1,848 research outputs found
Post-translational mechanisms which could underlie the postsynaptic expression of LTP and LTD
No full textCompartmentalized Calcium Signaling in Cilia Regulates Intraflagellar Transport
No full textIntraflagellar transport (IFT) underpins many of the important cellular roles of cilia and flagella in signaling and motility [1,2,3,4]. The microtubule motors kinesin-2 and cytoplasmic dynein 1b drive IFT particles (protein complexes carrying ciliary component proteins) along the axoneme to facilitate the assembly and maintenance of cilia. IFT is regulated primarily by cargo loading onto the IFT particles, although evidence suggests that IFT particles also exhibit differential rates of movement [5,6,7]. Here we demonstrate that intraflagellar Ca2+ elevations act to directly regulate the movement of IFT particles. IFT-driven movement of adherent flagella membrane glycoproteins in the model alga Chlamydomonas enables flagella-mediated gliding motility [8,9,10]. We find that surface contact promotes the localized accumulation of IFT particles in Chlamydomonas flagella. Highly compartmentalized intraflagellar Ca2+ elevations initiate retrograde transport of paused IFT particles to modulate their accumulation. Gliding motility induces mechanosensitive intraflagellar Ca2+ elevations in trailing (dragging) flagella only, acting to specifically clear the accumulated microtubule motors from individual flagella and prevent a futile tug-of-war. Our results demonstrate that compartmentalized intraciliary Ca2+ signaling can regulate the movement of IFT particles and is therefore likely to play a central role in directing the movement and distribution of many ciliary proteins
On the mechanism of long-term potentiation induced by (1S,3R)-1-aminocyclopentane-1,3-dicarboxylic acid (ACPD) in rat hippocampal slices
No full textWe have reported previously that transient application of a specific metabotropic glutamate receptor (mGluR) agonist (1S,3R)-1-aminocyclopentane-1,3-dicarboxylate (ACPD) can induce a slow-onset form of long-term potentiation (LTP) of synaptic transmission in the CA1 region of rat hippocampal slices [Bortolotto Z. A. and Collingridge G. L. (1993) Neuropharmacology 32, 1-9]. Here we have investigated further the mechanisms involved in the induction and expression of ACPD-induced LTP. Unless otherwise stated, field excitatory postsynaptic potentials (EPSPs) were recorded in stratum radiatum in response to low frequency (0.033 Hz stimulation) of the Schaffer collateral-commissural pathway and 10 microM ACPD was added for 20 min to the perfusate. ACPD-induced LTP was still observed following blockade of GABAA receptor-mediated synaptic inhibition using picrotoxin (50 microM) and was not the result of a change in the presynaptic fibre volley. Intracellular recording from area CA1 revealed an increase in the size of the EPSP but no associated change in membrane potential or input resistance. However, ACPD-induced potentiation was never seen when intracellular electrodes contained the Ca(2+)-chelating agent 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid (BAPTA; 0.5 M). In area CA3, ACPD elicited a slow-onset LTP of the intracellularly recorded EPSP, evoked by stimulation of associational fibres. In contrast to area CA1, 10 microM ACPD depolarized CA3 neurones. Unlike certain other forms of tetanus- and chemically-induced potentiation, ACPD-induced LTP was not affected by the L-type Ca2+ channel antagonist nimodipine (50 microM). It was, however, prevented by delivering low frequency stimulation (900 shocks at 1 Hz) immediately following termination of the application of ACPD; an effect which was inhibited by the specific N-methyl-D-aspartate (NMDA) receptor antagonist D-2-amino-5-phosphonopentanoate (AP5; 50 microM). ACPD failed to induce LTP of pharmacologically-isolated NMDA receptor-mediated EPSPs. The induction of ACPD-induced LTP was blocked by the alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionate (AMPA) receptor antagonist 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX), in a reversible manner. In slices in which area CA3 had been removed ACPD failed to induce LTP when applied alone or together with AMPA. However, a slow-onset form of LTP was induced, in slices lacking area CA3, when a tetanus (100 Hz, 1 sec) was delivered in the presence of ACPD and 50 microM AP5 (the latter applied to prevent conventional tetanus-induced LTP). ACPD-induced LTP was associated with a parallel increase in the sensitivity of CA1 neurones to AMPA. Considered together, these data suggest that ACPD-induced LTP is due to a direct increase in the AMPA receptor-mediated synaptic conductance and involves postsynaptic induction and expression mechanisms.We have reported previously that transient application of a specific metabotropic glutamate receptor (mGluR) agonist (1S,3R)-1-aminocyclopentane-1,3-dicarboxylate (ACPD) can induce a slow-onset form of long-term potentiation (LTP) of synaptic transmission in the CA1 region of rat hippocampal slices [Bortolotto Z. A. and Collingridge G. L. (1993) Neuropharmacology 32, 1-9]. Here we have investigated further the mechanisms involved in the induction and expression of ACPD-induced LTP. Unless otherwise stated, field excitatory postsynaptic potentials (EPSPs) were recorded in stratum radiatum in response to low frequency (0.033 Hz stimulation) of the Schaffer collateral-commissural pathway and 10 microM ACPD was added for 20 min to the perfusate. ACPD-induced LTP was still observed following blockade of GABAA receptor-mediated synaptic inhibition using picrotoxin (50 microM) and was not the result of a change in the presynaptic fibre volley. Intracellular recording from area CA1 revealed an increase in the size of the EPSP but no associated change in membrane potential or input resistance. However, ACPD-induced potentiation was never seen when intracellular electrodes contained the Ca(2+)-chelating agent 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid (BAPTA; 0.5 M). In area CA3, ACPD elicited a slow-onset LTP of the intracellularly recorded EPSP, evoked by stimulation of associational fibres. In contrast to area CA1, 10 microM ACPD depolarized CA3 neurones. Unlike certain other forms of tetanus- and chemically-induced