Michael Kintscher

ORCID: 0000-0003-2355-1369
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About
Contact & Profiles
Research Areas
  • Neuroscience and Neuropharmacology Research
  • Neural dynamics and brain function
  • Memory and Neural Mechanisms
  • Cellular transport and secretion
  • Photoreceptor and optogenetics research
  • Lipid Membrane Structure and Behavior
  • Genetics and Neurodevelopmental Disorders
  • Ion Transport and Channel Regulation
  • Neural and Behavioral Psychology Studies
  • Epilepsy research and treatment
  • Stress Responses and Cortisol
  • Biomedical Research and Pathophysiology
  • Cholesterol and Lipid Metabolism
  • Genomics and Rare Diseases
  • Adipose Tissue and Metabolism
  • Sphingolipid Metabolism and Signaling
  • Endoplasmic Reticulum Stress and Disease
  • Mitochondrial Function and Pathology
  • Ion channel regulation and function
  • RNA regulation and disease
  • Neurogenesis and neuroplasticity mechanisms
  • Sensor Technology and Measurement Systems
  • Cell Image Analysis Techniques
  • Calcium signaling and nucleotide metabolism
  • Retinal Development and Disorders

Charité - Universitätsmedizin Berlin
2009-2023

Freie Universität Berlin
2023

École Polytechnique Fédérale de Lausanne
2018-2023

Humboldt-Universität zu Berlin
2023

Hertie Institute for Clinical Brain Research
2023

Technische Universität Braunschweig
2009

The amygdala is a brain area critical for the formation of fear memories. However, nature teaching signal(s) that drive plasticity in are still under debate. Here, we use optogenetic methods to investigate contribution ventral tegmental (VTA) dopamine neurons auditory-cued learning male mice. Using anterograde and retrograde labeling, found sparse relatively evenly distributed population VTA projects basal (BA). In vivo optrode recordings behaving mice showed many neurons, among them...

10.1523/jneurosci.1796-19.2020 article EN cc-by-nc-sa Journal of Neuroscience 2020-04-10

Significance Brain function depends on neurotransmission, and alterations in this process are linked to neuropsychiatric disorders. Neurotransmitter release requires the rapid recycling of synaptic vesicles (SVs) by endocytosis. How synapses can rapidly regenerate SVs, yet preserve their molecular composition, is poorly understood. We demonstrate that mice lacking endocytic protein stonin 2 (Stn2) show changes exploratory behavior defects SV whereas speed at which SVs regenerated increased....

10.1073/pnas.1218432110 article EN Proceedings of the National Academy of Sciences 2013-01-23

IRSp53 is an essential intermediate between the activation of Rac and Cdc42 GTPases formation cellular protrusions; it affects cell shape by coupling membrane-deforming activity with actin cytoskeleton. highly expressed in neurons where also abundant component postsynaptic density (PSD). Here we analyze physiological function this protein mouse brain generating IRSp53-deficient mice. Neurons hippocampus young adult knock-out (KO) mice do not exhibit morphological abnormalities vivo....

10.1074/jbc.m808425200 article EN cc-by Journal of Biological Chemistry 2009-02-11

Learning about threats is essential for survival. During threat learning, an innocuous sensory percept such as a tone acquires emotional meaning when paired with aversive stimulus mild footshock. The amygdala critical memory formation, but little known upstream brain areas that process somatosensory information. Using optogenetic techniques in mice, we found silencing of the posterior insula during footshock reduced acute fear behavior and impaired 1-day memory. Insular cortex neurons...

10.1126/science.aaw0474 article EN Science 2019-05-16

During fear learning, defensive behaviors like freezing need to be finely balanced in the presence or absence of threat-predicting cues (conditioned stimulus, CS). Nevertheless, circuits underlying such balancing are largely unknown. Here, we investigate role ventral tail striatum (vTS) auditory-cued learning male mice. In vivo Ca 2+ imaging showed that sizable sub-populations direct (D1R+) and indirect pathway neurons (Adora+) vTS responded footshocks, initiation movements after freezing;...

