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Cajal–Retzius cells switch from expressing γ-less to γ-containing GABAA receptors during corticogenesis

Authors

  • Qing Cheng,

    1. Department of Physiology, Dartmouth Medical School, Dartmouth-Hitchcock Medical Center, One Medical Center Drive, Lebanon, NH 03756, USA Department of Neurobiology, Duke University Medical Center, Durham, NC 27710, USA
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  • Pamela W. L. Yeh,

    1. Department of Physiology, Dartmouth Medical School, Dartmouth-Hitchcock Medical Center, One Medical Center Drive, Lebanon, NH 03756, USA Department of Neurobiology, Duke University Medical Center, Durham, NC 27710, USA
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  • Hermes H. Yeh

    1. Department of Physiology, Dartmouth Medical School, Dartmouth-Hitchcock Medical Center, One Medical Center Drive, Lebanon, NH 03756, USA Department of Neurobiology, Duke University Medical Center, Durham, NC 27710, USA
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Dr Hermes H. Yeh, as above.
E-mail: hermes.yeh@dartmouth.edu

Abstract

Cajal–Retzius cells are implicated in regulating neuronal migration and lamination during corticogenesis. In rodents, Cajal–Retzius cells are transient, being prevalent in the marginal zone of the embryonic neocortex and declining over the first two postnatal weeks. While studies have examined in postnatal neocortex the properties of GABAA receptors in Cajal–Retzius cells, less is known about their disposition at embryonic stages. Here, we combined patch-clamp electrophysiology and single-cell mRNA profiling to probe the expression of GABAA receptors in Cajal–Retzius cells. In embryonic neocortical slices, GABA elicited GABAA receptor-mediated current responses that were diazepam-insensitive and inhibited by Zn2+, a pharmacological profile consistent with expression of γ-less GABAA receptor isoforms. Non-Cajal–Retzius cells in the same embryonic slices, on the other hand, were robustly potentiated by diazepam and were insensitive to Zn2+, typical of γ-containing GABAA receptor isoforms, as were Cajal–Retzius cells in the postnatal neocortex. Single-cell mRNA profiling and immunohistochemistry confirmed expression of GABAA receptor γ subunit transcript and protein, respectively, in individual reelin-expressing cells in the postnatal cortex but not in their embryonic counterparts. We conclude that Cajal–Retzius cells express γ-less GABAA receptors at embryonic stages and switch to expressing γ-containing GABAA receptor isoforms during postnatal neocortical development.

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