651 research outputs found
A Serviceable Villain: Eugenics, The Fear of the Underman, and Anti-Democratic Discourse in Texas Thought and Culture, 1900-1940
Zwischen RealitÀt und Utopie: Geschlechterkonzepte und Selbstbilder in der zeitgenössischen bildenden Kunst
"Die politische Emanzipationskraft der in den
1960er und 1970er Jahren entwickelten femi
nis tischen Kunst ist heute teilweise der
Genderdebatte zum Opfer gefallen. Weiterhin
notwendige feministische Arbeit wird
vernachlÀssigt, feministische Kunst musealisiert
und entpolitisiert. AuĂerdem fĂŒhrt die
populÀre BeschÀftigung mit Genderfragen
mit unter zur VernachlĂ€ssigung kĂŒnstlerischer
Fragen. Dabei bietet das âNeogeschlechtâ
spannenden Stoff fĂŒr kĂŒnstlerische SelbstreprĂ€sentation.
Die Grenzen zwischen den
Genres werden aufgelöst, auch die Grenzen
zwischen realem Abbild und Wunschprojektion,
klassischem SelbstportrÀt und gendersensitiver
Selbstinterpretation verfl ieĂen." (Autorenreferat)"Part of the emancipatory force of 1960s and
1970s feminist art was lost along the way because
the gender debate now dominates public
discourse. While feminist action is still necessary,
feminist art is being historicized and
depoliticised. In addition, the popular focus
on gender issues sometimes results in a neglect
of artistic issues. Nonetheless, âneogen
derâ offers exciting material for artistic
self-representation. The boundaries between
genres are melt away as do the distinctions
between realistic image and desired icon,
classic self-portrait and gender-sensitive selfinterpretation." (author's abstract
Is there a "native" band gap in ion conducting glasses?
It is suggested that the spectrum of ion site energies in glasses exhibits a
band gap, establishing an analogy between ion conducting glasses and intrinsic
semiconductors. This implies that ion conduction in glasses takes place via
vacancies and interstitial ions (as in crystals).Comment: 3 page
Poor transcript-protein correlation in the brain: negatively correlating gene products reveal neuronal polarity as a potential cause
International audienceTranscription, translation, and turnover of transcripts and proteins are essential for cellular function. The contribution of those factors to protein levels is under debate, as transcript levels and cognate protein levels do not necessarily correlate due to regulation of translation and protein turnover. Here we propose neuronal polarity as a third factor that is particularly evident in the CNS, leading to considerable distances between somata and axon terminals. Consequently, transcript levels may negatively correlate with cognate protein levels in CNS regions, i.e., transcript and protein levels behave reciprocally. To test this hypothesis, we performed an integrative interâomics study and analyzed three interconnected rat auditory brainstem regions (cochlear nuclear complex, CN; superior olivary complex, SOC; inferior colliculus, IC) and the rest of the brain as a reference. We obtained transcript and protein sets in these regions of interest (ROIs) by DNA microarrays and labelâfree mass spectrometry, and performed principal component and correlation analyses. We found 508 transcript|protein pairs and detected poor to moderate transcript|protein correlation in all ROIs, as evidenced by coefficients of determination from 0.34 to 0.54. We identified 57â80 negatively correlating gene products in the ROIs and intensively analyzed four of them for which the correlation was poorest. Three cognate proteins (Slc6a11, Syngr1, Tppp) were synaptic and hence candidates for a negative correlation because of protein transport into axon terminals. Thus, we systematically analyzed the negatively correlating gene products. Gene ontology analyses revealed overrepresented transport/synapseârelated proteins, supporting our hypothesis. We present 30 synapse/transportârelated proteins with poor transcript|protein correlation. In conclusion, our analyses support that protein transport in polar cells is a third factor that influences the protein level and, thereby, the transcript|protein correlation
ADF/Cofilin Controls Synaptic Actin Dynamics and Regulates Synaptic Vesicle Mobilization and Exocytosis.
Attention deficit/hyperactivity disorder-like phenotype in a mouse model with impaired actin dynamics.
