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  • 1
    Online Resource
    Online Resource
    Prolonged Epileptiform Discharges Induced by Altered Group I Metabotropic Glutamate Receptor-Mediated Synaptic Responses in Hippocampal Slices of a Fragile X Mouse Model
    Society for Neuroscience ; 2005
    In:  The Journal of Neuroscience Vol. 25, No. 35 ( 2005-08-31), p. 8048-8055
    Details
    In: The Journal of Neuroscience, Society for Neuroscience, Vol. 25, No. 35 ( 2005-08-31), p. 8048-8055
    Abstract: Mutations in FMR1 , which encodes the fragile X mental retardation protein (FMRP), are the cause of fragile X syndrome (FXS), an X-linked mental retardation disorder. Inactivation of the mouse gene Fmr1 confers a number of FXS-like phenotypes including an enhanced susceptibility to epileptogenesis during development. We find that in a FXS mouse model, in which the function of FMRP is suppressed, synaptically released glutamate induced prolonged epileptiform discharges resulting from enhanced group I metabotropic glutamate receptor (mGluR)-mediated responses in hippocampal slices. The induction of the group I mGluR-mediated, prolonged epileptiform discharges was inhibited in preparations that were pretreated with inhibitors of ERK1/2 (extracellular signal-regulated kinase 1/2) phosphorylation or of mRNA translation, and their maintenance was suppressed by group I mGluR antagonists. The results suggest that FMRP plays a key role in the control of signaling at the recurrent glutamatergic synapses in the hippocampus. The absence of this control causes the synaptically activated group I mGluRs to elicit translation-dependent epileptogenic activities.
    Type of Medium: Online Resource
    ISSN: 0270-6474 , 1529-2401
    URL: Article
    DOI: 10.1523/JNEUROSCI.1777-05.2005
    Language: English
    Publisher: Society for Neuroscience
    Publication Date: 2005
    detail.hit.zdb_id: 1475274-8
    SSG: 12
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  • 2
    Online Resource
    Online Resource
    BC RNA Mislocalization in the Fragile X Premutation
    Society for Neuroscience ; 2018
    In:  eneuro Vol. 5, No. 2 ( 2018-03), p. ENEURO.0091-18.2018-
    Details
    In: eneuro, Society for Neuroscience, Vol. 5, No. 2 ( 2018-03), p. ENEURO.0091-18.2018-
    Abstract: Fragile X premutation disorder is caused by CGG triplet repeat expansions in the 5′ untranslated region of FMR1 mRNA. The question of how expanded CGG repeats cause disease is a subject of continuing debate. Our work indicates that CGG-repeat structures compete with regulatory BC1 RNA for access to RNA transport factor hnRNP A2. As a result, BC1 RNA is mislocalized in vivo, as its synapto-dendritic presence is severely diminished in brains of CGG-repeat knock-in animals (a premutation mouse model). Lack of BC1 RNA is known to cause seizure activity and cognitive dysfunction. Our working hypothesis thus predicted that absence, or significantly reduced presence, of BC1 RNA in synapto-dendritic domains of premutation animal neurons would engender cognate phenotypic alterations. Testing this prediction, we established epileptogenic susceptibility and cognitive impairments as major phenotypic abnormalities of CGG premutation mice. In CA3 hippocampal neurons of such animals, synaptic release of glutamate elicits neuronal hyperexcitability in the form of group I metabotropic glutamate receptor–dependent prolonged epileptiform discharges. CGG-repeat knock-in animals are susceptible to sound-induced seizures and are cognitively impaired as revealed in the Attentional Set Shift Task. These phenotypic disturbances occur in young-adult premutation animals, indicating that a neurodevelopmental deficit is an early-initial manifestation of the disorder. The data are consistent with the notion that RNA mislocalization can contribute to pathogenesis.
    Type of Medium: Online Resource
    ISSN: 2373-2822
    URL: Article
    DOI: 10.1523/ENEURO.0091-18.2018
    Language: English
    Publisher: Society for Neuroscience
    Publication Date: 2018
    detail.hit.zdb_id: 2800598-3
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  • 3
    Online Resource
    Online Resource
    Neuronal Network Excitability in Alzheimer’s Disease: The Puzzle of Similar versus Divergent Roles of Amyloid β and Tau
    Society for Neuroscience ; 2021
    In:  eneuro Vol. 8, No. 2 ( 2021-03), p. ENEURO.0418-20.2020-
    Details
    In: eneuro, Society for Neuroscience, Vol. 8, No. 2 ( 2021-03), p. ENEURO.0418-20.2020-
    Abstract: Alzheimer’s disease (AD) is the most frequent neurodegenerative disorder that commonly causes dementia in the elderly. Recent evidence indicates that network abnormalities, including hypersynchrony, altered oscillatory rhythmic activity, interneuron dysfunction, and synaptic depression, may be key mediators of cognitive decline in AD. In this review, we discuss characteristics of neuronal network excitability in AD, and the role of Aβ and tau in the induction of network hyperexcitability. Many patients harboring genetic mutations that lead to increased Aβ production suffer from seizures and epilepsy before the development of plaques. Similarly, pathologic accumulation of hyperphosphorylated tau has been associated with hyperexcitability in the hippocampus. We present common and divergent roles of tau and Aβ on neuronal hyperexcitability in AD, and hypotheses that could serve as a template for future experiments.
