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Burg bei Magdeburg, Germany

Krautwald K.,Functional Neuroimaging Group | Angenstein F.,Leibniz Institute for Neurobiology Magdeburg | Angenstein F.,Otto Von Guericke University of Magdeburg | Angenstein F.,Center for Behavioural Brain science
Journal of Cerebral Blood Flow and Metabolism | Year: 2012

To study how various anesthetics affect the relationship between stimulus frequency and generated functional magnetic resonance imaging (fMRI) signals in the rat dentate gyrus, the perforant pathway was electrically stimulated with repetitive low frequency (i.e., 0.625, 1.25, 2.5, 5, and 10 Hz) stimulation trains under isoflurane/N 2 O, isoflurane, medetomidine, and α-chloralose. During stimulation, the blood oxygen level-dependent signal intensity (BOLD response) and local field potentials in the dentate gyrus were simultaneously recorded to prove whether the present anesthetic controls the generation of a BOLD response via targeting general hemodynamic parameters, by affecting mechanisms of neurovascular coupling, or by disrupting local signal processing. Using this combined electrophysiological/fMRI approach, we found that the threshold frequency (i.e., the minimal frequency required to trigger significant BOLD responses), the optimal frequency (i.e., the frequency that elicit the strongest BOLD response), and the spatial distribution of generated BOLD responses are specific for each anesthetic used. Concurrent with anesthetic-dependent characteristics of the BOLD response, we found the pattern of stimulus-induced neuronal activity in the dentate gyrus is also specific for each anesthetic. Consequently, the anesthetic-specific influence on local signaling processes is the underlying cause for the observation that an identical stimulus elicits different BOLD responses under various anesthetics. © 2012 ISCBFM All rights reserved.

Tiede R.,Leibniz Institute for Neurobiology | Krautwald K.,Functional Neuroimaging Group | Fincke A.,Leibniz Institute for Neurobiology | Angenstein F.,Leibniz Institute for Neurobiology | And 3 more authors.
Journal of Cerebral Blood Flow and Metabolism | Year: 2012

The role of N-methyl-D-aspartate (NMDA) receptor-mediated mechanisms in the formation of a blood oxygen level-dependent (BOLD) response was studied using electrical stimulation of the right perforant pathway. Stimulation of this fiber bundle triggered BOLD responses in the right hippocampal formation and in the left entorhinal cortex. The perforant pathway projects to and activates the dentate gyrus monosynaptically, activation in the contralateral entorhinal cortex is multisynaptic and requires forwarding and processing of signals. Application of the NMDA receptor antagonist MK801 during stimulation had no effect on BOLD responses in the right dentate gyrus, but reduced the BOLD responses in the left entorhinal cortex. In contrast, application of MK801 before the first stimulation train reduced the BOLD response in both regions. Electrophysiological recordings revealed that the initial stimulation trains changed the local processing of the incoming signals in the dentate gyrus. This altered electrophysiological response was not further changed by a subsequent application of MK801, which is in agreement with an unchanged BOLD response. When MK801 was present during the first stimulation train, a dissimilar electrophysiological response pattern was observed and corresponds to an altered BOLD response, indicating that NMDA-dependent mechanisms indirectly affect the BOLD response, mainly via modifying local signal processing and subsequent propagation. © 2012 ISCBFM All rights reserved.

Hoffmann M.B.,Otto Von Guericke University of Magdeburg | Hoffmann M.B.,Center for Behavioural Brain science | Thieme H.,Otto Von Guericke University of Magdeburg | Liedecke K.,Otto Von Guericke University of Magdeburg | And 3 more authors.
Investigative Ophthalmology and Visual Science | Year: 2015

