Prof. Dr. Uwe Heinemann

Former Heinemann group

Physiology and Pathophysiology of the hippocampal formation

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We are grieving for Professor Dr. Uwe Heinemann, the highly regarded and warmly regarded former long-standing Head of the Institute of Neurophysiology

Uwe Heinemann studied medicine in Munich. Following doctoral studies and training in Oxford, he returned to Germany, joining the Max-Planck-Institute for Physiology in Munich. In 1986, he was appointed Professor for Physiology and Pathophysiology at the University of Cologne. In 1993 he accepted a call to the Charité Berlin. His tireless commitment over the following 17 years saw the Institute of Neurophysiology develop into a research center of international renown. After retiring as Institute Head in 2010, he was appointed Senior Professor at the Neuroscience Research Center, Charité, in 2012.

Berlin's post-German unification neuroscience community was shaped to a great degree by Uwe Heinemann's tireless efforts in heading the former Institute of Physiology, later called Johannes-Müller-Institute of Physiology and his establishment of numerous large-scale research collaborative centers. He also laid the groundwork for the Charité's Cluster of Excellence NeuroCure, of which he was a founding member and co-director until 2010. His research and generous collaborative approach significantly influenced the today's Institute of Neurophysiology, specifically, and the wider field of neuroscience, more broadly.

His main research interests were mechanisms of and pharmacoresistance to epileptogenesis and, in later years, the mechanisms underlying learning and memory. Numerous international research awards and his participation in a wide range of expert panels, including those of the German Research Foundation and European Research Council, testify to the high regard he was held in by the scientific community both at home and abroad.

Research focus

  • General anaesthesia is required for surgical interventions or during treatment on intensive care units. Our principal aim is to understand possible pathophysiological mechanisms concerning neurological disorders related to anesthesia. We therefore investigate the effects of anesthetics on neuronal oscillations, neurotransmission, ion homeostasis and neuronal metabolism.

  • Blood-brain barrier dysfunction – a state of abnormal trafficking from blood to brain and vice versa – is common in patients suffering from stroke, traumatic brain injury, epilepsy, brain tumors or vascular dementia and likely influences their outcome. We induce increased BBB permeability using the neocortical photothrombosis model and investigate the role of network dysfunction, namely seizures and spreading depolarizations on tissue viability and BBB integrity.

  • Different oscillatory rhythms of the brain mediate different functions of the brain. Sharp wave ripples (SPW-Rs) in area CA3 and CA1 of the rat hippocampus occur during immobility, consummatory behavior and slow-wave sleep and play a critical role in memory consolidation. In acute rat brain slices, SPW-Rs occur together with dentate waves (DWs) of the dentate gyrus and the hilus. We investigate how neuronal ensembles can create, maintain, and modulate these rhythms.

  • Neurometabolic coupling: Energy metabolism and neural activity are tightly coupled processes. Metabolic substrates can alter neuronal activity by modulating different signaling pathways. This makes them alternative therapeutic targets for conditions like seizure disorders. Apart from glucose, the brain can utilize alternative energy substrates such aslactate, ketone bodies, glutamate etc. Lactate, once considered a mere glycolytic byproduct, has been shown to alter neuronal activity through a G protein-coupled receptor (GP81). Hence, we investigate the role of intrinsic lactate for neuronal metabolism, synaptic transmission, ionic homeostasis and pathological network activity in acute rat slices and neocortical slices from patients with temporal lobe epilepsy.

Methods

  • Simultaneous recordings of intra- and extracellular potentials, ion concentrations and partial Oxygen  pressure in acute brain slices and in-vivo in anesthetized animals under controlled Ventilation (CO2-Monitoring) and monitored cardiovascular System

  • Imaging of FAD, NAD(P)H and intracellular Calcium

  • In vivo imaging to assess vascular reactivity, BBB-permeability and cell viability

Team

Dr. Karl Schoknecht (Klinik für Neurologie / Experimentelle Neurologie, CCM, Charité)
Dr. Agustin Liotta (Klinik für Anästhesie mit Schwerpunkt operative Intensivmedizin, Charité)

Alumni

Dr. med. Sigrun Gabriel
Dr. rer. nat. Hans-Jürgen Gabriel
Prof. Dr. med. Oliver Kann

Dr. Eskedar Ayele Angamo
Dr. med. Christoph J. Behrens
Dr. Anne Boehlen
Dr. Gürsel Caliskan
Dr. Nora Dengler
Dr. Silvia Fano
Dr. Rizwan Ul Haq
Dr. Jan Oliver Hollnagel
 Dr. Sebastian Ivens
Dr. Simon Kim
Dr. Ezequiel Lapilover
Dr. Kristina Lippmann
Dr. Anna Maslarova
Dr. Julia Nichtweiß
Dipl. Biol. Anton Rösler
Dr. Seda Salar
Tanja Specowius
Dr. Anna Wójtowicz
Bifeng Wu
Dipl. Ing. Karin Berlin
Prof. Dr. med. Klaus Albus (Guest scientist)
Prof. Dr. Alon Friedman MD PhD (Guest scientist)

Publications

all publications of Prof. Dr. Uwe Heinemann

 

selected publications:

Schoknecht K, Berndt N, Rösner J, Heinemann U, Dreier JP,  Kovàcs R, Friedman A, Liotta A. Event-associated oxygen consumption rate increases ~5-fold when interictal activity transforms into seizure-like events in vitro. Int J Mol Sci 2017;18(9) PubMed Central

Rösner J, Liotta A, Angamo EA, Spies C, Heinemann U, Kovács R. Minimizing photodecomposition of flavin adenine dinucleotide fluorescence by the use of pulsed LEDs.J Microsc. 2016 Nov. PubMed 

Schoknecht K, David Y, Heinemann U. The blood–brain barrier—Gatekeeper to neuronal homeostasis: Clinical implications in the setting of stroke. Semin Cell Dev Biol 2015:38/35-42. PubMed

Schoknecht K, Prager O, Vazana U, Kamintsky L, Harhausen D, Zille M, Figge L, Chassidim Y, Schellenberger E, Kovács R, Heinemann U, Friedman A. Monitoring stroke progression: in vivo imaging of cortical perfusion, blood-brain barrier permeability and cellular damage in the rat photothrombosis model. J Cereb Blood Flow Metab 2014:34/11,1791-80. PubMed Central

Rösner J, Liotta A, Schmitz D, Heinemann U, Kovács R. A LED-based method for monitoring NAD(P)H and FAD fluorescence in cell cultures and brain slices. J Neurosci Methods. 2013 Jan. PubMed

Liotta A, Rösner J, Huchzermeyer C, Wojtowicz A, Kann O, Schmitz D, Heinemann U, Kovács R. Energy demand of synaptic transmission at the hippocampal Schaffer-collateral synapse. J Cereb Blood Flow Metab. 2012 Nov. PubMed

Liotta A, Caliskan G, ul Haq R, Hollnagel JO, Rösler A, Heinemann U, Behrens CJ. Partial disinhibition is required for transition of stimulus-induced sharp wave-ripple complexes into recurrent epileptiform discharges in rat hippocampal slices. J Neurophysiol. 2011 Jan. PubMed