    Type of Medium: Online Resource
    ISSN: 2373-2822
    URL: Article
    DOI: 10.1523/ENEURO.0418-20.2020
    Language: English
    Publisher: Society for Neuroscience
    Publication Date: 2021
    detail.hit.zdb_id: 2800598-3
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  • 4
    Online Resource
    Online Resource
    Cellular Mechanism of Neuronal Synchronization in Epilepsy
    American Association for the Advancement of Science (AAAS) ; 1982
    In:  Science Vol. 216, No. 4547 ( 1982-05-14), p. 745-747
    Details
    In: Science, American Association for the Advancement of Science (AAAS), Vol. 216, No. 4547 ( 1982-05-14), p. 745-747
    Type of Medium: Online Resource
    ISSN: 0036-8075 , 1095-9203
    URL: Article
    DOI: 10.1126/science.7079735
    RVK:
    TA 1000
    RVK:
    WA 15000
    Language: English
    Publisher: American Association for the Advancement of Science (AAAS)
    Publication Date: 1982
    detail.hit.zdb_id: 128410-1
    detail.hit.zdb_id: 2066996-3
    detail.hit.zdb_id: 2060783-0
    SSG: 11
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  • 5
    Online Resource
    Online Resource
    Latent synaptic pathways revealed after tetanic stimulation in the hippocampus
    Springer Science and Business Media LLC ; 1987
    In:  Nature Vol. 329, No. 6141 ( 1987-10), p. 724-726
    Details
    In: Nature, Springer Science and Business Media LLC, Vol. 329, No. 6141 ( 1987-10), p. 724-726
    Type of Medium: Online Resource
    ISSN: 0028-0836 , 1476-4687
    URL: Article
    DOI: 10.1038/329724a0
    RVK:
    TA 1000
    RVK:
    UA 1000
    RVK:
    WA 15000
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 1987
    detail.hit.zdb_id: 120714-3
    detail.hit.zdb_id: 1413423-8
    SSG: 11
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    Online Resource
  • 6
    Online Resource
    Online Resource
    Dual Regulation of Fragile X Mental Retardation Protein by Group I Metabotropic Glutamate Receptors Controls Translation-Dependent Epileptogenesis in the Hippocampus
    Society for Neuroscience ; 2011
    In:  The Journal of Neuroscience Vol. 31, No. 2 ( 2011-01-12), p. 725-734
    Details
    In: The Journal of Neuroscience, Society for Neuroscience, Vol. 31, No. 2 ( 2011-01-12), p. 725-734
    Abstract: Group I metabotropic glutamate receptors (mGluRs) stimulation activates translation-dependent epileptogenesis in the hippocampus. This translation is regulated by repressors, including BC1 RNA and fragile X mental retardation protein (FMRP). Recent data indicate that group I mGluR stimulation exerts bidirectional control over FMRP level by activating translation and ubiquitin-proteasome system (UPS)-dependent proteolysis for the up- and downregulation of the protein, respectively. At present, the temporal relationship of translation and proteolysis on FMRP and their interplay for group I mGluR-mediated translation and epileptogenesis are unknown. We addressed these issues by using mouse hippocampal slices. Agonist [( S )-3,5-dihydroxyphenylglycine (DHPG)] stimulation of group I mGluRs caused a biphasic change in FMRP level. An initial decrease (within 10 min) was followed by an increase at 30 min. When slices were pretreated with translation inhibitor (anisomycin or cycloheximide), group I mGluRs elicited a sustained decrease in FMRP. This decrease was prevented by a proteasome inhibitor [Z-Leu-Leu-Leu-CHO (MG-132)] . When slices were pretreated with MG-132 alone, DHPG no longer elicited any change in FMRP. MG-132 also suppressed increase in other proteins, including postsynaptic density-95and α-calcium/calmodulin-dependent protein kinase II, normally elicited by group I mGluR stimulation. Physiological experiments showed that proteasome inhibitor suppressed group I mGluR-induced prolonged synchronized discharges. However, proteasome inhibitor did not affect group I mGluR-induced prolonged synchronized discharges in Fmr1 −/− preparations, where functional FMRP is absent. The results suggest that constitutive FMRP in hippocampal cells acts as a brake on group I mGluR-mediated translation and epileptogenesis. FMRP downregulation via UPS removes this brake enabling group I mGluR-mediated translation and epileptogenesis.
