Positron emission tomography (PET) with 11C-deuterium-deprenyl in temporal lobe epilepsy : 1E. Kumlien, 3M. Bergström, 2A. Lilja, 3J. Andersson, 1C.-E. Westerberg, 3G. Westerberg, 3G. Antoni, and 3B. Lȧngström (Departments of 1Neurology, 2Diagnostic Radiology, and 3Uppsala PET Center, University Hospital, Uppsala)

Abstract

Tyrosine phosphorylation is a rapid and reversible process. It provides the cell with an efficient mechanism for altering protein and enzyme activity. The tyrosine phosphorylation events ultimately result in the stimulation of the activity of cellular proteins responsible for activating the gene transcriptional machinery that controls the growth, migration, morphology, and survival of neurons. The transmission of growth factor signals from the cell surface to the nucleus and the cytoskeleton involves the propagation and amplification of these signals by protein kinases and “adaptor” proteins. These proteins act as members of signaling pathways, radiating from the intracellular portion of the receptor tyrosine kinase (RTK) to various target proteins and transcription factors responsible for eliciting neurotrophic responses. A major goal of the neuronal signal transduction field is to identify how RTKs evoke the diverse array of responses to neurotrophic factors. The three tropomyosin-receptor-kinase (Trk) family members — TrkA, TrkB, and TrkC — each bind to a distinct subset of the neurotrophins; TrkA primarily binds nerve growth factor, TrkB binds brain-derived neurotrophic factor and NT-4/5, and TrkC binds NT-3. Both TrkA and TrkB can also bind NT-3 to a lesser extent, depending upon the cell type and perhaps the expression of other receptor subunits. NT-6, to date only identified in fish, has an activity on neurons consistent with interactions with TrkA. The Trk receptors are expressed in a temporally and specially distinct manner in the nervous system.