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  • 1
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    Online Resource
    Domains Responsible for Constitutive and Ca 2+ -Dependent Interactions between Calmodulin and Small Conductance Ca 2+ -Activated Potassium Channels
    Society for Neuroscience ; 1999
    In:  The Journal of Neuroscience Vol. 19, No. 20 ( 1999-10-15), p. 8830-8838
    Details
    In: The Journal of Neuroscience, Society for Neuroscience, Vol. 19, No. 20 ( 1999-10-15), p. 8830-8838
    Abstract: Small conductance Ca 2+ -activated potassium channels (SK channels) are coassembled complexes of pore-forming SK α subunits and calmodulin. We proposed a model for channel activation in which Ca 2+ binding to calmodulin induces conformational rearrangements in calmodulin and the α subunits that result in channel gating. We now report fluorescence measurements that indicate conformational changes in the α subunit after calmodulin binding and Ca 2+ binding to the α subunit–calmodulin complex. Two-hybrid experiments showed that the Ca 2+ -independent interaction of calmodulin with the α subunits requires only the C-terminal domain of calmodulin and is mediated by two noncontiguous subregions; the ability of the E-F hands to bind Ca 2+ is not required. Although SK α subunits lack a consensus calmodulin-binding motif, mutagenesis experiments identified two positively charged residues required for Ca 2+ -independent interactions with calmodulin. Electrophysiological recordings of SK2 channels in membrane patches from oocytes coexpressing mutant calmodulins revealed that channel gating is mediated by Ca 2+ binding to the first and second E-F hand motifs in the N-terminal domain of calmodulin. Taken together, the results support a calmodulin- and Ca 2+ -calmodulin-dependent conformational change in the channel α subunits, in which different domains of calmodulin are responsible for Ca 2+ -dependent and Ca 2+ -independent interactions. In addition, calmodulin is associated with each α subunit and must bind at least one Ca 2+ ion for channel gating. Based on these results, a state model for Ca 2+ gating was developed that simulates alterations in SK channel Ca 2+ sensitivity and cooperativity associated with mutations in CaM.
    Type of Medium: Online Resource
    ISSN: 0270-6474 , 1529-2401
    URL: Article
    DOI: 10.1523/JNEUROSCI.19-20-08830.1999
    Language: English
    Publisher: Society for Neuroscience
    Publication Date: 1999
    detail.hit.zdb_id: 1475274-8
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  • 2
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    Online Resource
    Ovarian Hormone Deficiency Reduces Intrinsic Excitability and Abolishes Acute Estrogen Sensitivity in Hippocampal CA1 Pyramidal Neurons
    Society for Neuroscience ; 2011
    In:  The Journal of Neuroscience Vol. 31, No. 7 ( 2011-02-16), p. 2638-2648
    Details
    In: The Journal of Neuroscience, Society for Neuroscience, Vol. 31, No. 7 ( 2011-02-16), p. 2638-2648
    Abstract: Premature and uncompensated loss of ovarian hormones following ovariectomy (OVX) elevates the risks of cognitive impairment and dementia. These risks are prevented with estrogen (E 2 )-containing hormone replacement therapy initiated shortly following OVX but not after substantial delay. Currently, the cellular bases underlying these clinical findings are unknown. At the cellular level, intrinsic membrane properties regulate the efficiency of synaptic inputs to initiate output action potentials (APs), thereby affecting neuronal communication, hence cognitive processing. This study tested the hypothesis that in CA1 pyramidal neurons, intrinsic membrane properties and their acute regulation by E 2 require ovarian hormones for maintenance. Whole-cell current-clamp recordings were performed on neurons from ∼7-month-old OVX rats that experienced either short-term (10 d, control OVX) or long-term (5 months, OVX LT ) ovarian hormone deficiency. The results reveal that long-term hormone deficiency reduced intrinsic membrane excitability (IE) as measured by the number of evoked APs and firing duration for a given current injection. This was accompanied by AP broadening, an increased slow afterhyperpolarization (sAHP), and faster accumulation of Na V channel inactivation during repetitive firing. In the control OVX neurons, E 2 acutely increased IE and reduced the sAHP. In contrast, acute regulation of IE by E 2 was absent in the OVX LT neurons. Since the degree of IE of hippocampal pyramidal neurons is positively related with hippocampus-dependent learning ability, and modulation of IE is observed following successful learning, these findings provide a framework for understanding hormone deficiency-related cognitive impairment and the critical window for therapy initiation.