    Type of Medium: Online Resource
    ISSN: 0270-6474 , 1529-2401
    URL: Article
    DOI: 10.1523/JNEUROSCI.2915-10.2011
    Language: English
    Publisher: Society for Neuroscience
    Publication Date: 2011
    detail.hit.zdb_id: 1475274-8
    SSG: 12
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  • 7
    Online Resource
    Online Resource
    Extracellular Signal-Regulated Kinase 1/2 Is Required for the Induction of Group I Metabotropic Glutamate Receptor-Mediated Epileptiform Discharges
    Society for Neuroscience ; 2004
    In:  The Journal of Neuroscience Vol. 24, No. 1 ( 2004-01-07), p. 76-84
    Details
    In: The Journal of Neuroscience, Society for Neuroscience, Vol. 24, No. 1 ( 2004-01-07), p. 76-84
    Abstract: Transient stimulation of group I metabotropic glutamate receptors (mGluRs) induces persistent prolonged epileptiform discharges in hippocampal slices via a protein synthesis-dependent process. At present, the signaling process underlying the induction of these epileptiform discharges remains unknown. We examined the possible role of extracellular signal-regulated kinases (ERK1 and ERK2) because these kinases can be activated by group I mGluRs, and their activation may regulate gene expression and alter protein synthesis. The group I mGluR agonist ( S )-3,5-dihydroxyphenylglycine (DHPG; 50 μ m ) induced activation of ERK1/2 in hippocampal slices. 2-(2-Diamino-3-methoxyphenyl-4H-1-benzopyran-4-one (PD98059) (50 μ m ) a specific inhibitor of mitogen-activated protein kinase kinase (MEK), suppressed ERK1/2 activation by DHPG. PD98059 or another MEK inhibitor, 1,4-diamino-2,3-dicyano-1,4-bis[2-aminophenylthio]butadiene (10 μ m ), also prevented the induction of the prolonged epileptiform discharges by DHPG. In the presence of ionotropic glutamate receptor inhibitors and tetrodotoxin (blockers), DHPG-induced epileptiform discharges were suppressed, whereas ERK1/2 activation persisted. Protein kinase C inhibitors (2-[1-(3-dimethylaminopropyl)-5-methoxyindol-3-yl]-3-(1H-indol-3-yl) maleimide, 1 μ m ; or chelerythrine, 10 μ m ) did not prevent the generation of DHPG-induced epileptiform discharges, nor did they suppress the activation of ERK1/2 by DHPG in slices pretreated with the blockers. Genistein (30 μ m ), a broad-spectrum tyrosine kinase inhibitor, suppressed the DHPG-induced epileptiform discharges and the ERK1/2 activation in the presence of blockers. Induction of DHPG-mediated epileptiform discharges was also suppressed by 4-amino-5-(4-chlorophenyl)-7-(t-butyl)pyrazolo[3,4- d ]pyrimidine (10 μ m ), an Src-family tyrosine kinase inhibitor. The study shows that group I mGluRs activate ERK1/2 through a tyrosine kinase-dependent process and that this activation of ERK1/2 is necessary for the induction of prolonged epileptiform discharges in the hippocampus.