10.7554/elife.75703 article EN cc-by eLife 2023-01-19

STX1 is a major neuronal syntaxin protein located at the plasma membrane of tissues. Rodent has two highly similar paralogs, STX1A and STX1B, that are thought to be functionally redundant. Interestingly, some studies have shown distribution patterns STX1B central peripheral nervous systems only partially overlapped, implying there might differential functions between these paralogs. In current study, we generated an knockout (KO) mouse line studied impact removal in neurons several brain...

10.1152/jn.00577.2015 article EN Journal of Neurophysiology 2015-07-23

Activation of the basal forebrain (BF) has been associated with increased attention, arousal, and a heightened cortical representation external world. In addition, BF implicated in regulation default mode network (DMN) behaviors. Here, we provide causal evidence for role DMN regulation, highlighting prominent parvalbumin (PV) GABAergic neurons. The optogenetic activation PV neurons reliably drives animals toward DMN-like behaviors, no effect on memory encoding. contrast, electrical...

10.1016/j.celrep.2020.108359 article EN cc-by Cell Reports 2020-11-01

The maturation of glutamatergic synapses in the CNS is regulated by NMDA receptors (NMDARs) that gradually change from a GluN2B- to GluN2A-dominated subunit composition during postnatal development. Here we show NMDARs control activity small GTPase ADP-ribosylation factor 6 (Arf6) consecutively recruiting two related brefeldin A-resistant Arf guanine nucleotide exchange factors, BRAG1 and BRAG2, GluN2 subunit-dependent manner. In young cortical cultures, GluN2B tonically activated Arf6....

10.1074/jbc.m115.691717 article EN cc-by Journal of Biological Chemistry 2016-02-17

The subiculum (SUB) is a pivotal structure positioned between the hippocampus proper and various cortical subcortical areas. Despite growing body of anatomical intrinsic electrophysiological data subicular neurons, modulation synaptic transmission in SUB not well understood. In present study we investigated role group II metabotropic glutamate receptors (mGluRs), which have been shown to be involved regulation by suppressing presynaptic cAMP activity. Using field potential patch-clamp whole...

10.1371/journal.pone.0045039 article EN cc-by PLoS ONE 2012-09-11

Abstract The Phospholipid Phosphatase Related 4 gene (PLPPR4, *607813) encodes the Plasticity-Related-Gene-1 (PRG-1) protein. This cerebral synaptic transmembrane-protein modulates cortical excitatory transmission on glutamatergic neurons. In mice, homozygous Prg-1 deficiency causes juvenile epilepsy. Its epileptogenic potential in humans was unknown. Thus, we screened 18 patients with infantile epileptic spasms syndrome (IESS) and 98 benign familial neonatal/infantile seizures (BFNS/BFIS)...

10.1093/cercor/bhad051 article EN Cerebral Cortex 2023-03-28

Summary The amygdala is a brain area critical for the formation of threat memories. However, nature teaching signal(s) that drive plasticity in are still under debate. Here, we use optogenetic methods to investigate whether dopamine release contributes fear learning. Antero- and retrograde labeling showed sparse, relatively evenly distributed population ventral tegmental (VTA) neurons projects basal (BA). In-vivo optrode recordings behaving mice many VTA neurons, amongst them putative...

10.1101/716589 preprint EN cc-by-nc-nd bioRxiv (Cold Spring Harbor Laboratory) 2019-07-26

ABSTRACT Plasticity related gene 1 encodes a cerebral neuron-specific synaptic transmembrane protein that modulates hippocampal excitatory transmission on glutamatergic neurons. In mice, homozygous Prg1-deficiency results in juvenile epilepsy. Screening cohort of 18 patients with infantile spasms (West syndrome), we identified one patient heterozygous mutation the highly conserved third extracellular phosphatase domain (p.T299S). The functional relevance this was verified by in-utero...

10.1101/282871 preprint EN bioRxiv (Cold Spring Harbor Laboratory) 2018-03-15
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