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  • 1
    Online Resource
    Online Resource
    δ Subunit Inhibits Neurosteroid Modulation of GABA A Receptors
    Society for Neuroscience ; 1996
    In:  The Journal of Neuroscience Vol. 16, No. 21 ( 1996-11-01), p. 6648-6656
    Details
    In: The Journal of Neuroscience, Society for Neuroscience, Vol. 16, No. 21 ( 1996-11-01), p. 6648-6656
    Abstract: Neurosteroid modulation of GABA A receptors has been observed with all subunit combinations investigated; however, hetero-oligomeric GABA A receptors containing δ subunits were not studied previously. We describe the effect of δ subunit expression on 3α,21-dihydroxy-5α-pregnan-20-1 (THDOC)-induced potentiation of GABA-gated currents in transfected HEK 293 cells and in cerebellar granule cells in vitro . THDOC (100 n m ) significantly potentiated GABA-gated currents in cells transfected with combinations of α1, α6, β3, and γ2 subunit cDNAs, whereas cotransfection of δ subunit cDNA inhibited this potentiation. In contrast, the direct Cl − channel activation by THDOC at higher concentrations (1–10 μ m ) was not significantly dependent on δ subunit cotransfection. These results suggest that the presence of the δ subunit inhibits GABA A receptor modulation but not the direct activation by neurosteroids. Cotransfection with δ subunit also affected the negative allosteric modulation by pregnenolone sulfate. THDOC potentiation of GABA-gated currents was greater in cerebellar granule cell cultures at 4 d in vitro (DIV) compared with those at 14 DIV. Single-cell reverse transcription-PCR analysis of the mRNAs expressed in cultured cerebellar granule cells shows that an increased number of granule cells at 14 DIV express δ subunit mRNAs as compared with 4 DIV granule cells. The presence of δ subunit mRNAs detected in individual cells correlated well with the lack of sensitivity to THDOC. These results suggest that developmental expression of GABA A receptor δ subunits may play an important role in determining the region-specific neurosteroid-induced modification of fast inhibitory synaptic function.
    Type of Medium: Online Resource
    ISSN: 0270-6474 , 1529-2401
    URL: Article
    DOI: 10.1523/JNEUROSCI.16-21-06648.1996
    Language: English
    Publisher: Society for Neuroscience
    Publication Date: 1996
    detail.hit.zdb_id: 1475274-8
    SSG: 12
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  • 2
    Online Resource
    Online Resource
    GABA A Receptor α1 Subunit Deletion Prevents Developmental Changes of Inhibitory Synaptic Currents in Cerebellar Neurons
    Society for Neuroscience ; 2001
    In:  The Journal of Neuroscience Vol. 21, No. 9 ( 2001-05-01), p. 3009-3016
    Details
    In: The Journal of Neuroscience, Society for Neuroscience, Vol. 21, No. 9 ( 2001-05-01), p. 3009-3016
    Abstract: Developmental changes in miniature IPSC (mIPSC) kinetics have been demonstrated previously in cerebellar neurons in rodents. We report that these kinetic changes in mice are determined primarily by developmental changes in GABA A receptor subunit expression. mIPSCs were studied by whole-cell recordings in cerebellar slices, prepared from postnatal day 11 (P11) and P35 mice. Similar to reports in granule neurons, wild-type cerebellar stellate neuron mIPSCs at P11 had slow decay kinetics, whereas P35 mIPSCs decayed five times faster. When mIPSCs in cerebellar stellate neurons were compared between wild-type (+/+) and GABA A receptor α1 subunit-deficient (−/−) littermates at P35, we observed dramatically slower mIPSC decay rates in −/− animals. We took advantage of the greater potency of imidazopyridines for GABA current potentiation with α1 subunit-containing receptors to characterize the relative contribution of α1 subunits in native receptors on inhibitory synapses of cerebellar granule neurons. Zolpidem-induced prolongation of mIPSC decay was variable among distinct cells, but it increased during development in wild-type mice. Similarly, Zolpidem prolongation of mIPSC decay rate was significantly greater in adult +/+ mice than in knock-outs. We propose that an increased α1 subunit assembly in postsynaptic receptors of cerebellar inhibitory synapses is responsible for the fast inhibitory synaptic currents that are normally observed during postnatal development.
