Neuroscience MCAT Practice Question
A 54-year-old man with a 6-month history of visual hallucinations undergoes neuroimaging that reveals a small cell lung cancer with metastases to the visual cortex. His hallucinations are characterized by seeing flashing lights and geometric patterns, particularly when he tries to focus on objects. A research team studying his cortical biopsy specimen applies optogenetics to activate parvalbumin-positive GABAergic interneurons in the visual cortex while simultaneously recording from layer 5 pyramidal neurons. Upon light stimulation of the interneurons, the pyramidal neurons demonstrate membrane hyperpolarization and suppression of their spontaneous firing despite continued presentation of visual stimuli to the tissue preparation. Which of the following best explains the mechanism by which GABAergic interneuron activation suppresses pyramidal neuron firing?
Answer choices
- AGABA binding to postsynaptic GABA-A receptors opens chloride channels, causing chloride influx and membrane hyperpolarizationCorrect answer
- BGABA-B receptor activation opens potassium channels on pyramidal neurons, leading to potassium efflux and depolarization
- CGABAergic interneurons inhibit the presynaptic terminals of thalamocortical glutamatergic neurons, reducing excitatory neurotransmitter release
- DGABA competitively blocks glutamate binding sites on AMPA receptors, preventing excitatory synaptic transmission
- EGABAergic interneurons depolarize pyramidal neurons to threshold, causing sodium channel inactivation and refractory period prolongation
- FGABA inhibits the release of neuropeptides from pyramidal neurons that are required for action potential generation
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