhibition of dynamin disrupts the recycling of synaptic vesicles, leading to a depletion of vesicles ready for neurotransmitter release.
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Transcribed Image Text:### Experiment Overview: Impact of Various Drugs on Synaptic Transmission in Cholinergic Neurons
You are performing experiments on **cholinergic neurons** in mutant vs. WT *C. elegans* looking for mutants that are drug resistant. Your experiments involve using various drugs (listed below) that impact different steps in chemical neurotransmission. Forget what might be going on in the mutants. Let's just focus on the predicted responses of the WT neurons. For each drug, describe which step in synaptic transmission would be impacted and how.
#### Drugs and Their Impact on Synaptic Transmission:
**Drug 1: Aldicarb, an acetylcholinesterase inhibitor**
- **Impact:** Aldicarb inhibits the enzyme acetylcholinesterase, which is responsible for breaking down the neurotransmitter acetylcholine in the synaptic cleft. Inhibition of this enzyme results in an accumulation of acetylcholine, leading to prolonged activation of acetylcholine receptors on the postsynaptic neuron.
**Drug 2: Dyhydropyridine, a calcium channel blocker**
- **Impact:** Dyhydropyridine blocks voltage-gated calcium channels on the presynaptic neuron. This prevents the influx of calcium ions, which is necessary for vesicle fusion and release of neurotransmitters into the synaptic cleft. Consequently, neurotransmitter release is reduced or inhibited.
**Drug 3: Levamisole, an acetylcholine receptor agonist (activator)**
- **Impact:** Levamisole acts as an agonist at acetylcholine receptors, meaning it binds to these receptors and activates them in a manner similar to acetylcholine. This leads to increased activation of the postsynaptic neuron.
**Drug 4: Botulism toxin, a drug that cleaves and deactivates SNARE proteins**
- **Impact:** Botulism toxin cleaves SNARE proteins, which are critical for the fusion of synaptic vesicles with the presynaptic membrane. By deactivating these proteins, the toxin prevents the release of acetylcholine into the synaptic cleft, thus inhibiting synaptic transmission.
**Drug 5: Dynasore, a drug that inhibits dynamin**
- **Impact:** Dynasore inhibits dynamin, a GTPase required for the endocytosis of synaptic vesicles. Inhibition of dynamin disrupts the recycling of synaptic vesicles, leading to a depletion of vesicles ready for neurotransmitter release.
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