Excess of which neurotransmitter is associated with brain damage after strokes?

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Multiple Choice

Excess of which neurotransmitter is associated with brain damage after strokes?

Explanation:
Excess glutamate leads to brain damage after strokes through a process called excitotoxicity. When a stroke cuts off blood flow, neurons lose energy and can’t dispose of glutamate efficiently. This causes glutamate to accumulate outside cells and overactivate glutamate receptors (like NMDA and AMPA) on nearby neurons. The result is a surge of calcium ions into the cells, which sets off a cascade of destructive processes: activating enzymes that degrade proteins and membranes, disrupting mitochondria, producing free radicals, and triggering cell death pathways. That’s why glutamate is the neurotransmitter most closely linked to post-stroke brain injury—the damage isn’t caused by glutamine (a precursor), but by the excess glutamate itself. GABA, in contrast, is inhibitory and would tend to dampen neural activity rather than cause excitotoxic damage. Acetylcholine and endorphins aren’t the primary drivers of this injury mechanism in stroke.

Excess glutamate leads to brain damage after strokes through a process called excitotoxicity. When a stroke cuts off blood flow, neurons lose energy and can’t dispose of glutamate efficiently. This causes glutamate to accumulate outside cells and overactivate glutamate receptors (like NMDA and AMPA) on nearby neurons. The result is a surge of calcium ions into the cells, which sets off a cascade of destructive processes: activating enzymes that degrade proteins and membranes, disrupting mitochondria, producing free radicals, and triggering cell death pathways. That’s why glutamate is the neurotransmitter most closely linked to post-stroke brain injury—the damage isn’t caused by glutamine (a precursor), but by the excess glutamate itself.

GABA, in contrast, is inhibitory and would tend to dampen neural activity rather than cause excitotoxic damage. Acetylcholine and endorphins aren’t the primary drivers of this injury mechanism in stroke.

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