Cajal-Retzius cells in early postnatal mouse cortex selectively express functional metabotropic glutamate receptors

Authors

  • Juan Ramón Martínez-Galán,

    1. Instituto de Neurociencias, CSIC, Universidad Miguel Hernández, Campus de San Juan, Apartado 18, 03550 San Juan de Alicante, Spain
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    • *Present address: Facultad de Medicina, Universidad de Castilla-La Mancha, Edificio Benjamín Palencia, 02071 Albacete, Spain
  • Guillermina López-Bendito,

    1. Instituto de Neurociencias, CSIC, Universidad Miguel Hernández, Campus de San Juan, Apartado 18, 03550 San Juan de Alicante, Spain
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  • Rafael Luján,

    1. Instituto de Neurociencias, CSIC, Universidad Miguel Hernández, Campus de San Juan, Apartado 18, 03550 San Juan de Alicante, Spain
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    • *Present address: Facultad de Medicina, Universidad de Castilla-La Mancha, Edificio Benjamín Palencia, 02071 Albacete, Spain
  • Ryuichi Shigemoto,

    1. Laboratory of Cerebral Structure, National Institute for Physiological Sciences, Myodaiji, Okazaki 444–8585, Japan
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  • Alfonso Fairén,

    1. Instituto de Neurociencias, CSIC, Universidad Miguel Hernández, Campus de San Juan, Apartado 18, 03550 San Juan de Alicante, Spain
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  • Miguel Valdeolmillos

    1. Instituto de Neurociencias, CSIC, Universidad Miguel Hernández, Campus de San Juan, Apartado 18, 03550 San Juan de Alicante, Spain
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: Dr Miguel Valdeolmillos, as above for offprints.
E-mail: miguel.valdeolmillos@umh.es

Abstract

Glutamate receptors have been linked to the regulation of several developmental events in the CNS. By using cortical slices of early postnatal mice, we show that in layer I cells, glutamate produces intracellular calcium ([Ca2+]i) elevations mediated by ionotropic and metabotropic glutamate receptors (mGluRs). The contribution of mGluRs to these responses was demonstrated by application of tACPD, an agonist to groups I and II mGluRs, which evoked [Ca2+]i increases that could be reversibly blocked by MCPG, an antagonist to groups I and II mGluRs. In the absence of extracellular Ca2+, repetitive applications of tACPD or quisqualate, an agonist to group I mGluRs, elicited decreasing [Ca2+]i responses that were restored by refilling a thapsigargin-sensitive Ca2+ store. The use of specific group I mGluR agonists CHPG and DHPG indicated that the functional mGluR in layer I was of the mGluR1 subtype. Subtype specific antibodies confirmed the presence of mGlur1α, but not mGluR5, in Cajal-Retzius (Reelin-immunoreactive) neurons.

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