Excitatory GABA Responses in Embryonic and Neonatal Cortical Slices Demonstrated by Gramicidin Perforated-Patch Recordings and Calcium Imaging
Open accessAbstract
Gramicidin perforated-patch-clamp recordings in brain slices were used to obtain an accurate assessment of the developmental change in the GABA A receptor reversal potential (EGABA A) in embryonic and early postnatal rat neocortical cells including neuroepithelial precursor cells, cortical plate neurons, and postnatal neocortical neurons. Our results demonstrate that there is a progressive negative shift in EGABA A, with the most positive values found in the youngest cortical precursor cells. At the early stages of neocortical development,EGABA Ais determined by the chloride (Cl−) gradient, and the internal chloride concentration ([Cl−]i) decreases with development.EGABA Ais positive to the resting potential, indicating that GABA serves to depolarize developing neocortical cells. Consistent with this conclusion, GABA A receptor activation with muscimol was found to increase the internal calcium concentration ([Ca 2+]i) in both embryonic and early postnatal neocortical cells through the activation of voltage-gated calcium channels (VGCCs). Postnatal cells exhibit spontaneous postsynaptic synaptic currents, which are eliminated by bicuculline methiodide (BMI) but not glutamate receptor antagonists and reverse at the Cl−equilibrium potential. Likewise, brief spontaneous increases in [Ca 2+]i, sensitive to BMI and TTX, are observed at the same ages, suggesting that endogenous synaptic GABA A receptor activation can depolarize cells and activate VGCCs. These results suggest that GABA A receptor-mediated depolarization may influence early neocortical developmental events, including neurogenesis and synaptogenesis, through the activation of Ca 2+-dependent signal transduction pathways.
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Initially being excitatory through the GABAA receptors expressed on radial glia cells and migrating interneurons, GABA plays a role in proliferation, migration and synaptogenesis.
“Initially being excitatory through the GABAA receptors expressed on radial glia cells and migrating interneurons, GABA plays a role in proliferation, migration and synaptogenesis [183–186].”
From Development of prefrontal cortex (2022) · cites this paper as [186]
The paper reports excitatory GABAA responses in immature cortical cells and, in its discussion of calcium-dependent development (page not provided), describes possible effects on proliferation and migration and a possible role in forming or strengthening synapses. It does not identify radial glia and migrating interneurons as the receptor-expressing cells in this account, and it presents the developmental roles as possibilities rather than established effects. (LLM, conf=0.88)
Experimental — accuracy not yet measuredGABA either promotes or arrests radial migration depending on cell maturity, due to developmental regulation of the chloride gradient.
“GABA either promotes or arrests radial migration dependent on cell maturity. This is due to developmental regulation of the chloride gradient”
From Hippocampal GABAergic Inhibitory Interneurons (2017) · cites this paper as [872]
This early activity is quickly replaced by synapse-driven network events in which interneurons play a key role via depolarizing actions of GABA on principal cells during early development.
“this activity is quickly replaced by synapse-driven network events in which interneurons play a key role via depolarizing actions of GABA on PCs during early development”
From Hippocampal GABAergic Inhibitory Interneurons (2017) · cites this paper as [872]
As neurons mature, the reversal potential for chloride becomes shunting/hyperpolarizing, leading to inhibitory GABAergic transmission.
“As neurons mature, the reversal potential for chloride becomes shunting/hyperpolarizing, leading to inhibitory GABAergic transmission”
From Hippocampal GABAergic Inhibitory Interneurons (2017) · cites this paper as [872]
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- Authors
- Owens, D. F., Boyce, L. H., Davis, M. B. E., & Kriegstein, A. R.
- Affiliations
- Columbia University Irving Medical Center (US)
- Venue
- The Journal of Neuroscience
- Publisher
- Society for Neuroscience
- Published
- 1996-10-15
- Volume
- 16
- Issue
- 20
- Pages
- 6414-6423
- ISSN
- 0270-6474 (ISSN-L)
- 1529-2401
- PMC
- PMC6578913
- OpenAlex
- W1705218924
- Cited by
- 721
- References
- 53
- Citations by year
- 2026: 4 · 2025: 1 · 2024: 7 · 2023: 12 · 2022: 18 · 2021: 15 · 2020: 15 · 2019: 13 · 2018: 12 · 2017: 16 · 2016: 18 · 2015: 27 · 2014: 16 · 2013: 27 · 2012: 24
- FWCI
- 9.18
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Journal of Neuroscience (publishedVersion, public-domain)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- March of Dimes Foundation
- National Institutes of Health
- National Institute of Neurological Disorders and Stroke (NS-21223, K12NS001698, NS01698, R01NS021223)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Life Sciences › Neuroscience › Cognitive Neuroscience › Neural dynamics and brain function
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Ion channel regulation and function
- Keywords
- GABAA receptor, GABA reversal potential, chloride equilibrium potential, embryonic neocortex, cortical development, muscimol, voltage-gated calcium channels, spontaneous postsynaptic currents, bicuculline methiodide, tetrodotoxin, calcium imaging, neurogenesis, synaptogenesis
- MeSH terms
- Animals, Animals, Newborn, Calcium, Cerebral Cortex, gamma-Aminobutyric Acid, Gramicidin, Muscimol, Time Factors, Rats, Sprague-Dawley, Receptors, GABA, Patch-Clamp Techniques, Rats
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