The disruption of the nerve growth factor (NGF) gene in trans-\ud genic mice leads to a lethal phenotype (Crowley et al., 1994)\ud and hinders the study of NGF functions in the adult. In this\ud study the phenotypic knockout of NGF in adult mice was\ud achieved by expressing transgenic anti-NGF antibodies, under\ud the control of the human cytomegalovirus promoter. In adult\ud mice, antibody levels are 2000-fold higher than in newborns.\ud Classical NGF targets, including sympathetic and sensory neu-\ud rons, are severely affected. In the CNS, basal forebrain and\ud hippocampal cholinergic neurons are not affected in the early\ud postnatal period, whereas they are greatly reduced in the adult\ud (55 and 62% reduction, respectively). Adult mice show a re-\ud duced ability in spatial learning behavioral tasks. Adult, but not\ud neonatal, transgenic mice further show a new phenotype at the\ud level of peripheral tissues, such as apoptosis in the spleen and\ud dystrophy of skeletal muscles. The analysis of this novel com-\ud prehensive transgenic model settles the controversial issue\ud regarding the NGF dependence of cholinergic neurons in adult\ud animals and reveals new NGF functions in adult non-neuronal\ud tissues. The results demonstrate that the decreased availability\ud of NGF in the adult causes phenotypic effects via processes\ud that are at least partially distinct from early developmental\ud effects of NGF deprivation
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