ArticleCerebral cortex (New York, N.Y. : 1991)2014
Accumulation of GABAergic neurons, causing a focal ambient GABA gradient, and downregulation of KCC2 are induced during microgyrus formation in a mouse model of polymicrogyria.
Article in Cerebral cortex (New York, N.Y. : 1991), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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13 citing papers in PubMed, 28 citations in OpenAlex.
- Synaptic Dysregulation Drives Hyperexcitability in Pyramidal Neurons Surrounding Freeze-Induced Neocortical Malformations in Rats.International journal of molecular sciences · 2025Article
- The Role of Galanin in Cerebellar Granule Cell Migration in the Early Postnatal Mouse during Normal Development and after Injury.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021Article
- Targeting the WNK-SPAK/OSR1 Pathway and Cation-Chloride Cotransporters for the Therapy of Stroke.International journal of molecular sciences · 2021Review
- Targeting CDK5 in Astrocytes Promotes Calcium Homeostasis Under Excitotoxic Conditions.Frontiers in cellular neuroscience · 2021Article
- Different exercises can modulate the differentiation/maturation of neural stem/progenitor cells after photochemically induced focal cerebral infarction.Brain and behavior · 2020Article
- Alterations of GABAergic Neuron-Associated Extracellular Matrix and Synaptic Responses inFrontiers in cellular neuroscience · 2018Article
- Ion channels, guidance molecules, intracellular signaling and transcription factors regulating nervous and vascular system development.The journal of physiological sciences : JPS · 2016Review
- Control of cortical neuronal migration by glutamate and GABA.Frontiers in cellular neuroscience · 2015Review
- Gabapentin attenuates hyperexcitability in the freeze-lesion model of developmental cortical malformation.Neurobiology of disease · 2014Article
- Excitatory and inhibitory synaptic connectivity to layer V fast-spiking interneurons in the freeze lesion model of cortical microgyria.Journal of neurophysiology · 2014Article
- Early susceptibility for epileptiform activity in malformed cortex.Epilepsy research · 2014Article
- Roles of taurine-mediated tonic GABAA receptor activation in the radial migration of neurons in the fetal mouse cerebral cortex.Frontiers in cellular neuroscience · 2014Article
- Pathophysiological power of improper tonic GABA(A) conductances in mature and immature models.Frontiers in neural circuits · 2013Review
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8 authors at 4 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Although focal cortical malformations are considered neuronal migration disorders, their formation mechanisms remain unknown. We addressed how the γ-aminobutyric acid (GABA)ergic system affects the GABAergic and glutamatergic neuronal migration underlying such malformations. A focal freeze-lesion (FFL) of the postnatal day zero (P0) glutamic acid decarboxylase-green fluorescent protein knock-in mouse neocortex produced a 3- or 4-layered microgyrus at P7. GABAergic interneurons accumulated around the necrosis including the superficial region during microgyrus formation at P4, whereas E17.5-born, Cux1-positive pyramidal neurons outlined the GABAergic neurons and were absent from the superficial layer, forming cell-dense areas in layer 2 of the P7 microgyrus. GABA imaging showed that an extracellular GABA level temporally increased in the GABAergic neuron-positive area, including the necrotic center, at P4. The expression of the Cl(-) transporter KCC2 was downregulated in the microgyrus-forming GABAergic and E17.5-born glutamatergic neurons at P4; these cells may need a high intracellular Cl(-) concentration to induce depolarizing GABA effects. Bicuculline decreased the frequency of spontaneous Ca(2+) oscillations in these microgyrus-forming cells. Thus, neonatal FFL causes specific neuronal accumulation, preceded by an increase in ambient GABA during microgyrus formation. This GABA increase induces GABAA receptor-mediated Ca(2+) oscillation in KCC2-downregulated microgyrus-forming cells, as seen in migrating cells during early neocortical development.
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