GABAergic interneurons play a key role in the formation and tuning of network oscillations in the cerebral cortex and hippocampus, and have been implicated in the pathophysiology of neurodevelopmental disorders, such as schizophrenia, autism spectrum disorders, and several types of encephalopathic epilepsies. The interneurons shape diverse aspects of cortical and hippocampal circuit maturation and regulate information processing in mature circuits by maintaining appropriate excitation-inhibition (E-I) balance. The two major populations of GABAergic interneurons originate from the medial and caudal portions of the ganglionic eminence (MGE and CGE), respectively. MGE-derived interneurons include parvalbumin-positive (PV+) and somatostatin-positive (SSt+) interneurons, which account for approximately 40 and 30% of the overall number of GABAergic interneurons. In addition, approximately half of all hippocampal neuroglia form-type cells (NGFCs), including the Ivy cells, originate from the MGE. CGE-derived interneurons (such as, VIP+, CCK+, and reelin+ interneurons) are characterized by the expression of 5-HT3 serotonin receptors. PV+ and SSt+ interneurons are dysfunctional in schizophrenia and stress-related disorders, respectively. In addition, interneurons are targeted by medications in psychiatric disorders. For example, (S)-ketamine, a drug recently approved for the treatment of depression, inhibits PV+ interneurons acting as a slow NMDA channel blocker, and the antidepressant vortioxetine inhibits CGE-derived interneurons as a result of 5-HT3 blockade.
Cortical and hippocampal interneurons, have distinct molecular, anatomical, and physiological properties. However, the molecular mechanisms regulating their maturation are only partially elucidated. Unravelling these mechanisms might disclose the nature of the developmental trajectory of the cerebral cortex and hippocampus in the postnatal life and pave the way to novel treatments for neurodevelopmental disorders
It is the right time for a Research Topic addressing the mechanisms regulating interneuron maturation and function during postnatal development, placing emphasis on how neurotransmitters and trophic factors shape the activity of the different types of interneurons and how this regulation might have an impact on the pathophysiology of neurologic and psychiatric disorders
We would like to receive research articles and reviews.
GABAergic interneurons play a key role in the formation and tuning of network oscillations in the cerebral cortex and hippocampus, and have been implicated in the pathophysiology of neurodevelopmental disorders, such as schizophrenia, autism spectrum disorders, and several types of encephalopathic epilepsies. The interneurons shape diverse aspects of cortical and hippocampal circuit maturation and regulate information processing in mature circuits by maintaining appropriate excitation-inhibition (E-I) balance. The two major populations of GABAergic interneurons originate from the medial and caudal portions of the ganglionic eminence (MGE and CGE), respectively. MGE-derived interneurons include parvalbumin-positive (PV+) and somatostatin-positive (SSt+) interneurons, which account for approximately 40 and 30% of the overall number of GABAergic interneurons. In addition, approximately half of all hippocampal neuroglia form-type cells (NGFCs), including the Ivy cells, originate from the MGE. CGE-derived interneurons (such as, VIP+, CCK+, and reelin+ interneurons) are characterized by the expression of 5-HT3 serotonin receptors. PV+ and SSt+ interneurons are dysfunctional in schizophrenia and stress-related disorders, respectively. In addition, interneurons are targeted by medications in psychiatric disorders. For example, (S)-ketamine, a drug recently approved for the treatment of depression, inhibits PV+ interneurons acting as a slow NMDA channel blocker, and the antidepressant vortioxetine inhibits CGE-derived interneurons as a result of 5-HT3 blockade.
Cortical and hippocampal interneurons, have distinct molecular, anatomical, and physiological properties. However, the molecular mechanisms regulating their maturation are only partially elucidated. Unravelling these mechanisms might disclose the nature of the developmental trajectory of the cerebral cortex and hippocampus in the postnatal life and pave the way to novel treatments for neurodevelopmental disorders
It is the right time for a Research Topic addressing the mechanisms regulating interneuron maturation and function during postnatal development, placing emphasis on how neurotransmitters and trophic factors shape the activity of the different types of interneurons and how this regulation might have an impact on the pathophysiology of neurologic and psychiatric disorders
We would like to receive research articles and reviews.
