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Bilder der Anderen : die Digitalisierung des ethnographischen Bildarchivs des Frobenius-Instituts
(2006)
Für viele Drogenprostituierte ist »die Szene« nicht nur Drogenmarkt, Arbeitsmarkt und Stätte des Konsums, sondern Lebensraum überhaupt, ein Lebensraum, in dem es allerdings mehr ums Überleben als ums Miteinanderleben geht. Wie Junkies, die Geld mit Prostitution verdienen, ihr Gewerbe betreiben, hat die Forschergruppe mit ihren 26 Interviews im Frankfurter Bahnhofsviertel ebenso beleuchtet wie Lebenswege, Perspektiven und Lebensträume der drogenabhängigen Prostituierten.
In Amerika wird Crack, eine rauchbare Form von Kokain, seit Mitte der 1980er Jahre konsumiert. In Deutschland wähnte man sich vor dieser »Ghetto-Droge« sicher. Doch seit Mitte der 1990er Jahre gibt es auch in Frankfurt und Hamburg Crack-Szenen. In der Main-Metropole war es zunächst eine kleine, von den Heroin-Süchtigen getrennte Raucherszene, aber schon 2002 hatte Crack das Kokain-Pulver völlig verdrängt und sogar das Heroin als bisher meistgebrauchte Droge auf den zweiten Rang verwiesen. Heute konsumieren 60 Prozent der Frankfurter Szene-Junkies mehrmals in der Woche Heroin, aber über 80 Prozent – oftmals dieselben Drogenabhängigen – auch mehrmals in der Woche Crack. Da bei dieser Droge der Kick zwar stark, aber nicht nachhaltig ist und die Junkies sich deshalb nie gesättigt fühlen, treibt die Abhängigen eine enorme Unruhe. Beobachtungen und Interviews mit Betroffenen zeigen, wie sich der Konsum dieser Droge verschärfend auf das Leben der Junkies und damit auf die gesamte Szene auswirkt.
Poster presentation: Light is the main phase-adjusting stimulus of the circadian clock located in the suprachiasmatic nucleus (SCN). A candidate pathway transmitting photic information at the postsynaptic site in the SCN is the extracellular signal-regulated kinase (ERK 1/2) which has been previously shown to be an essential element in the photoentrainment of the circadian rhythm. An upstream activator of the ERK signalling route is the small intracellular GTPase Ras. Here we observed that endogenous Ras activity in the SCN was subjected to rhythmic changes, reaching maximum levels at the late subjective day and minimum levels at the late subjective night (CT22). In order to investigate if Ras would modulate the circadian cycle, we used transgenic mice expressing constitutively activated Val-12 Ha-Ras selectively in neurons (synRas mice). In these mice Ras activity was also cycling during the circadian rhythm yet, Ras activities were up-regulated at each time point measured. We investigated if this change in Ras activity translates into a behavioral phenotype by monitoring free-running activity rhythms under conditions of constant darkness. SynRas mice exhibited circadian rhythms in locomotor activities similar to WT mice. However, when challenged by applying a 15 minutes light pulse at CT22 to promote phase advance shifts, synRas mice were completely non-responsive. As a first step towards the possible intracellular mechanism of this behavioral change we analyzed ERK1/2 activities in more details: We found a 1,7-fold increase of circadian peak levels of ERK 1/2 activities at CT10 and CT14 in synRas mice, while at minimum levels (CT18, CT22) no differences were found between ERK1/2 activities of WT and synRas mice. In WT animals the 15 minutes light pulse at CT22 resulted in rapid up regulations of Ras, ERK1/2 and CREB activities as described previously by others. However, in correlation with the lack of a behavioral response, ERK1/2 but not Ras and CREB activities remained unchanged in synRas mice, suggesting that Ras-dependent and Ras-independent pathways may co-exist to regulate ERK1/2 and behavioral phase shifts in response to the acute light treatment. Next we investigated the length "tau" of the locomotor activity rhythm during constant darkness and found a slight shortening by about 10 minutes in synRas mice as compared to the WT littermates. Recently, "tau" has been discussed to be modulated by the interaction between glycogen synthase 3beta (GSK3beta) and a clock gene product (Per 2) that is involved in the determination of circadian phase durations. We describe here a down-regulation of GSK3beta phosphorylation in synRas mice as a possible mechanism of "tau" shortening. Taken together, cycling of Ras activity at elevated levels in the SCN during the circadian rhythm results in a distinct pattern of behavioral phenotype changes correlating with de-regulated ERK1/2 or GSK3beta activities.
Poster presentation: Hyperphosphorylation of tau is a characteristic of Alzheimer's disease (AD). Our group has established a model for tau hyperphosphorylation by mutating 10 residues from Ser/Thr to Glu to simulate the negative charge of phosphorylated residues ("pseudohyperphosphorylated (PHP)-tau"). In order to analyze temporal and spatial effects of hyperphosphorylation of tau in a systemic context, we have established transgenic mouse lines that express human wild-type (wt)- or PHP-tau under the control of the CamKIIalpha-promoter that leads to a forebrain specific moderate expression in neurons, i.e. the region where also tau-pathology in AD is abundant. For the evaluation of tau-induced changes in the transgenic mice, we quantified spine densities in the neocortex and hippocampus of transgenic mice. The spine densitiy was significantly increased in PHP-tau compared to wt-tau expressing mice. It is known that AD is associated with aberrant pre- and postsynaptic sprouting. Axonal sprouting is also observed in transgenic mice expressing mutated amyloid precursor protein (APP), which suggests that Abeta plays a significant role in this process. We deduce from our results, that (pseudo)-hyperphosphorylation of tau is sufficient to induce aberrant sprouting in the absence of Abeta. Analyses whether this sprouting is induced by pre- or postsynaptic changes and if functionally active synapses are formed are in progress. It will be interesting to determine if stabilization of these newly formed synapses slows or – in contrary – accelerates the progression of the disease. Sprouting as observed in our PHP-tau expressing mice is part of neuronal differentiation. One family of enzymes that is involved in cell differentiation are mitogen-acitvated protein kinases (MAPK). Western blot analysis was performed with brain lysates from transgenic mice to check whether PHP-tau induced sprouting is associated with MAPK activation. In fact, we also observed an increased activation of the MAPK ERK1/2 evident by phosphorylation of the residues Thr202 and Tyr204. ERK1/2 is also known to phosphorylate tau at sites characteristic for AD. Our results suggest the presence of a vicious circle by which (pseudo)-hyperphosphorylated tau activates ERK1/2 which in turn phosphorylates tau.