Intermediate zone cells express calcium-permeable AMPA receptors and establish close contact with growing axons.
Recent studies have shown that cells in the intermediate zone (IZ) of the embryonic neocortex originate in the basal telencephalon and migrate tangentially in the cortical wall (;; ). We had previously observed growing cortical axons closely apposed to calbindin-positive, tangentially oriented cells in the IZ (), and it has been shown that neurites in the IZ express a glutamate transporter (). To test if glutamate released by corticofugal growth cones could influence the tangential IZ cells, we characterized the glutamate receptors expressed by IZ cells using patch-clamp techniques, histochemical labeling, and immunostaining on slices of embryonic mice forebrain. We show that tangential IZ cells express inwardly rectifying kainate responses, but not NMDA responses, and accumulate cobalt after AMPA receptor activation. We conclude that IZ cells express calcium-permeable AMPA receptors. This property correlates with our observation that the GluR2 subunit is not expressed in the IZ. AMPA receptors are activated by a millimolar concentration of glutamate. To know whether this high level of glutamate could occur at the surface of IZ cells, we examined contacts made by corticofugal growth cones and calbindin-positive IZ cells using electron microscopy. We show vesicle-containing neurites tightly apposed to calbindin-positive IZ cells over remarkably long length. This suggests that glutamate released by growing corticofugal axons could reach high concentrations close to AMPA receptors of tangential IZ cells and efficiently activate them to control the intracellular calcium in embryonic IZ cells.
Métin
C
C
Equipe Régionalisation Nerveuse, Centre National de la Recherche Scientifique (CNRS) Unité Mixte de Recherche 8542, Niveau 8, Ecole Normale Supérieure, 75230 Paris Cédex 05, France. metin@biologie.ens.fr
Denizot
J P
JP
Ropert
N
N
D000200:Action Potentials / Q000187:drug effects / Q000502:physiology; D000818:Animals; D001369:Axons / Q000187:drug effects / Q000502:physiology* / Q000648:ultrastructure; D001569:Benzodiazepines / Q000494:pharmacology; D001692:Biological Transport / Q000187:drug effects; D064026:Calbindins; D002118:Calcium / Q000378:metabolism*; D002540:Cerebral Cortex / Q000166:cytology / Q000502:physiology; D003035:Cobalt / Q000493:pharmacokinetics / Q000494:pharmacology; D018691:Excitatory Amino Acid Antagonists / Q000494:pharmacology; D005865:Gestational Age; D066298:In Vitro Techniques; D007608:Kainic Acid / Q000494:pharmacology; D051379:Mice; D008810:Mice, Inbred C57BL; D008815:Mice, Inbred Strains; D016202:N-Methylaspartate / Q000494:pharmacology; D016501:Neurites / Q000502:physiology / Q000648:ultrastructure; D009474:Neurons / Q000166:cytology / Q000187:drug effects / Q000502:physiology*; D016548:Prosencephalon / Q000166:cytology / Q000196:embryology / Q000502:physiology*; D011810:Quinoxalines / Q000494:pharmacology; D018091:Receptors, AMPA / Q000378:metabolism*; D064030:S100 Calcium Binding Protein G / Q000032:analysis; D013779:Tetrodotoxin / Q000494:pharmacology; D005680:gamma-Aminobutyric Acid / Q000494:pharmacology
D064026:Calbindins; D018691:Excitatory Amino Acid Antagonists; D011810:Quinoxalines; D018091:Receptors, AMPA; D064030:S100 Calcium Binding Protein G; D001569:Benzodiazepines; D003035:Cobalt; D013779:Tetrodotoxin; D005680:gamma-Aminobutyric Acid; C056723:FG 9041; D016202:N-Methylaspartate; C118651:GYKI 53784; D007608:Kainic Acid; D002118:Calcium