Zwischen Realität 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 vernachlässigt, feministische Kunst musealisiert und entpolitisiert. Außerdem führt die populäre Beschäftigung mit Genderfragen mit unter zur Vernachlässigung künstlerischer Fragen. Dabei bietet das „Neogeschlecht“ spannenden Stoff für künstlerische Selbstrepräsentation. Die Grenzen zwischen den Genres werden aufgelöst, auch die Grenzen zwischen realem Abbild und Wunschprojektion, klassischem Selbstporträt und gendersensitiver Selbstinterpretation verfl ießen." (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, “neogen der” 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 inter‐omics 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 label‐free 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 57‐80 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/synapse‐related proteins, supporting our hypothesis. We present 30 synapse/transport‐related 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

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 Ministère de la Recherche et de l’Enseignement Supérieur, 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