The article by Benes and Berretta discusses the role of GABAergic interneurons in the corticolimbic circuitry and their implications for understanding schizophrenia and bipolar disorder. GABAergic interneurons, which are crucial for modulating cortical and hippocampal circuits, exhibit various subtypes defined by their morphological, synaptic, and electrophysiological properties. These interneurons play essential roles in generating oscillatory rhythms, discriminative information processing, and gating sensory information. Recent postmortem studies have provided evidence that defects in GABAergic neurotransmission may contribute to both schizophrenia and bipolar disorder, possibly through disturbances in early development and the formation of normal lamination. The basolateral nucleus of the amygdala is proposed to contribute to these abnormalities through increased excitatory activity. Research using partial modeling has induced changes in the GABA system similar to those seen in these disorders in the rat hippocampus. Future investigations into the GABA system in rodent, primate, and human brains, as well as the characterization of specific phenotypic subclasses of interneurons, are expected to provide new insights into the integration of this transmitter system in neuropsychiatric diseases.The article by Benes and Berretta discusses the role of GABAergic interneurons in the corticolimbic circuitry and their implications for understanding schizophrenia and bipolar disorder. GABAergic interneurons, which are crucial for modulating cortical and hippocampal circuits, exhibit various subtypes defined by their morphological, synaptic, and electrophysiological properties. These interneurons play essential roles in generating oscillatory rhythms, discriminative information processing, and gating sensory information. Recent postmortem studies have provided evidence that defects in GABAergic neurotransmission may contribute to both schizophrenia and bipolar disorder, possibly through disturbances in early development and the formation of normal lamination. The basolateral nucleus of the amygdala is proposed to contribute to these abnormalities through increased excitatory activity. Research using partial modeling has induced changes in the GABA system similar to those seen in these disorders in the rat hippocampus. Future investigations into the GABA system in rodent, primate, and human brains, as well as the characterization of specific phenotypic subclasses of interneurons, are expected to provide new insights into the integration of this transmitter system in neuropsychiatric diseases.