T-Mobile 11:45 PM × Bio337-lecture#4 questions.docx 1. Picrotoxin is a non-compe
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T-Mobile 11:45 PM × Bio337-lecture#4 questions.docx 1. Picrotoxin is a non-competitive antagonist of GABAA receptors. What is the most likely site of action of picrotoxin? 2. In terms of factors affecting the post-synaptic potential (number of release sites, release probability, quantal size), which factor would you most likely increase if you increased the number of AMPA receptors in the postsynaptic neuron? 3. At a release site and during a release event, the postsynaptic receptors are saturated. If you increase the amount of neurotransmitter released during a release event what would this do to quantal size? 4. You are recording synaptic currents from GABAergic interneuron. You stimulate glutamatergic input and record excitatory post-synaptic currents (EPSCs) at-100 and +50 mVs. At which potential would the current be larger? a. NMDAR-component b. AMPAR-component 5. If you used an anti-body against the vesicular glutamate transporter (VGlut) you would identify what type of neuron?Explanation / Answer
1. Picrotoxin is a poisonous plant compound which interacts with the inhibitory neurotransmitter GABA. It acts as a stimulant as well as a convulsant.
GABA (gamma aminobutyric acid) is an inhibitory neurotransmitter that is widely distributed in the neurons of cortex. This neurotransmitter contributes to motor control, vision and also regulates anxiety.
Picrotoxin acts as a non-competitive antagonist at GABAA receptor. It binds to the allosteric (non-agonist) site of the receptor and thus prevents the activation of GABAA receptor. Picrotoxin blocks the gamma-aminobutyric acid-activated chloride ionophore and mainly impacts the central nervous system (CNS). Hence, it has been used as a CNS stimulant and an antidote in poisoning by CNS depressants.
Therefore, the most likely site of action of picrotoxin is the CNS.
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