The main focus of our research is proteins that play a role in synaptic plasticity. We monitor changes in the function of these proteins and their role in synaptic disease.
The main objective of our research is to investigate the molecular and cellular determinants of behavior and cognition. Specifically, we focus on the role of distinct proteins in synaptic plasticity and pathology of the brain. Change in the function of these proteins may contribute to or be a result of synaptic disease. Our main approach to research on synaptic plasticity is quantitative analysis of images of CNS synapses.
The brain contains about 100 billion neurons. These nerve cells communicate with each other through 164 trillion points of contact or synapses. Recent research shows that these synapses have highly developed capacities for change. Continuously, new synapses appear, old ones disappear, existing synapses change their qualities and strengths. These processes are collectively called synaptic plasticity. In fact, synapses are not a cumbersome machinery to merely transmit information from one neuron to the next, but they carry the essence of the brain, its capacity to change.
At these points of contact, the flow of information throughout the brain may continuously be regulated and adjusted, providing the individual organism with a means of learning from the experiences it makes during interaction with its physical and social environment. Thus, these experiences may lead to new ways to perceive, interpret and act within this environment. They may be small, but synapses are incredibly complicated. Interaction between a battery of ions, cytoplasmic and membrane proteins make each synapse a molecular microcomputer in itself. Synapses are fascinating and complex, but they are also subject to strains and diseases in manners that we know only a few details about.
Currently, we are interested in projects which focus on the following proteins: glutamate receptors; SNARE proteins (VAMP2, SNAP-25, syntaxin, and also synaptotagmin; these proteins regulate synaptic vesicular exocytosis); PICK1 and GRIP (synaptic trafficking of glutamate receptors); the Exocyst proteins (synaptic vesicle and receptor trafficking); and Arc (an immediate early gene involved in synaptic plasticity). These proteins interact in order to regulate the strength and efficacy of glutamatergic synaptic transmission, and may underlie synaptic changes during stress, depression, epilepsy, and stroke.
We typically use electron microscopy, light microscopy, confocal microscopy, and in vivo brain imaging, often in combination with immunocytochemical labeling to quantify the localization and concentration of synaptic proteins within different synaptic regions during different physiological or pathological conditions. In some cases we employ MR techniques to investigate changes in brain function. In parallel with these anatomical methods, we use both biochemical (e.g., western blot and subcellular fractionation) or molecular biological (e.g. cloning and transfection of genes).
We are associated with the ”Scientific Excellence Research Thematic Area” (SERTA) Developing and Adaptive Brain at the University of Oslo. We have and have had collaborations with a number of other labs in Oslo (UiO, the Biotechnology Center, Rikshospitalet), Bergen, Trondheim, Ås, and in Denmark, UK, France, Germany, Hong Kong, and the US.