    Type of Medium: Online Resource
    ISSN: 0270-6474 , 1529-2401
    URL: Article
    DOI: 10.1523/JNEUROSCI.21-09-03009.2001
    Language: English
    Publisher: Society for Neuroscience
    Publication Date: 2001
    detail.hit.zdb_id: 1475274-8
    SSG: 12
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  • 3
    Online Resource
    Online Resource
    Distinct Roles for Somatically and Dendritically Synthesized Brain-Derived Neurotrophic Factor in Morphogenesis of Dendritic Spines
    Society for Neuroscience ; 2013
    In:  Journal of Neuroscience Vol. 33, No. 28 ( 2013-07-10), p. 11618-11632
    Details
    In: Journal of Neuroscience, Society for Neuroscience, Vol. 33, No. 28 ( 2013-07-10), p. 11618-11632
    Type of Medium: Online Resource
    ISSN: 0270-6474 , 1529-2401
    URL: Article
    DOI: 10.1523/JNEUROSCI.0012-13.2013
    Language: English
    Publisher: Society for Neuroscience
    Publication Date: 2013
    detail.hit.zdb_id: 1475274-8
    SSG: 12
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  • 4
    Online Resource
    Online Resource
    Glutamate-activated currents in outside-out patches from spiny versus aspiny hilar neurons of rat hippocampal slices
    Society for Neuroscience ; 1993
    In:  The Journal of Neuroscience Vol. 13, No. 12 ( 1993-12-01), p. 5324-5333
    Details
    In: The Journal of Neuroscience, Society for Neuroscience, Vol. 13, No. 12 ( 1993-12-01), p. 5324-5333
    Abstract: The desensitization rate of non-NMDA glutamate receptors was investigated in outside-out membrane patches obtained from morphologically identified spiny “mossy cells” (SMCs) and aspiny hilar interneurons (AHIs) in young rat hippocampal slices. The fast application of a 1 mM step of L-glutamate for 50–100 msec in the presence of TTX and dizolcipine (MK-801) onto patches excised from these neurons produced large glutamate-activated currents (GACs) that decayed with a single or double exponential time course despite the continued presence of agonist. These desensitization rates of alpha- amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA)/kainate- sensitive receptors differed markedly between patches obtained from the two cell types. The fast time constant of desensitization in AHIs (n = 34) averaged 3.3 +/- 0.93 msec (mean +/- SD), while that of SMCs (n = 57) averaged 6.8 +/- 2.0 msec. Current-voltage relationships of the GACs did not differ between SMCs and AHIs, with comparable reversal potentials and no evidence of inward rectification. We also failed to observe significant Ca2+ permeability in either cell type. However, brief ( 〈 1 msec) pulses of 1 mM glutamate produced rapidly decaying GACs with distinct kinetics in the two neuronal classes. Furthermore, analysis of the single glutamate-activated channel currents in outside- out patches from hilar neurons revealed a larger predominant single- channel current in AHIs versus SMCs. Lastly, we observed a greater sensitivity to cyclothiazide in SMCs versus AHIs, with half-maximal removal of desensitization being 90 mM and 200 mM, respectively. Taken together, these differences in GACs between SMCs and AHIs might indicate a functional correlate to the substantial heterogeneity in the molecular structure of glutamate receptor subunits or might be related to posttranslational modifications of these subunits, perhaps provided by the unique microenvironment in the spines covering SMCs.
