Chloride homeostasis is an important mechanism involved in a variety of cellular events such as volume regulation, proliferation and migration. In neurons the setting of intracellular chloride concentration is in addition crucial for the changes in GABAA mediated transmission that take place during development and in pathophysiological conditions. Our previous research has demonstrated an important role of chloride homeostasis in the mechanism for neuronal survival, apoptosis and rewiring.
Our current aim is to investigate in more detail these mechanisms with particular emphasis on interneurons both during development (perinatal maturation) and following a post- traumatic event (e.g. status epilepticus, TBI and ischemic stroke).
in vitro live cell imaging: ratiometric imaging of calcium and chloride ions, FRET and FRAP imaging, dendritic spine dynamics, neuron progenitor migration,
In vivo: 2 –photon calcium imaging, optogenetic and chemogenetic activation and inactivation of neuronal activity. Multichannel intracortical recordings in anesthetised and awake head restrained mice combined with locomotion tracking.
Abnormal fast GABAergic transmission and chloride homeostasis are implicated in the pathology of many brain diseases including post-traumatic epilepsy and Autism Spectrum Disorders. Our work may help to find novel and refined therapeutically approaches to ameliorate their sequelae.
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