GABAergic interneurons are crucial components of corticolimbic circuits, playing roles in inhibitory and disinhibitory modulation of cortical and hippocampal circuits, and in generating oscillatory rhythms, information processing, and sensory information gating. Abnormalities in these functions are associated with schizophrenia and bipolar disorder. Postmortem studies suggest that GABAergic neurotransmission defects may contribute to these disorders, possibly due to developmental disruptions affecting cell migration and lamination. The mesocortical dopamine projections may trigger GABA system defects, especially under stress. The basolateral nucleus of the amygdala may contribute to these abnormalities through increased excitatory activity. In rat hippocampus, changes in the GABA system similar to those in schizophrenia and bipolar disorder have been induced using partial modeling. Continued research on the GABA system in rodents, primates, and humans, along with characterization of interneuron phenotypic subclasses in these disorders, will provide new insights into how the GABA system integrates in neuropsychiatric disease. GABAergic interneurons in the cortex and hippocampus have distinct morphological, neurochemical, and electrophysiological properties. They include basket cells, chandelier cells, double bouquet cells, and axon tuft cells, each with specific synaptic connections and roles in modulating neuronal activity. Neurochemical markers such as GAD, parvalbumin, calbindin D28k, calretinin, and somatostatin help identify these subtypes. GABAergic interneurons receive intrinsic and extrinsic excitatory inputs, as well as inhibitory inputs from other interneurons. These inputs are crucial for regulating neuronal activity and network oscillations, which are essential for cognitive functions. Dysfunction in GABAergic systems has been linked to schizophrenia, with postmortem studies showing reduced densities of nonpyramidal neurons in the anterior cingulate cortex and hippocampus. These findings suggest that GABAergic dysfunction may contribute to the pathophysiology of schizophrenia and bipolar disorder. Further research is needed to understand the precise mechanisms and potential therapeutic targets.GABAergic interneurons are crucial components of corticolimbic circuits, playing roles in inhibitory and disinhibitory modulation of cortical and hippocampal circuits, and in generating oscillatory rhythms, information processing, and sensory information gating. Abnormalities in these functions are associated with schizophrenia and bipolar disorder. Postmortem studies suggest that GABAergic neurotransmission defects may contribute to these disorders, possibly due to developmental disruptions affecting cell migration and lamination. The mesocortical dopamine projections may trigger GABA system defects, especially under stress. The basolateral nucleus of the amygdala may contribute to these abnormalities through increased excitatory activity. In rat hippocampus, changes in the GABA system similar to those in schizophrenia and bipolar disorder have been induced using partial modeling. Continued research on the GABA system in rodents, primates, and humans, along with characterization of interneuron phenotypic subclasses in these disorders, will provide new insights into how the GABA system integrates in neuropsychiatric disease. GABAergic interneurons in the cortex and hippocampus have distinct morphological, neurochemical, and electrophysiological properties. They include basket cells, chandelier cells, double bouquet cells, and axon tuft cells, each with specific synaptic connections and roles in modulating neuronal activity. Neurochemical markers such as GAD, parvalbumin, calbindin D28k, calretinin, and somatostatin help identify these subtypes. GABAergic interneurons receive intrinsic and extrinsic excitatory inputs, as well as inhibitory inputs from other interneurons. These inputs are crucial for regulating neuronal activity and network oscillations, which are essential for cognitive functions. Dysfunction in GABAergic systems has been linked to schizophrenia, with postmortem studies showing reduced densities of nonpyramidal neurons in the anterior cingulate cortex and hippocampus. These findings suggest that GABAergic dysfunction may contribute to the pathophysiology of schizophrenia and bipolar disorder. Further research is needed to understand the precise mechanisms and potential therapeutic targets.