Transgenic mice overexpressing truncated trkB neurotrophin receptors in neurons have impaired long-term spatial memory but normal hippocampal LTP

• Published in: Synapse (New York, N.Y.) N.Y.), 2000-10, Vol.38 (1), p.102-104
• Main Authors: Saarelainen, Tommi, Pussinen, Raimo, Koponen, Eija, Alhonen, Leena, Wong, Garry, Sirviö, Jouni, Castrén, Eero
• Format: Article
• Language: English
• Subjects: Animals; Brain-Derived Neurotrophic Factor - metabolism; Gene Expression Regulation - physiology; Hippocampus - pathology; Hippocampus - physiopathology; Long-Term Potentiation - physiology; Male; Maze Learning - physiology; Memory Disorders - physiopathology; Mice; Mice, Transgenic; Receptor, trkB - genetics; Receptor, trkB - metabolism; Space life sciences; Space Perception - physiology
• ISSN: 0887-4476; 1098-2396
• DOI: 10.1002/1098-2396(200010)38:1<102::AID-SYN11>3.0.CO;2-K

Neurotrophins, particularly brain-derived neurotrophic factor (BDNF), have been implicated in the regulation of synaptic plasticity and in learning and memory. BDNF mRNA expression is strongly increased upon the induction of long-term potentiation (LTP), a widely used neurobiological model for learning and memory and exogenous administration of BDNF enhances synaptic transmission. Moreover, the late phase of LTP is compromised in mice that are missing one or both alleles of BDNF and this impairment can be overcome by exogenous administration of BDNF. In order to investigate the physiological role of endogenous BDNF signaling, we have taken advantage of the inhibitory receptor isoform and developed a mouse model that overexpresses truncated isoform trkB.T1 in postnatal neurons, including hippocampus and cortex. We report here that these mice have mildly impaired spatial memory but the LTP in the CA1 area is normal.