potentiation, ACPD-induced LTP was not affected by the L-type Ca2+ channel antagonist nimodipine (50 microM). It was, however, prevented by delivering low frequency stimulation (900 shocks at 1 Hz) immediately following termination of the application of ACPD; an effect which was inhibited by the specific N-methyl-D-aspartate (NMDA) receptor antagonist D-2-amino-5-phosphonopentanoate (AP5; 50 microM). ACPD failed to induce LTP of pharmacologically-isolated NMDA receptor-mediated EPSPs. The induction of ACPD-induced LTP was blocked by the alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionate (AMPA) receptor antagonist 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX), in a reversible manner. In slices in which area CA3 had been removed ACPD failed to induce LTP when applied alone or together with AMPA. However, a slow-onset form of LTP was induced, in slices lacking area CA3, when a tetanus (100 Hz, 1 sec) was delivered in the presence of ACPD and 50 microM AP5 (the latter applied to prevent conventional tetanus-induced LTP). ACPD-induced LTP was associated with a parallel increase in the sensitivity of CA1 neurones to AMPA. Considered together, these data suggest that ACPD-induced LTP is due to a direct increase in the AMPA receptor-mediated synaptic conductance and involves postsynaptic induction and expression mechanisms
Globalization of Distinguished Supercuspidal Representations of GL(n)
No full textAn irreducible supercuspidal representation of = GL(n, ), where is a nonarchimedean local field of characteristic zero, is said to be “distinguished” by a subgroup of and a quasicharacter of if Hom(, ) ≠ 0. There is a suitable global analogue of this notion for an irreducible, automorphic, cuspidal representation associated to GL(n). Under certain general hypotheses, it is shown in this paper that every distinguished, irreducible, supercuspidal representation may be realized as a local component of a distinguished, irreducible automorphic, cuspidal representation. Applications to the theory of distinguished supercuspidal representations are provided
Restriction of Representations of GL (n + 1, ℂ) to GL (n, ℂ) and Action of the Lie Overalgebra
No full textConsider a restriction of an irreducible finite dimensional holomorphic representation of GL(n+1,C) to the subgroup GL(n,C). We write explicitly formulas for generators of the Lie algebra gl(n+1) in the direct sum of representations of GL(n,C). Nontrivial generators act as differential-difference operators, the differential part has order n − 1, the difference part acts on the space of parameters (highest weights) of representations. We also formulate a conjecture about unitary principal series of GL(n,C).© The Author(s) 201
Gluk1 Receptor Antagonists and Hippocampal Mossy Fiber Function
No full textKainate receptors, one of the three subtypes of ionotropic receptors for the excitatory transmitter l-glutamate, play a variety of functions in the regulation of synaptic activity. Their physiological properties and functional roles have been identified only recently, following the discovery of selective pharmacological tools that allow for isolation of kainate receptor-mediated events. A considerable amount of data indicates that this class of glutamate receptors is located both at the pre- and postsynaptic site, playing a special role in regulating transmission and controlling short- and long-term plasticity. In this review, we summarize some data obtained in our laboratory over the last decade illustrating how various ligands have contributed to our understanding of the physiological role for neuronal kainate receptors. In particular, we show that the GluK1-containing KARs are important for regulating synaptic facilitation and LTP induction at hippocampal mossy fiber synapses
The Balanced Voronoi Formulas for
No full textAbstract
In this article, we show how the Voronoi summation formula of [13] can be rewritten to incorporate hyper-Kloosterman sums of various dimensions on both sides. This generalizes a formula for with ordinary Kloosterman sums on both sides that was used in [1] to prove nonvanishing of GL(4) -functions by GL(2)-twists, and later by the second-named author in [16].</jats:p
Bethe Vectors for Composite Models with gl(2|1) and gl(1|2) Supersymmetry
No full textSupersymmetric composite generalized quantum integrable models solvable by the algebraic Bethe ansatz are studied. Using a coproduct in the bialgebra of monodromy matrix elements and their action on Bethe vectors, formulas for Bethe vectors in the composite models with supersymmetry based on the super-Yangians Y[gl(2|1)] and Y[gl(1|2)] are derived.The author wants to express his gratitude to N.A. Slavnov for the proposal to investigate this
topic and discussions. He thanks also to S. Pakuliak for discussions and to A.P. Isaev and
C. Burd´ık for their support. The work of the author has been supported by the Grant Agency ˇ
of the Czech Technical University in Prague, grant No. SGS15/215/OHK4/3T/14, and by the
Grant of the Plenipotentiary of the Czech Republic at JINR, Dubna
Combinatorial results on (1,2,1,2)-avoiding -orbit closures on
No full text35 pages, 18 figuresInternational audienceUsing recent results of the second author which explicitly identify the "-avoiding" -orbit closures on the flag manifold as certain Richardson varieties, we give combinatorial criteria for determining smoothness, lci-ness, and Gorensteinness of such orbit closures. (In the case of smoothness, this gives a new proof of a theorem of W.M. McGovern.) Going a step further, we also describe a straightforward way to compute the singular locus, the non-lci locus, and the non-Gorenstein locus of any such orbit closure. We then describe a manifestly positive combinatorial formula for the Kazhdan-Lusztig-Vogan polynomial in the case where corresponds to the trivial local system on a -avoiding orbit closure and corresponds to the trivial local system on any orbit contained in . This combines the aforementioned result of the second author, results of A. Knutson, the first author, and A. Yong, and a formula of Lascoux and Sch\"{u}tzenberger which computes the ordinary (type ) Kazhdan-Lusztig polynomial whenever is cograssmannian
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