    Type of Medium: Online Resource
    ISSN: 0270-6474 , 1529-2401
    URL: Article
    DOI: 10.1523/JNEUROSCI.6081-10.2011
    Language: English
    Publisher: Society for Neuroscience
    Publication Date: 2011
    detail.hit.zdb_id: 1475274-8
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  • 3
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    Online Resource
    Coassembly and Coupling of SK2 Channels and mGlu 5 Receptors
    Society for Neuroscience ; 2014
    In:  The Journal of Neuroscience Vol. 34, No. 44 ( 2014-10-29), p. 14793-14802
    Details
    In: The Journal of Neuroscience, Society for Neuroscience, Vol. 34, No. 44 ( 2014-10-29), p. 14793-14802
    Abstract: Group I metabotropic glutamate (mGlu) receptors regulate hippocampal CA1 pyramidal neuron excitability via Ca 2+ wave-dependent activation of small-conductance Ca 2+ -activated K + (SK) channels. Here, we show that mGlu 5 receptors and SK2 channels coassemble in heterologous coexpression systems and in rat brain. Further, in cotransfected cells or rat primary hippocampal neurons, mGlu 5 receptor stimulation activated apamin-sensitive SK2-mediated K + currents. In addition, coexpression of mGlu 5 receptors and SK2 channels promoted plasma membrane targeting of both proteins and correlated with increased mGlu 5 receptor function that was unexpectedly blocked by apamin. These results demonstrate a reciprocal functional interaction between mGlu 5 receptors and SK2 channels that reflects their molecular coassembly.
    Type of Medium: Online Resource
    ISSN: 0270-6474 , 1529-2401
    URL: Article
    DOI: 10.1523/JNEUROSCI.2038-14.2014
    Language: English
    Publisher: Society for Neuroscience
    Publication Date: 2014
    detail.hit.zdb_id: 1475274-8
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  • 4
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    Online Resource
    Episodic Ataxia Mutations in Kv1.1 Alter Potassium Channel Function by Dominant Negative Effects or Haploinsufficiency
    Society for Neuroscience ; 1998
    In:  The Journal of Neuroscience Vol. 18, No. 8 ( 1998-04-15), p. 2842-2848
    Details
    In: The Journal of Neuroscience, Society for Neuroscience, Vol. 18, No. 8 ( 1998-04-15), p. 2842-2848
    Abstract: Subunits of the voltage-gated potassium channel Kv1.1 containing mutations responsible for episodic ataxia (EA), a human inherited neurological disease, were expressed in Xenopus oocytes. Five EA subunits formed functional homomeric channels with lower current amplitudes and altered gating properties compared with wild type. Two EA mutations located in the first cytoplasmic loop, R239S and F249I, yielded minimal or no detectable current, and Western blot analysis showed reduced protein levels. Coinjection of equal amounts of EA and wild-type mRNAs, mimicking the heterozygous condition, resulted in current amplitudes and gating properties that were intermediate between wild-type and EA homomeric channels, suggesting that heteromeric channels are formed with a mixed stoichiometry of EA and wild-type subunits. To examine the relative contribution of EA subunits in forming heteromeric EA and wild-type channels, each EA subunit was made insensitive to TEA, TEA-tagged, and coexpressed with wild-type subunits. TEA-tagged R239S and F249I induced the smallest shift in TEA sensitivity compared with homomeric wild-type channels, whereas the other TEA-tagged EA subunits yielded TEA sensitivities similar to coexpression of wild-type and TEA-tagged wild-type subunits. Taken together, these results show that the different mutations in Kv1.1 affect channel function and indicate that both dominant negative effects and haplotype insufficiency may result in the symptoms of EA.
