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Systemische Neurophysiologie

Arbeitsgruppenleiter
Prof. Dr. rer. nat. Cornelius Schwarz
Tel. 07071 29 80462
Fax 07071 29 5724

Ziele

  1. Interaktion von Bewegungssignalen und taktiler Wahrnehmung. Ratten führen palpatorische Bewegungen ihrer Vibrissen aus um Objektoberflächen und  -formen zu diskriminieren. Mittels Multielektrodenexperimenten in sensorischen und motorischen neocortikalen Arealen in Ratten, die Vibrissenbewegung und/oder taktile Diskriminationsaufgaben ausführen, wird untersucht wie motorische Signale taktile Signalprozessierung beeinflussen.
  2. Untersuchung von Grundlagen der Multielektrodenstimulation im Vibrissensystem. Es sollen Methoden für die zielgerichtete Nutzung von ZNS-Multielektrodenimplantaten für die neurologische Rehabilitation entwickelt werden.


Methoden

  1. Operantes Training von Ratten
  2. Echtzeitmessung von Vibrissentrajektorien und taktile Vibrissenstimulation
  3. Elektrophysiologische Registrierungen über implantierte Mikroelektrodenarrays
  4. Multielektroden Mikrostimulation


Schlüsselpublikationen

  • Haiss F, Schwarz C (2005) Spatial segregation of different modes of movement control in the whisker representation of rat primary motor cortex. J Neurosci 25:1579-1587
  • Hentschke H, Haiss F, Schwarz C (2006) Central signals rapidly switch tactile processing in rat barrel cortex during whisker movements. Cerebral Cortex 16:1142-1156
  • Stüttgen MC, Rüter J, Schwarz C (2006) Two psychophysical channels of whisker deflection in rats align with two neuronal classes of primary afferents. J Neurosci 26:7933-7941.
  • Stüttgen MC, Schwarz C (2008) Psychophysical and neurometric detection performance under stimulus uncertainty. Nat Neurosci 11:1091-1099
  • Gerdjikov TV, Bergner CG, Stüttgen MC, Waiblinger C, Schwarz C (2010) Discrimination of vibrotactile stimuli in the rat whisker system - behavior and neurometrics. Neuron 65:530-540
  • Butovas S, Schwarz C (2003) Spatiotemporal effects of microstimulation in rat neocortex: a parametric study using multielectrode recordings. J Neurophysiol 90: 3024
  • Butovas S, Hormuzdi SG, Monyer H, Schwarz C (2006) Effects of electrically coupled inhibitory networks on local neuronal responses to intracortical microstimulation. J Neurophysiol 96:1227-1236.
  • Butovas S, Schwarz C (2007) Intracortical microstimulation in barrel cortex of awake, head-restraint rats: assessment of detection thresholds. Eur J Neurosci 25:2161-2169


Lehre

  1. Lecture Neurophysiology Graduate School of Cognitive and Behavioural Neuroscience (Schwarz, Pedroarena, Antkowiak). Winter term. In English.
  2. Lab Practical Neurophysiology (Schwarz, Pedroarena, Antkowiak, Hentschke). Open for students of the Graduate School of Cognitive and Behavioural Neuroscience, Medicine, Psychology, Sciences. HIH Otfried Müller Str. 27, August, 1 week block. In English.



In vitro Electrophysiology Lab

Head
Christine Pedroarena, MD

Intrinsic and synaptic mechanisms determining cerebellar nuclei neurons spike output
Although all forms of cerebellar dysfunction are characterized by severe impairment in the timing of muscular activation and consequent uncoordinated movements, the cellular underpinnings of the cerebellum control of movement remains unknown. Our research is focused on the neurons of the deep cerebellar nuclei (DCN) which carry almost all cerebellar output signals and are the main target of the cerebellar cortex signals. Despite their central position in the cerebellar system, the internal micro-circuits and cellular mechanisms determining DCN output are still poorly understood. Moreover, in many types of cerebellar diseases, deep cerebellar nuclei neurons are spared and their function is altered only secondarily to the alterations occurring at the cerebellar cortex. Hence, cerebellar nuclei are a natural place for compensatory mechanisms for diseases affecting the cerebellar cortex. The general aim of this research is to understand the cellular mechanism that control DCNs output. Particularly, three areas are currently investigated:

  1. The ionic mechanisms controlling spontaneous end evoked firing of DCNs.
  2. How synaptic and intrinsic mechanisms interact to support transfer of information from the Purkinje cells to the DCNs.
  3. DCN neurons are a heterogeneous population with different neurotransmitter content and projection patterns. We are investigating how connectivity and cellular properties of each DCN type determine its specific output.

Finally we are interested in the potential plasticity of the above mentioned mechanisms.

Methods

  1. in vitro electrophysiology using whole cell patch recordings
  2. brain slices taken from wild type and transgenic animals
  3. immuno-histochemistry and intracellular staining techniques  

 

Key publications

  • Pedroarena CM, Kamphausen S (2008) Glycinergic synaptic currents in the deep cerebellar nuclei. Neuropharmacology 54: 784-795.
  • Sausbier M, Hu H, Arntz C, Feil S, Kamm S, Adelsberger H, Sausbier U, Sailer CA, Feil R, Hofmann F, Korth M, Shipston MJ, Knaus HG, Wolfer DP, Pedroarena CM, Storm JF, Ruth P (2004) Cerebellar ataxia and Purkinje cell dysfunction caused by Ca2+-activated K+ channel deficiency. Proc Natl Acad Sci U S A 101: 9474-9478.
  • Linnemann C, Sultan F, Pedroarena CM, Schwarz C, Thier P (2004) Lurcher mice exhibit potentiation of GABA(A)-receptor-mediated conductance in cerebellar nuclei neurons in close temporal relationship to Purkinje cell death. J Neurophysiol 91: 1102-1107.
  • Pedroarena CM, Schwarz C (2003) Efficacy and short-term plasticity at GABAergic synapses between Purkinje and cerebellar nuclei neurons. J Neurophysiol 89: 704-715.