@article{HeckmannPauli2022,
  author    = {Heckmann, Manfred and Pauli, Martin},
  title     = {Visualizing presynaptic active zones and synaptic vesicles},
  series = {Frontiers in Synaptic Neuroscience},
  volume    = {14},
  journal   = {Frontiers in Synaptic Neuroscience},
  issn      = {1663-3563},
  doi       = {10.3389/fnsyn.2022.901341},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-274687},
  year      = {2022},
  abstract  = {The presynaptic active zone (AZ) of chemical synapses is a highly dynamic compartment where synaptic vesicle fusion and neurotransmitter release take place. During evolution the AZ was optimized for speed, accuracy, and reliability of chemical synaptic transmission in combination with miniaturization and plasticity. Single-molecule localization microscopy (SMLM) offers nanometer spatial resolution as well as information about copy number, localization, and orientation of proteins of interest in AZs. This type of imaging allows quantifications of activity dependent AZ reorganizations, e.g., in the context of presynaptic homeostatic potentiation. In combination with high-pressure freezing and optogenetic or electrical stimulation AZs can be imaged with millisecond temporal resolution during synaptic activity. Therefore SMLM allows the determination of key parameters in the complex spatial environment of AZs, necessary for next generation simulations of chemical synapses with realistic protein arrangements.},
  language  = {en}
}
@article{PauliPaulProppertetal.2021,
  author    = {Pauli, Martin and Paul, Mila M. and Proppert, Sven and Mrestani, Achmed and Sharifi, Marzieh and Repp, Felix and K{\"u}rzinger, Lydia and Kollmannsberger, Philip and Sauer, Markus and Heckmann, Manfred and Sir{\´e}n, Anna-Leena},
  title     = {Targeted volumetric single-molecule localization microscopy of defined presynaptic structures in brain sections},
  series = {Communications Biology},
  volume    = {4},
  journal   = {Communications Biology},
  doi       = {10.1038/s42003-021-01939-z},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-259830},
  pages     = {407},
  year      = {2021},
  abstract  = {Revealing the molecular organization of anatomically precisely defined brain regions is necessary for refined understanding of synaptic plasticity. Although three-dimensional (3D) single-molecule localization microscopy can provide the required resolution, imaging more than a few micrometers deep into tissue remains challenging. To quantify presynaptic active zones (AZ) of entire, large, conditional detonator hippocampal mossy fiber (MF) boutons with diameters as large as 10 mu m, we developed a method for targeted volumetric direct stochastic optical reconstruction microscopy (dSTORM). An optimized protocol for fast repeated axial scanning and efficient sequential labeling of the AZ scaffold Bassoon and membrane bound GFP with Alexa Fluor 647 enabled 3D-dSTORM imaging of 25 mu m thick mouse brain sections and assignment of AZs to specific neuronal substructures. Quantitative data analysis revealed large differences in Bassoon cluster size and density for distinct hippocampal regions with largest clusters in MF boutons. Pauli et al. develop targeted volumetric dSTORM in order to image large hippocampal mossy fiber boutons (MFBs) in brain slices. They can identify synaptic targets of individual MFBs and measured size and density of Bassoon clusters within individual untruncated MFBs at nanoscopic resolution.},
  language  = {en}
}
@article{BeckEhmannAndlaueretal.2015,
  author    = {Beck, Katherina and Ehmann, Nadine and Andlauer, Till F. M. and Ljaschenko, Dmitrij and Strecker, Katrin and Fischer, Matthias and Kittel, Robert J. and Raabe, Thomas},
  title     = {Loss of the Coffin-Lowry syndrome-associated gene RSK2 alters ERK activity, synaptic function and axonal transport in Drosophila motoneurons},
  series = {Disease Models \& Mechanisms},
  volume    = {8},
  journal   = {Disease Models \& Mechanisms},
  doi       = {10.1242/dmm.021246},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-145185},
  pages     = {1389-1400},
  year      = {2015},
  abstract  = {Plastic changes in synaptic properties are considered as fundamental for adaptive behaviors. Extracellular-signal-regulated kinase (ERK)-mediated signaling has been implicated in regulation of synaptic plasticity. Ribosomal S6 kinase 2 (RSK2) acts as a regulator and downstream effector of ERK. In the brain, RSK2 is predominantly expressed in regions required for learning and memory. Loss-of-function mutations in human RSK2 cause Coffin-Lowry syndrome, which is characterized by severe mental retardation and low IQ scores in affected males. Knockout of RSK2 in mice or the RSK ortholog in Drosophila results in a variety of learning and memory defects. However, overall brain structure in these animals is not affected, leaving open the question of the pathophysiological consequences. Using the fly neuromuscular system as a model for excitatory glutamatergic synapses, we show that removal of RSK function causes distinct defects in motoneurons and at the neuromuscular junction. Based on histochemical and electrophysiological analyses, we conclude that RSK is required for normal synaptic morphology and function. Furthermore, loss of RSK function interferes with ERK signaling at different levels. Elevated ERK activity was evident in the somata of motoneurons, whereas decreased ERK activity was observed in axons and the presynapse. In addition, we uncovered a novel function of RSK in anterograde axonal transport. Our results emphasize the importance of fine-tuning ERK activity in neuronal processes underlying higher brain functions. In this context, RSK acts as a modulator of ERK signaling.},
  language  = {en}
}