Brain and Muscle Energy Group &

Electron Microscopy Laboratory,

Department of Oral Biology      

 

 

Linda Hildegard Bergersen, PhD  

Professor of Physiology, University of Oslo, Norway

Professor Neurobiology of Aging, University of Copenhagen, Denmark


Affiliation details:

  Professor of Physiology

Department of Oral Biology (DOB)

 

  Group Leader  

Brain and Muscle Energy Group & Electron Microscopy Laboratory 

Department of Oral Biology 

 

  Group Leader / Researcher

Brain and Muscle Energy Group & SN Lab
Division of Anatomy, Department of Molecular Medicine, Institute of Basic Medical Sciences (
IMB) &

Centre for Molecular Biology and Neuroscience (CMBN) / SERTA Healthy Brain Aging
University of Oslo, Norway

 

  Professor in Neurobiology of Aging 
Center for Healthy Aging (
CEHA) &
Department of Neuroscience and Pharmacology (
INF)
Panum Institute, Building 18.1

University of Copenhagen, Denmark

 

  Board Member

Nansen Neuroscience Network

 

Post: PO Box 1052 Blindern, 0316 Oslo, Norway

Visit: Domus Odontologica, Room A1.M068, Sognsvannsveien 9, 0372 Oslo, Norway

Telephone: +47 22840288 / Mobile telephone: +47 97032049

Email: l.h.bergersen@odont.uio.no   l.h.bergersen@medisin.uio.no

 

 

 

Linda Hildegard Bergersen obtained her PhD at the University of Oslo in 2001 under the supervision of Ole Petter Ottersen. After a postdoc period with Jon Storm-Mathisen 2002-2004, encompassing a year in Lausanne with Pierre Magistretti and Luc Pellerin in 2003, she established her own groups, in Oslo and in Copenhagen. She was leader of the SN-Lab of the CMBN and IMB 2009-2012.

Her joint positions at the Center for Healthy Aging  (CEHA), University of Copenhagen, and at the Departments of Oral Biology and of Molecular Medicine, University of Oslo, provide optimized gain from her combined expertise in molecular biology and neuroscience, particularly for healthy brain ageing and dementia research.

 
17 Linda_Bergersen Compr
 

 

 

 

 

 

 

 

 


Photo:  Elmer Laahne, for Nasjonalt medisinsk museum/Norsk teknisk museum

 

 

Overview

The function of both brain and muscle depends crucially on their energy supply. The brain uses most of its energy on electrical signalling, along and between neurons. Brain energy supply is highly dependent on glucose, but can also be sustained by lactate, eg, entering from blood during physical exercise. Lactate is produced by the brain, such as in aerobic glycolysis, for fast ATP production and generation of anabolic products for protein and lipid synthesis, and acts as a signalling molecule transmitting signals about the energy state of active brain cells. The latter concept was substantiated by our discovery of the existence and action of the lactate receptor, HCAR1 (also known as HCA1 or GPR81), in the brain (Fig 1). Our main research focus is now on the hypothesis that HCAR1 mediates some of the dementia-protective and other ameliorative effects of physical exercise on diseases of the brain. Of particular interest is whether HCAR1 activation can delay or stop cognitive decline from mild cognitive impairment into dementia.

Brain neurons contact each other at synapses. A synapse consists of a presynaptic terminal and a postsynaptic dendrite, separated by a 20 nm wide synaptic cleft, into which the neurotransmitter (eg, glutamate and GABA) is released from presynaptic vesicle stores to activate receptor proteins at outward facing binding sites. Glial cells, primarily astrocytes, tightly surround the synapse, contributing to signalling as the third member of the ‘tripartite synapse’ (Fig 2). Information transmission at synapses is based on ion fluxes through the postsynaptic cell membrane. The ions that enter or leave the cell must later be pumped out or in again, consuming energy. Whereas glutamate and GABA exert their primary effects at the synapse, part of the released transmitter molecules escape the synaptic gap and diffuse to deliver their signal via extracellular receptors in a larger volume of brain tissue surrounding the active synapse. This phenomenon is known as ‘volume transmission’ as opposed to the classical ‘wiring transmission’ restricted to the synapse.

 

 

 

 

Fig 1.  L-lactate transport and action at the ‘tripartite synapse’ of axon, dendrite, and astrocyte, and at the glio-vascular junction. Lactate, formed by glycolysis in brain cells or entering from blood, migrates down concentration gradients (of lactate and cotransported proton) between intracellular and extracellular compartments of neurons, astrocytes, and endothelial cells (orange circle), catalyzed by monocarboxylate transporters (MCT1, MCT2, and MCT4, red ovals). Lactate also migrates along the extracellular space, as well as throughout the astrocytic syncytial network via connexin gap junctions (Cx, orange oval). HCAR1 (red rectangles), lactate receptors. GLUT1 and GLUT3 (green ovals), glucose transporters. Positions of ionotropic glutamate receptors (AMPA-R, purple rectangles) and metabotropic glutamate receptors (blue serpents), influencing and influenced by lactate, are indicated. Mitochondria (dark-blue symbols) shun dendritic spines and thin astroglial processes. Astroglial processes contain glycogen particles (green spheres). From Bergersen LH (2015) Lactate transport and signaling in the brain: potential therapeutic targets and roles in body-brain interaction. J Cereb Blood Flow Metab 35(2):176-185