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Lovastatin Corrects Excess Protein Synthesis and Prevents Epileptogenesis in a Mouse Model of Fragile X Syndrome
It is discovered that lovastatin, a drug that is widely prescribed for the treatment of high cholesterol, can correct excess hippocampalprotein synthesis in the mouse model of FXS and can prevent one of the robust functional consequences of increased protein synthesis in FXS, epileptogenesis. Expand
Prolonged Epileptiform Discharges Induced by Altered Group I Metabotropic Glutamate Receptor-Mediated Synaptic Responses in Hippocampal Slices of a Fragile X Mouse Model
- S. Chuang, Wangfa Zhao, R. Bauchwitz, Q. Yan, R. Bianchi, R. Wong
- Biology, Medicine
- The Journal of Neuroscience
- 31 August 2005
The results suggest that FMRP plays a key role in the control of signaling at the recurrent glutamatergic synapses in the hippocampus, and the absence of this control causes the synaptically activated group I mGluRs to elicit translation-dependent epileptogenic activities. Expand
Genetic dissection of theta rhythm heterogeneity in mice.
- Jong-Seung Shin, Daesoo Kim, R. Bianchi, R. Wong, Hee-Sup Shin
- Biology, Medicine
- Proceedings of the National Academy of Sciences…
- 13 December 2005
It is shown that mice harboring a PLC-beta1(-/-) mutation lack one subset of theta rhythms normally observed during urethane anesthesia, alert immobility, and passive whole-body rotation, while the other subset observed during walking or running was intact in these mutants. Expand
BC1 Regulation of Metabotropic Glutamate Receptor-Mediated Neuronal Excitability
It is reported that neuronal BC1 RNA plays an instrumental role in the protein-synthesis-dependent implementation of neuronal excitation–repression equilibria and the significance of small RNA control in neuronal plasticity is highlighted. Expand
Group I metabotropic glutamate receptor‐dependent TRPC channel trafficking in hippocampal neurons
- M. Wang, R. Bianchi, S. Chuang, Wangfa Zhao, R. Wong
- Biology, Medicine
- Journal of neurochemistry
- 1 April 2007
The results suggest that TRPC channels are involved in generating DHPG‐induced prolonged epileptiform discharges, which is associated with a neuronal activity‐ and PLCβ1‐dependent translocation of TRPC4 and TRPC5 proteins from the plasmalemma to the cytoplasmic compartment. Expand
Group I mGluR activation causes voltage-dependent and -independent Ca2+ rises in hippocampal pyramidal cells.
Activation of group I mGluRs produced a biphasic accumulation of [Ca2+]i via two paths: a transient release from intracellular stores, and subsequently, by influx through voltage-gated Ca2+ channels. Expand
Receptor protein tyrosine phosphatase α is essential for hippocampal neuronal migration and long‐term potentiation
It is reported that absence of RPTPα compromises correct positioning of pyramidal neurons during development of mouse hippocampus, and is identified as a novel member of the functional class of genes that control radial neuronal migration. Expand
Excitatory synaptic potentials dependent on metabotropic glutamate receptor activation in guinea‐pig hippocampal pyramidal cells.
The results suggest that the long burst‐associated depolarizations are synaptic potentials dependent on mGluR activation and may also be involved in the generation of synchronized long bursts in the CA3 region. Expand
Role of synaptic metabotropic glutamate receptors in epileptiform discharges in hippocampal slices.
- Angela Lee, R. Wong, S. Chuang, Hee-Sup Shin, R. Bianchi
- Chemistry, Medicine
- Journal of neurophysiology
- 1 October 2002
The results suggest that mGluR1 and mGlamR5 are activated synaptically during prolonged epileptiform discharges induced by bicuculline and 4-AP and indicate that the synaptic effects of the group I mGLURs on the duration of epilepsy discharges were mediated by a PLCbeta1-independent mechanism. Expand
Signaling mechanisms underlying group I mGluR-induced persistent AHP suppression in CA3 hippocampal neurons.
It is shown that persistent AHP suppression differs from short-term, transient suppression in that distinct and additional signaling processes are required to render the suppression persistent. Expand