Oliver M. Schlüter

ORCID: 0000-0001-8958-5815
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About
Contact & Profiles
Research Areas
  • Neuroscience and Neuropharmacology Research
  • Neurotransmitter Receptor Influence on Behavior
  • Neural dynamics and brain function
  • Memory and Neural Mechanisms
  • Receptor Mechanisms and Signaling
  • Cellular transport and secretion
  • Retinal Development and Disorders
  • Photoreceptor and optogenetics research
  • Parkinson's Disease Mechanisms and Treatments
  • Sleep and Wakefulness Research
  • Zebrafish Biomedical Research Applications
  • Alzheimer's disease research and treatments
  • Neuroscience and Neural Engineering
  • Nerve injury and regeneration
  • Cannabis and Cannabinoid Research
  • Neuroinflammation and Neurodegeneration Mechanisms
  • Erythrocyte Function and Pathophysiology
  • Treatment of Major Depression
  • Gene Regulatory Network Analysis
  • Lipid Membrane Structure and Behavior
  • Nuclear Receptors and Signaling
  • Signaling Pathways in Disease
  • Neuroendocrine regulation and behavior
  • Neurological diseases and metabolism
  • Neurobiology and Insect Physiology Research

University of Pittsburgh
2014-2024

Universitätsmedizin Göttingen
2017-2024

University of Göttingen
2009-2023

Institut du Cerveau
2022

Leibniz Institute for Agricultural Engineering and Bioeconomy
2010-2021

University of Bologna
2021

European Neuroscience Institute Göttingen
2008-2020

Nanoscale Microscopy and Molecular Physiology of the Brain Cluster of Excellence 171 — DFG Research Center 103
2012-2017

Max Planck Institute of Experimental Medicine
2000-2010

Stanford University
2006-2009

In animals, sporadic injections of the mitochondrial toxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) selectively damage dopaminergic neurons but do not fully reproduce features human Parkinson's disease. We have now developed a mouse disease model that is based on continuous MPTP administration with an osmotic minipump and mimics many Although both led to severe striatal dopamine depletion nigral cell loss, we find only produced progressive behavioral changes triggered formation...

10.1073/pnas.0409713102 article EN Proceedings of the National Academy of Sciences 2005-02-16

Rab3A, Rab3B, Rab3C, and Rab3D are closely related GTP-binding proteins of synaptic vesicles that may function in neurotransmitter release. We have produced knock-out (KO) mice for Rab3B Rab3C crossed them with previously generated Rab3A 3D to generate double, triple, quadruple Rab3 mice. found all single double viable fertile. Most triple perish whenever is one the three deleted proteins, whereas express Finally, die shortly after birth. Quadruple KO initially develop normally born alive...

10.1523/jneurosci.1610-04.2004 article EN cc-by-nc-sa Journal of Neuroscience 2004-07-21

Presynaptic vesicle trafficking and priming are important steps in regulating synaptic transmission plasticity. The four closely related small GTP-binding proteins Rab3A, Rab3B, Rab3C, Rab3D believed to be for these steps. In mice, the complete absence of all Rab3s leads perinatal lethality accompanied by a 30% reduction probability Ca 2+ -triggered release. This study examines role Rab3 during release more detail identifies its impact on short-term Using patch-clamp electrophysiology...

10.1523/jneurosci.3553-05.2006 article EN cc-by-nc-sa Journal of Neuroscience 2006-01-25

Locomotor sensitization is a common and robust behavioral alteration in rodents whereby following exposure to abused drugs such as cocaine, the animal becomes significantly more hyperactive response an acute drug challenge. Here, we further analyzed role of cocaine-induced silent synapses nucleus accumbens (NAc) shell their contribution development locomotor sensitization. Using combination viral vector-mediated genetic manipulations, biochemistry, electrophysiology paradigm with repeated,...

10.1523/jneurosci.0016-11.2011 article EN cc-by-nc-sa Journal of Neuroscience 2011-06-01

Significance Experimental animals are usually raised in small, so-called standard cages, depriving them of numerous natural stimuli. We show that raising mice an enriched environment, allowing enhanced physical, social, and cognitive stimulation, preserved a juvenile brain into adulthood. Enrichment also rejuvenated the visual cortex after extended periods cage rearing protected adult from stroke-induced impairments cortical plasticity. Because local inhibitory tone was not only...

10.1073/pnas.1313385111 article EN Proceedings of the National Academy of Sciences 2014-01-06

Significance During critical periods, cortical neural circuits are refined to optimize their functional properties. The prevailing notion is that the balance between excitation and inhibition determines onset closure of periods. Here, we show postsynaptic density protein-95 (PSD-95)–dependent maturation silent glutamatergic synapses onto principal neurons was sufficient govern duration period for ocular dominance plasticity (ODP) in visual cortex mice. Loss PSD-95 before CPs resulted...

10.1073/pnas.1506488112 article EN Proceedings of the National Academy of Sciences 2015-05-26

Rab3A and rab3C are GTP-binding proteins of synaptic vesicles that regulate vesicle exocytosis. Rabphilin is a candidate rab3 effector at the synapse because it binds to rab3s in GTP-dependent manner, co-localized with on vesicles, dissociates from during contains two C(2) domains, which could function as Ca(2+) sensors exocytosis phosphorylated stimulation. However, unknown what essential function, if any, rabphilin performs. One controversial question regards respective roles localizing...

10.1523/jneurosci.19-14-05834.1999 article EN cc-by-nc-sa Journal of Neuroscience 1999-07-15

Rab3A, Rab3B, Rab3C, and Rab3D constitute a family of GTP-binding proteins that are implicated in regulated exocytosis. Various localizations distinct functions have been proposed for different occasionally even the same Rab3 protein. This is exemplified by studies demonstrating deletion Rab3A knock-out mice results dysregulation final stages exocytosis, whereas overexpression neuroendocrine cells causes nearly complete inhibition Ca2+-triggered We now examined properties all assays, with...

10.1074/jbc.m203704200 article EN cc-by Journal of Biological Chemistry 2002-10-01

Drug-induced malfunction of nucleus accumbens (NAc) neurons underlies a key pathophysiology drug addiction. changes in intrinsic membrane excitability NAc are thought to be critical for producing behavioral alterations. Previous studies demonstrate that, after short-term (2 d) or long-term (21 withdrawal from noncontingent cocaine injection, the shell (NAcSh) is decreased, and decreased NAcSh increases acute locomotor response cocaine. However, animals exhibit distinct cellular alterations...

10.1523/jneurosci.4063-09.2010 article EN cc-by-nc-sa Journal of Neuroscience 2010-03-10

Stable brain function relies on homeostatic maintenance of the functional output individual neurons. In general, neurons by converting synaptic input to as action potential firing. To determine mechanisms that balance this input–output/synapse–membrane interaction, we focused nucleus accumbens (NAc) and demonstrated a novel form synapse-to-membrane regulation, synapse-driven membrane plasticity ( h SMP). Through SMP, NAc adjusted their excitability functionally compensate for basal shifts in...

10.1523/jneurosci.5703-08.2009 article EN cc-by-nc-sa Journal of Neuroscience 2009-05-06
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