    Type of Medium: Online Resource
    ISSN: 0270-6474 , 1529-2401
    URL: Article
    DOI: 10.1523/JNEUROSCI.13-12-05324.1993
    Language: English
    Publisher: Society for Neuroscience
    Publication Date: 1993
    detail.hit.zdb_id: 1475274-8
    SSG: 12
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  • 5
    Online Resource
    Online Resource
    Glutamate receptor subtypes mediate excitatory synaptic currents of dopamine neurons in midbrain slices
    Society for Neuroscience ; 1991
    In:  The Journal of Neuroscience Vol. 11, No. 5 ( 1991-05-01), p. 1359-1366
    Details
    In: The Journal of Neuroscience, Society for Neuroscience, Vol. 11, No. 5 ( 1991-05-01), p. 1359-1366
    Abstract: Although dopamine (DA)-containing neurons participate in a number of important cerebral functions, the physiology of their synaptic connections is poorly understood. By using whole-cell patch-clamp recording in thin slices of rat mesencephalon, we have investigated the biophysical properties of synaptic events and the nature of neurotransmitter(s) and receptors involved in the synaptic input to DA neurons in substantia nigra. The histological and electrophysiological characteristics of these cells were consistent with those described by recent in vivo and in vitro studies, thus allowing their unequivocal identification. Under appropriate experimental conditions, intranigral stimulation produced excitatory synaptic inputs in DA neurons. By voltage-clamp analysis, most of these excitatory postsynaptic currents (EPSCs) had a rise time of about 1.0 msec and a decay phase that could be fit by the sum of two exponential curves so that a fast and a slow component could be distinguished. The slow component was enhanced by glycine, by removing Mg2+ from the bath medium, or by membrane depolarization. Moreover, the slow component was consistently decreased by selective antagonists of NMDA receptors, whereas an antagonist for the non-NMDA receptors abolished the fast component slightly affecting the slow component and reduced peak EPSC amplitude. The results indicate that both NMDA-sensitive and non-NMDA-sensitive glutamate receptors contribute to EPSCs of DA neurons. Therefore, it is suggested that these receptors may play a critical role in the physiology (control of excitability, pacemaker firing, and dendritic DA release) as well as pathology (neuronal death in Parkinson's disease, psychosis, and mechanism of action of drugs of abuse, such as ethanol) related to DA neurons.
    Type of Medium: Online Resource
    ISSN: 0270-6474 , 1529-2401
    URL: Article
    DOI: 10.1523/JNEUROSCI.11-05-01359.1991
    Language: English
    Publisher: Society for Neuroscience
    Publication Date: 1991
    detail.hit.zdb_id: 1475274-8
    SSG: 12
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  • 6
    Online Resource
    Online Resource
    Electroconvulsive Shock Enhances Responsive Motility and Purinergic Currents in Microglia in the Mouse Hippocampus
    Society for Neuroscience ; 2019
    In:  eneuro Vol. 6, No. 2 ( 2019-03), p. ENEURO.0056-19.2019-
    Details
    In: eneuro, Society for Neuroscience, Vol. 6, No. 2 ( 2019-03), p. ENEURO.0056-19.2019-
    Abstract: Microglia are in a privileged position to both affect and be affected by neuroinflammation, neuronal activity and injury, which are all hallmarks of seizures and the epilepsies. Hippocampal microglia become activated after prolonged, damaging seizures known as status epilepticus (SE). However, since SE causes both hyperactivity and injury of neurons, the mechanisms triggering this activation remain unclear, as does the relevance of the microglial activation to the ensuing epileptogenic processes. In this study, we use electroconvulsive shock (ECS) to study the effect of neuronal hyperactivity without neuronal degeneration on mouse hippocampal microglia. Unlike SE, ECS did not alter hippocampal CA1 microglial density, morphology, or baseline motility. In contrast, both ECS and SE produced a similar increase in ATP-directed microglial process motility in acute slices, and similarly upregulated expression of the chemokine C-C motif chemokine ligand 2 (CCL2). Whole-cell patch-clamp recordings of hippocampal CA1 sr microglia showed that ECS enhanced purinergic currents mediated by P2X7 receptors in the absence of changes in passive properties or voltage-gated currents, or changes in receptor expression. This differs from previously described alterations in intrinsic characteristics which coincided with enhanced purinergic currents following SE. These ECS-induced effects point to a “seizure signature” in hippocampal microglia characterized by altered purinergic signaling. These data demonstrate that ictal activity per se can drive alterations in microglial physiology without neuronal injury. These physiological changes, which up until now have been associated with prolonged and damaging seizures, are of added interest as they may be relevant to electroconvulsive therapy (ECT), which remains a gold-standard treatment for depression.
    Type of Medium: Online Resource
    ISSN: 2373-2822
    URL: Article
    DOI: 10.1523/ENEURO.0056-19.2019
    Language: English
    Publisher: Society for Neuroscience
    Publication Date: 2019
    detail.hit.zdb_id: 2800598-3
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