    Type of Medium: Online Resource
    ISSN: 0270-6474 , 1529-2401
    URL: Article
    DOI: 10.1523/JNEUROSCI.4515-03.2004
    Language: English
    Publisher: Society for Neuroscience
    Publication Date: 2004
    detail.hit.zdb_id: 1475274-8
    SSG: 12
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  • 8
    Online Resource
    Online Resource
    Excitatory Synaptic Responses Mediated by GABA A Receptors in the Hippocampus
    American Association for the Advancement of Science (AAAS) ; 1991
    In:  Science Vol. 253, No. 5026 ( 1991-09-20), p. 1420-1423
    Details
    In: Science, American Association for the Advancement of Science (AAAS), Vol. 253, No. 5026 ( 1991-09-20), p. 1420-1423
    Type of Medium: Online Resource
    ISSN: 0036-8075 , 1095-9203
    URL: Article
    DOI: 10.1126/science.1654594
    RVK:
    TA 1000
    RVK:
    WA 15000
    Language: English
    Publisher: American Association for the Advancement of Science (AAAS)
    Publication Date: 1991
    detail.hit.zdb_id: 128410-1
    detail.hit.zdb_id: 2066996-3
    detail.hit.zdb_id: 2060783-0
    SSG: 11
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  • 9
    Online Resource
    Online Resource
    Activation of group I mGluRs elicits different responses in murine CA1 and CA3 pyramidal cells
    Wiley ; 2002
    In:  The Journal of Physiology Vol. 541, No. 1 ( 2002-05), p. 113-121
    Details
    In: The Journal of Physiology, Wiley, Vol. 541, No. 1 ( 2002-05), p. 113-121
    Abstract: The group I metabotropic glutamate receptor agonist DHPG has been shown to produce two major effects on CA3 pyramidal cells at rest: a reduction in the background conductance and an activation of a voltage‐gated inward current ( I mGluR(V) ). Both effects contribute to depolarising CA3 pyramidal cells and the latter has been implicated in eliciting prolonged epileptiform population bursts. We observed that DHPG‐induced depolarisation was smaller in CA1 pyramidal cells than in CA3 cells. Voltage clamp studies revealed that while DHPG elicited I mGluR(V) in CA3 pyramidal cells, such a response was absent in CA1 pyramidal cells. Both mGluR1 and mGluR5 have been localised in CA3 pyramidal cells, whereas only mGluR5 has been detected in CA1 pyramidal cells. Using mGluR1 knockout mice, we evaluated whether the absence of an I mGluR(V) response can be correlated with the absence of mGluR1. In these experiments, DHPG failed to elicit I mGluR(V) in CA3 pyramidal cells. This suggests that the smaller depolarising effects of DHPG on wild‐type CA1 pyramidal cells is caused, at least in part, by the absence of I mGluR(V) in these cells and that the difference in the responses of CA1 and CA3 cells may be attributable to the lack of mGluR1 in CA1 pyramidal cells.
    Type of Medium: Online Resource
    ISSN: 0022-3751 , 1469-7793
    URL: Article
    DOI: 10.1113/jphysiol.2001.013309
    RVK:
    WA 15000
    Language: English
    Publisher: Wiley
    Publication Date: 2002
    detail.hit.zdb_id: 1475290-6
    SSG: 12
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  • 10
    Online Resource
    Online Resource
    Fast ripples reflect increased excitability that primes epileptiform spikes
    Oxford University Press (OUP) ; 2023
    In:  Brain Communications Vol. 5, No. 5 ( 2023-08-31)
    Details
    In: Brain Communications, Oxford University Press (OUP), Vol. 5, No. 5 ( 2023-08-31)
    Abstract: The neuronal circuit disturbances that drive inter-ictal and ictal epileptiform discharges remain elusive. Using a combination of extra-operative macro-electrode and micro-electrode inter-ictal recordings in six pre-surgical patients during non-rapid eye movement sleep, we found that, exclusively in the seizure onset zone, fast ripples (200–600 Hz), but not ripples (80–200 Hz), frequently occur & lt;300 ms before an inter-ictal intra-cranial EEG spike with a probability exceeding chance (bootstrapping, P & lt; 1e−5). Such fast ripple events are associated with higher spectral power (P & lt; 1e−10) and correlated with more vigorous neuronal firing than solitary fast ripple (generalized linear mixed-effects model, P & lt; 1e−9). During the intra-cranial EEG spike that follows a fast ripple, action potential firing is lower than during an intra-cranial EEG spike alone (generalized linear mixed-effects model, P & lt; 0.05), reflecting an inhibitory restraint of intra-cranial EEG spike initiation. In contrast, ripples do not appear to prime epileptiform spikes. We next investigated the clinical significance of pre-spike fast ripple in a separate cohort of 23 patients implanted with stereo EEG electrodes, who underwent resections. In non-rapid eye movement sleep recordings, sites containing a high proportion of fast ripple preceding intra-cranial EEG spikes correlate with brain areas where seizures begin more than solitary fast ripple (P & lt; 1e−5). Despite this correlation, removal of these sites does not guarantee seizure freedom. These results are consistent with the hypothesis that fast ripple preceding EEG spikes reflect an increase in local excitability that primes EEG spike discharges preferentially in the seizure onset zone and that epileptogenic brain regions are necessary, but not sufficient, for initiating inter-ictal epileptiform discharges.
    Type of Medium: Online Resource
    ISSN: 2632-1297
    URL: Article
    DOI: 10.1093/braincomms/fcad242
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2023
    detail.hit.zdb_id: 3020013-1
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