    Type of Medium: Online Resource
    ISSN: 0270-6474 , 1529-2401
    URL: Article
    DOI: 10.1523/JNEUROSCI.18-08-02842.1998
    Language: English
    Publisher: Society for Neuroscience
    Publication Date: 1998
    detail.hit.zdb_id: 1475274-8
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  • 5
    Online Resource
    Online Resource
    dSLo Interacting Protein 1, a Novel Protein That Interacts with Large-Conductance Calcium-Activated Potassium Channels
    Society for Neuroscience ; 1998
    In:  The Journal of Neuroscience Vol. 18, No. 7 ( 1998-04-01), p. 2360-2369
    Details
    In: The Journal of Neuroscience, Society for Neuroscience, Vol. 18, No. 7 ( 1998-04-01), p. 2360-2369
    Abstract: Large-conductance calcium-activated potassium channels (BK channels) are activated by depolarized membrane potential and elevated levels of intracellular calcium. BK channel activity underlies the fast afterhyperpolarization that follows an action potential and attenuates neurotransmitter and hormone secretion. Using a modified two-hybrid approach, the interaction trap, we have identified a novel protein from Drosophila , dSLIP1 (dSLo interacting protein), which specifically interacts with Drosophila and human BK channels and has partial homology to the PDZ domain of α1 syntrophin. The dSLIP1 and dSlo mRNAs are expressed coincidently throughout the Drosophila nervous system, the two proteins interact in vitro , and they may be coimmunoprecipitated from transfected cells. Coexpression of dSLIP1 with dSlo or hSlo BK channels in Xenopus oocytes results in reduced currents as compared with expression of BK channels alone; current amplitudes may be rescued by coexpression with the channel domain that interacts with dSLIP1. Single-channel recordings and immunostaining of transfected tissue culture cells suggest that dSLIP1 selectively reduces Slo BK currents by reducing the number of BK channels in the plasma membrane.
    Type of Medium: Online Resource
    ISSN: 0270-6474 , 1529-2401
    URL: Article
    DOI: 10.1523/JNEUROSCI.18-07-02360.1998
    Language: English
    Publisher: Society for Neuroscience
    Publication Date: 1998
    detail.hit.zdb_id: 1475274-8
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  • 6
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    Online Resource
    Localization of the Activation Gate for Small Conductance Ca 2+ -activated K + Channels
    Society for Neuroscience ; 2002
    In:  The Journal of Neuroscience Vol. 22, No. 15 ( 2002-08-01), p. 6499-6506
    Details
    In: The Journal of Neuroscience, Society for Neuroscience, Vol. 22, No. 15 ( 2002-08-01), p. 6499-6506
    Type of Medium: Online Resource
    ISSN: 0270-6474 , 1529-2401
    URL: Article
    DOI: 10.1523/JNEUROSCI.22-15-06499.2002
    Language: English
    Publisher: Society for Neuroscience
    Publication Date: 2002
    detail.hit.zdb_id: 1475274-8
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  • 7
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    Online Resource
    Small Conductance Ca 2+ -Activated K + Channels Modulate Synaptic Plasticity and Memory Encoding
    Society for Neuroscience ; 2002
    In:  The Journal of Neuroscience Vol. 22, No. 23 ( 2002-12-01), p. 10163-10171
    Details
    In: The Journal of Neuroscience, Society for Neuroscience, Vol. 22, No. 23 ( 2002-12-01), p. 10163-10171
    Type of Medium: Online Resource
    ISSN: 0270-6474 , 1529-2401
    URL: Article
    DOI: 10.1523/JNEUROSCI.22-23-10163.2002
    Language: English
    Publisher: Society for Neuroscience
    Publication Date: 2002
    detail.hit.zdb_id: 1475274-8
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  • 8
    Online Resource
    Online Resource
    Ovarian Hormone Loss Impairs Excitatory Synaptic Transmission at Hippocampal CA3–CA1 Synapses
    Society for Neuroscience ; 2013
    In:  The Journal of Neuroscience Vol. 33, No. 41 ( 2013-10-09), p. 16158-16169
    Details
    In: The Journal of Neuroscience, Society for Neuroscience, Vol. 33, No. 41 ( 2013-10-09), p. 16158-16169
    Abstract: Premature and long-term ovarian hormone loss following ovariectomy (OVX) is associated with cognitive impairment. This condition is prevented by estradiol (E 2 ) therapy when initiated shortly following OVX but not after substantial delay. To determine whether these clinical findings are correlated with changes in synaptic functions, we used adult OVX rats to evaluate the consequences of short-term (7–10 d, OVX Control ) and long-term (∼5 months, OVX LT ) ovarian hormone loss, as well as subsequent in vivo E 2 treatment, on excitatory synaptic transmission at the hippocampal CA3–CA1 synapses important for learning and memory. The results show that ovarian hormone loss was associated with a marked decrease in synaptic strength. E 2 treatment increased synaptic strength in OVX Control but not OVX LT rats, demonstrating a change in the efficacy for E 2 5 months following OVX. E 2 also had a more rapid effect: within minutes of bath application, E 2 acutely increased synaptic strength in all groups except OVX LT rats that did not receive in vivo E 2 treatment. E 2 's acute effect was mediated postsynaptically, and required Ca 2+ influx through the voltage-gated Ca 2+ channels. Despite E 2 's acute effect, synaptic strength of OVX LT rats remained significantly lower than that of OVX Control rats. Thus, changes in CA3–CA1 synaptic transmission associated with ovarian hormone loss cannot be fully reversed with delayed E 2 treatment. Given that synaptic strength at CA3–CA1 synapses is related to the ability to learn hippocampus-dependent tasks, these findings provide additional insights for understanding cognitive impairment-associated long-term ovarian hormone loss and ineffectiveness for delayed E 2 treatment to maintain cognitive functions.