PURPOSE. Numerous animal studies demonstrated the importance of components of the ephrin/Eph system for correct visual system development. Analogous investigations in humans are entirely missing. Here, we examined the visual system in humans with ephrin-B1 deficiency, which is x-linked and associated with the cranio-fronto-nasal syndrome (CFNS) in heterozygous females. METHODS. For one male hemizygous for ephrin-B1 deficiency and three affected heterozygous females with molecular-genetically confirmed mutations, the integrity of the partial decussation of the optic nerves was assessed with visual evoked potentials (VEPs) and compared with albinotic, achiasmic, and control participants with healthy vision. Further, retinal morphology and function and the gross-retinotopic representation of the primary visual cortex were examined with spectral-domain optical coherence tomography (SD-OCT), ERG, and multifocal (mf) VEPs for the male participant and part of the carriers. RESULTS. Strabismus and lack of stereovision was evident in the male and two of the females. Other characteristics of the visual system organization and function were normal: (1) retina: SD-OCT and funduscopy indicated normal foveal and optic nerve head morphology. Electroretinograms indicated normal retinal function, (2) optic chiasm: conventional (c)VEP showed no evidence for misrouting and mfVEPs were only suggestive of, if any, very minor local misrouting, and (3) visual cortex: mfVEP characteristics indicated normal retinotopic gross-representations of the contralateral visual hemifield in each hemisphere. CONCLUSIONS. While ephrin-B1 deficiency leads to abnormal visual pathways in mice, it leaves the human visual system, apart from deficits in binocular vision, largely normal. We presume that other components of the ephrin-system can substitute the lack of ephrin-B1 in humans. © 2015 The Association for Research in Vision and Ophthalmology, Inc.

Sharvit A.,Haifa University | Segal M.,Weizmann Institute of Science | Kehat O.,Haifa University | Stork O.,Otto Von Guericke University of Magdeburg | And 2 more authors.
Stress | Year: 2015

Depending on its severity, timing and context, stress has been shown to have a differential regional effect on hippocampal synaptic plasticity. While the focus of attention in most recent studies is on excitatory synapses and generation, modifications of inhibitory synapses and local interneurons cannot be ignored. We have now examined the effects of corticosterone (CORT) on extrinsic afferent and local circuit plasticity of the perforant path on the dentate gyrus (DG) and the ventral hippocampal commissure on CA1. Local circuit activity was measured by responses to paired-pulse stimulation. Control rats expressed afferent long-term potentiation (LTP) and local circuit plasticity in both the DG and CA1. Administration of a high dosage of CORT-reduced paired-pulse inhibition and increased facilitation in DG but not in CA1, whereas administration of a moderate CORT dosage had no effect. Moderate CORT doses caused enhancement of LTP in the DG but not in CA1, while high CORT doses converted LTP to long-term depression in the CA1 but had no effect in the DG. CORT blocked theta burst stimulation-induced local circuit plasticity otherwise found in control DG. These findings suggest that elevation of the level of CORT results in a regionally differentiated physiological response. In addition, the results indicate that CORT affects aspects of local circuit activity and plasticity in the DG but less so in the CA1. It is possible that these differentiated alterations underlie some of the behavioral consequences and memory processes under stressful conditions. © 2015 © 2015 Informa UK Ltd.

Teuber J.,Otto Von Guericke University of Magdeburg | Mueller B.,Otto Von Guericke University of Magdeburg | Fukabori R.,Otto Von Guericke University of Magdeburg | Lang D.,Otto Von Guericke University of Magdeburg | And 3 more authors.
PLoS ONE | Year: 2013

Evidence suggests that regulated ubiquitination of proteins plays a critical role in the development and plasticity of the central nervous system. We have previously identified the ubiquitin ligase Praja1 as a gene product induced during fear memory consolidation. However, the neuronal function of this enzyme still needs to be clarified. Here, we investigate its involvement in the nerve growth factor (NGF)-induced differentiation of rat pheochromocytoma (PC12) cells. Praja1 co-localizes with cytoskeleton components and the neurotrophin receptor interacting MAGE homologue (NRAGE). We observed an enhanced expression of Praja1 after 3 days of NGF treatment and a suppression of neurite formation upon Praja1 overexpression in stably transfected PC12 cell lines, which was associated with a proteasome-dependent reduction of NRAGE levels. Our data suggest that Praja1, through ubiquitination and degradation of NRAGE, inhibits neuronal differentiation. The two murine isoforms, Praja1.1 and Praja1.2, appear to be functionally homologous in this respect. © 2013 Teuber et al.

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