Which neurotransmitter is inhibitory throughout the CNS, most active in the striatum, hypothalamus, spinal cord, and temporal lobe; deficiency is linked to Huntington's disease, stiff-person syndrome, and antiseizure medications can increase it?

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Multiple Choice

Which neurotransmitter is inhibitory throughout the CNS, most active in the striatum, hypothalamus, spinal cord, and temporal lobe; deficiency is linked to Huntington's disease, stiff-person syndrome, and antiseizure medications can increase it?

GABA is the brain’s main inhibitory transmitter, reducing neuronal excitability by acting on GABA_A and GABA_B receptors to hyperpolarize neurons. It is especially important in areas like the striatum, hypothalamus, spinal cord, and temporal lobe, where it helps regulate movement, autonomic functions, and overall network stability. When GABAergic signaling is diminished in the striatum, as occurs in Huntington’s disease, the loss of inhibition in basal ganglia circuits contributes to the characteristic involuntary movements. In stiff-person syndrome, autoantibodies against the enzyme that synthesizes GABA (glutamic acid decarboxylase) lower GABA levels, leading to rigidity and spasms. Many antiseizure drugs work by increasing GABAergic activity—benzodiazepines and barbiturates enhance GABA_A receptor action, valproic acid boosts GABA synthesis, and GABA transaminase inhibitors raise GABA levels—thereby enhancing inhibitory tone to reduce hyperexcitability. This combination of widespread inhibitory function, specific involvement of the striatum and related regions, and the links to Huntington’s, stiff-person syndrome, and antiseizure medications all point to GABA as the correct neurotransmitter.

GABA is the brain’s main inhibitory transmitter, reducing neuronal excitability by acting on GABA_A and GABA_B receptors to hyperpolarize neurons. It is especially important in areas like the striatum, hypothalamus, spinal cord, and temporal lobe, where it helps regulate movement, autonomic functions, and overall network stability. When GABAergic signaling is diminished in the striatum, as occurs in Huntington’s disease, the loss of inhibition in basal ganglia circuits contributes to the characteristic involuntary movements. In stiff-person syndrome, autoantibodies against the enzyme that synthesizes GABA (glutamic acid decarboxylase) lower GABA levels, leading to rigidity and spasms. Many antiseizure drugs work by increasing GABAergic activity—benzodiazepines and barbiturates enhance GABA_A receptor action, valproic acid boosts GABA synthesis, and GABA transaminase inhibitors raise GABA levels—thereby enhancing inhibitory tone to reduce hyperexcitability. This combination of widespread inhibitory function, specific involvement of the striatum and related regions, and the links to Huntington’s, stiff-person syndrome, and antiseizure medications all point to GABA as the correct neurotransmitter.

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