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The cerebral cortex contains 2 types of neurons: principal (mostly pyramidal) neurons, which constitute approximately 80% of the total population, and local interneurons, which constitute approximately 20% of the total population, with some species variation. Pyramidal cells are excitatory glutamatergic neurons that participate in cortico-cortical connections or project to subcortical areas. Local interneurons utilize γ-aminobutyric acid (GABA) as their primary neurotransmitter and participate in local circuits in the cerebral cortex. Normal sensory perception, attention, and planning and execution of behaviors depend on interactions among canonical neocortical circuits involving excitatory and inhibitory neurons. Cortical interneurons have a fundamental role in shaping cortical circuits and controlling neocortical network interactions. These interneurons form functionally distinct networks that are temporally coordinated by electrical coupling via gap junctions and establish GABAergic synapses not only with pyramidal neurons but also among each other. Via these interactions, GABAergic interneurons control the timing of pyramidal cell firing, generation of cortical rhythms, organization of sensory fields, and cortical plasticity. Impaired activity of neocortical inhibitory interneurons has been associated with several neurologic and psychiatric disorders, including epilepsy, mental retardation, schizophrenia, and autism. There are many comprehensive reviews on GABAergic interneuron heterogeneity, development, plasticity, function in shaping cortical activity, and involvement in disease.1–13
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- © 2013 American Academy of Neurology
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