RT Journal Article
SR Electronic
T1 Plasticity of the GABAergic Phenotype of the “Glutamatergic” Granule Cells of the Rat Dentate Gyrus
JF The Journal of Neuroscience
JO J. Neurosci.
FD Society for Neuroscience
SP 5594
OP 5598
DO 10.1523/JNEUROSCI.23-13-05594.2003
VO 23
IS 13
A1 Rafael Gutiérrez
A1 Héctor Romo-Parra
A1 Jasmín Maqueda
A1 Carmen Vivar
A1 Mónica Ramìrez
A1 Miguel A. Morales
A1 Mónica Lamas
YR 2003
UL http://www.jneurosci.org/content/23/13/5594.abstract
AB The “glutamatergic” granule cells of the dentate gyrus transiently express a GABAergic phenotype when a state of hyperexcitability is induced in the adult rat. Consequently, granule cell (GC) activation provokes monosynaptic GABAergic responses in their targets of area CA3. Because GABA exerts a trophic action on neonatal CA3 and mossy fibers (MF) constitute its main input, we hypothesized that the GABAergic phenotype of the MF could also be transiently expressed early in life. We addressed this possibility with a multidisciplinary approach. Electrophysiological recordings in developing rats revealed that, until day 22–23 of age, glutamate receptor antagonists block the excitatory response evoked in pyramidal cells by GCs, isolating a fast metabotropic glutamate receptor-sensitive GABAergic response. In a clear-cut manner from day 23–24 of age, GC activation in the presence of glutamatergic antagonists was unable to evoke synaptic responses in CA3. Immunohistological experiments showed the presence of GABA and GAD67 (glutamate decarboxylase 67 kDa isoform) in the developing GCs and their MF, and, using reverse transcription-PCR, we confirmed the expression of vesicular GABA transporter mRNA in the developing dentate gyrus and its downregulation in the adult. The GABAergic markers were upregulated and MF inhibitory transmission reappeared when hyperexcitability was induced in adult rats. Our data evidence for the first time a developmental and activity-dependent regulation of the complex phenotype of the GC. At early ages, the GABAergic input from the MF may add to the interneuronal input to CA3 to foster development, and, in the adult, it can possibly protect the system from enhanced excitability.