    Type of Medium: Online Resource
    ISSN: 0270-6474 , 1529-2401
    URL: Article
    DOI: 10.1523/JNEUROSCI.2001-13.2013
    Language: English
    Publisher: Society for Neuroscience
    Publication Date: 2013
    detail.hit.zdb_id: 1475274-8
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  • 9
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    Online Resource
    Episodic Ataxia Type 1 Mutations in the Human Kv1.1 Potassium Channel Alter hKvβ1-Induced N-Type Inactivation
    Society for Neuroscience ; 2002
    In:  The Journal of Neuroscience Vol. 22, No. 12 ( 2002-06-15), p. 4786-4793
    Details
    In: The Journal of Neuroscience, Society for Neuroscience, Vol. 22, No. 12 ( 2002-06-15), p. 4786-4793
    Type of Medium: Online Resource
    ISSN: 0270-6474 , 1529-2401
    URL: Article
    DOI: 10.1523/JNEUROSCI.22-12-04786.2002
    Language: English
    Publisher: Society for Neuroscience
    Publication Date: 2002
    detail.hit.zdb_id: 1475274-8
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  • 10
    Online Resource
    Online Resource
    Coupled Activity-Dependent Trafficking of Synaptic SK2 Channels and AMPA Receptors
    Society for Neuroscience ; 2010
    In:  The Journal of Neuroscience Vol. 30, No. 35 ( 2010-09-01), p. 11726-11734
    Details
    In: The Journal of Neuroscience, Society for Neuroscience, Vol. 30, No. 35 ( 2010-09-01), p. 11726-11734
    Abstract: Small conductance Ca 2+ -activated K + type 2 (SK2) channels are expressed in the postsynaptic density of CA1 neurons where they are activated by synaptically evoked Ca 2+ influx to limit the size of EPSPs and spine Ca 2+ transients. At Schaffer collateral synapses, the induction of long-term potentiation (LTP) increases the α-amino-3-hydroxyl-5-methyl-4-isoxazole-propionate receptor (AMPAR)-mediated contribution to synaptic transmission and decreases the synaptic SK2 channel contribution through protein kinase A-dependent channel endocytosis. Using a combination of electrophysiology and immunoelectron microscopy in mice, the relationship between the dynamics of spine SK2 channels and AMPARs was investigated. Unlike AMPARs, synaptic SK2 channels under basal conditions do not rapidly recycle. Furthermore, SK2 channels occupy a distinct population of endosomes separate from AMPARs. However, blocking vesicular exocytosis or the delivery of synaptic GluA1-containing AMPARs during the induction of LTP blocks SK2 channel endocytosis. By ∼2 h after the induction of LTP, synaptic SK2 channel expression and function are restored. Thus, LTP-dependent endocytosis of SK2 is coupled to LTP-dependent AMPA exocytosis, and the ∼2 h window after the induction of LTP during which synaptic SK2 activity is absent may be important for consolidating the later phases of LTP.
    Type of Medium: Online Resource
    ISSN: 0270-6474 , 1529-2401
    URL: Article
    DOI: 10.1523/JNEUROSCI.1411-10.2010
    Language: English
    Publisher: Society for Neuroscience
    Publication Date: 2010
    detail.hit.zdb_id: 1475274-8
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