The Journal of Neuroscience, May 31, 2006, ():
Glutamate Acting on AMPA But Not NMDA Receptors Modulates the Migration of Hippocampal Interneurons
J. Neurosci. Manent et al.
26: 5901
Supplemental data
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Figure S1. Proliferation and cell survival.
A) Histogram illustrating (± standard deviation) the density of BrdU+ cells (cells per surface unit) in the lateral ganglionic eminence (LGE) after 2 hours in vitro without any treatment control condition (CTRL) or in the presence of antagonists of GABAA 50µM bicuculline (BICU), NMDA (10 µM MK801) and AMPA (30 µM CNQX) receptors.
B) Histogram illustrating (± standard deviation) the number of PI+ cells per field in the hippocampal primordium after 1DIV and 3DIV without any treatment control condition (CTRL) or in the presence of antagonists of GABAA 50µM bicuculline (BICU), NMDA (10 µM MK801) and AMPA (30 µM CNQX) receptors.
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Figure S2. Proposed model for reciprocal interactions between glutamatergic and GABAergic neurons in the developing embryonic hippocampus.
Pioneer glutamatergic neurons (in blue) are present in the hippocampal primordium before the arrival of GABAergic interneurons (by E14, A). They likely release glutamate that exert a positive influence on the migration of interneurons (in red) via the activation of AMPA receptors. Cajal-Retzius cells (in green) located along the migratory pathway to the hippocampal primordium would also release glutamate, influencing interneuronal migration. Once interneurons have entered the hippocampal plate (by E15, A), they likely release GABA, facilitating the migration of glutamatergic neuroblasts via the activation of GABAA receptors, with the cooperation of glutamate acting on NMDA receptors. More glutamatergic cells reach then the hippocampal plate, which in turn will help the migration of more interneurons. This model (B) proposes a positive cooperation between the two neuronal subtypes.