N-Cofilin Can Compensate for the Loss of ADF in Excitatory Synapses
Actin plays important roles in a number of synaptic processes, including synaptic vesicle organization and exocytosis, mobility of postsynaptic receptors, and synaptic plasticity. However, little is known about the mechanisms that control actin at synapses. Actin dynamics crucially depend on LIM kinase 1 (LIMK1) that controls the activity of the actin depolymerizing proteins of the ADF/cofilin family. While analyses of mouse mutants revealed the importance of LIMK1 for both pre- and postsynaptic mechanisms, the ADF/cofilin family member n-cofilin appears to be relevant merely for postsynaptic plasticity, and not for presynaptic physiology. By means of immunogold electron microscopy and immunocytochemistry, we here demonstrate the presence of ADF (actin depolymerizing factor), a close homolog of n-cofilin, in excitatory synapses, where it is particularly enriched in presynaptic terminals. Surprisingly, genetic ablation of ADF in mice had no adverse effects on synapse structure or density as assessed by electron microscopy and by the morphological analysis of Golgi-stained hippocampal pyramidal cells. Moreover, a series of electrophysiological recordings in acute hippocampal slices revealed that presynaptic recruitment and exocytosis of synaptic vesicles as well as postsynaptic plasticity were unchanged in ADF mutant mice. The lack of synaptic defects may be explained by the elevated n-cofilin levels observed in synaptic structures of ADF mutants. Indeed, synaptic actin regulation was impaired in compound mutants lacking both ADF and n-cofilin, but not in ADF single mutants. From our results we conclude that n-cofilin can compensate for the loss of ADF in excitatory synapses. Further, our data suggest that ADF and n-cofilin cooperate in controlling synaptic actin content
Precisely timed inhibition facilitates action potential firing for spatial coding in the auditory brainstem
The integration of excitatory and inhibitory synaptic inputs is fundamental to neuronal processing. In the mammalian auditory brainstem, neurons compare excitatory and inhibitory inputs from the ipsilateral and contralateral ear, respectively, for sound localization. However, the temporal precision and functional roles of inhibition in this integration process are unclear. Here, we demonstrate by in vivo recordings from the lateral superior olive (LSO) that inhibition controls spiking with microsecond precision throughout high frequency click trains. Depending on the relative timing of excitation and inhibition, neuronal spike probability is either suppressed or-unexpectedly-facilitated. In vitro conductance-clamp LSO recordings establish that a reduction in the voltage threshold for spike initiation due to a prior hyperpolarization results in post-inhibitory facilitation of otherwise sub-threshold synaptic events. Thus, microsecond-precise differences in the arrival of inhibition relative to excitation can facilitate spiking in the LSO, thereby promoting spatial sensitivity during the processing of faint sounds
The adipocyte hormone leptin sets the emergence of hippocampal inhibition in mice
This is the author accepted manuscript. The final version is available from eLife Sciences Publications via the DOI in this record.Brain computations rely on a proper balance between excitation and inhibition which progressively emerges during postnatal development in rodent. g-aminobutyric acid (GABA) neurotransmission supports inhibition in the adult brain but excites immature rodent neurons. Alterations in the timing of the GABA switch contribute to neurological disorders, so unveiling the involved regulators may be a promising strategy for treatment. Here we show that the adipocyte hormone leptin sets the tempo for the emergence of GABAergic inhibition in the newborn rodent hippocampus. In the absence of leptin signaling, hippocampal neurons show an advanced emergence of GABAergic inhibition. Conversely, maternal obesity associated with hyperleptinemia delays the excitatory to inhibitory switch of GABA action in offspring. This study uncovers a developmental function of leptin that may be linked to the pathogenesis of neurological disorders and helps understanding how maternal environment can adversely impact offspring brain development.This work was supported by the MinistĂšre de la Recherche et de lâEnseignement SupĂ©rieur, Neurochlore (CD) and the National Institutes of Health (Grant MH086032, GW)
Decreased Immunoreactivities and Functions of the Chloride Transporters, KCC2 and NKCC1, in the Lateral Superior Olive Neurons of Circling Mice
Objectives. We tested the possibility of differential expression and function of the potassium-chloride (KCC2) and sodium-potassium-2 chloride (NKCC1) co-transporters in the lateral superior olive (LSO) of heterozygous (+/cir) or homozygous (cir/cir) mice.Methods. Mice pups aged from postnatal (P) day 9 to 16 were used. Tails from mice were cut for DNA typing. For Immunohistochemical analysis, rabbit polyclonal anti-KCC2 or rabbit polyclonal anti-NKCC1 was used and the density of immunolabelings was evaluated using the NTH image program. For functional analysis, whole cell voltage clamp technique was used in brain stem slices and the changes of reversal potentials were evaluated at various membrane potentials.Results. Immunohistochemical analysis revealed both KCC2 and NKCC1 immunoreactivities were more prominent in heterozygous (+/cir) than homozygous (cir/cir) mice on P day 16. In P9-P12 heterozygous (+/cir) mice, the reversal potential (E(gly)) of glycine-induced currents was shifted to a more negative potential by 50 mu M bumetanide, a known NKCC1 blocker, and the negatively shifted EA, was restored by additional application of 1 mM furosemide, a KCC2 blocker (-58.9 +/- 2.6 mV to -66.0 +/- 1.5 mV [bumetanide], -66.0 1.5 mV to -59.8 +/- 2.8 mV [furosemide+bumetanide], n=11). However, only bumetanide was weakly, but significantly effective (-60.1 +/- 2.9 mV to -62.7 +/- 2.6 mV [bumetanide], -62.7 +/- 2.6 mV to -62.1 +/- 2.5 mV [furosernide+bumetanide], n=7) in P9-P12 homozygous (cir/cir) mice.Conclusion. The less prominent immunoreactivities and weak or absent responses to bumetanide or furosemide suggest impaired function or delayed development of both transporters in homozygous (cir/cir) mice
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