Transgenic mice with neuronal overexpression of bcl-2 gene present navigation disabilites in a water task

• Published in: Neuroscience Vol. 104; no. 1; pp. 207 - 215
• Main Authors: Rondi-Reig, L, Lemaigre-Dubreuil, Y, Montécot, C, Müller, D, Martinou, J.C, Caston, J, Mariani, J
• Format: Journal Article
• Language: English
• Published: Oxford Elsevier Ltd 01.04.2001; Elsevier
• Subjects: Bcl-2 gene; Behavioral psychophysiology; Biological and medical sciences; cell death; development; Fundamental and applied biological sciences. Psychology; Miscellaneous; Psychology. Psychoanalysis. Psychiatry; Psychology. Psychophysiology; spatial learning; NSE, neuron-specific enolase; development; cell death; ANOVA, analysis of variance; spatial learning; EPSPs, excitatory postsynaptic potentials; LTP, long-term potentiation; NMDA, N-methyl- d-aspartate; Rodentia; Central nervous system; Transgenic animal; Gene overexpression; Space perception; Vertebrata; Mammalia; Acquisition process; Mouse; Cell death; Animal; Development; Perception; Perceptive learning; Hippocampus; Brain (vertebrata)
• ISSN: 0306-4522; 1873-7544
• DOI: 10.1016/S0306-4522(01)00050-1

In the CNS, Bcl-2 is an antiapoptotic gene involved in the regulation of neuronal death. Transgenic mice overexpressing the human gene Bcl-2 (Hu-bcl-2 mice) showed delayed acquisition in two tasks requiring them to find a hidden platform starting from either a random or a constant starting location. The same mice were not deficient in another task requiring them to find a visible platform suggesting that the delay observed was not due to motor, visual or motivational deficits in the water. The delay observed in Hu-bcl-2 mice was more important in the random starting test in which the allocentric demand for navigation was stronger. The results suggested that allocentric navigation is particularly sensitive to abnormal CNS maturation following the overexpression of the bcl-2 gene. The specific deficits (motor learning, fear-related behavior and allocentric navigation) observed in Hu-bcl-2 mice suggest that the regulation of developmental neuronal death is crucial for multisensorial learning and emotional behavior.