Nerve growth factor (NGF) promotes survival of septal cholinergic neurons after fimbrial transections in adult rats. The study investigated whether NGF could affect the survival of central cholinergic neurons following axonal transections. Unilateral fimbrial transections reduced the number of large cell bodies in the medial septal nucleus and the vertical limb of the diagonal band of Broca, as visualized by Nissl staining. Additionally, the number of AChE-positive cells in these areas was reduced after pretreatment with diisopropylfluorophosphate. However, in animals chronically treated with NGF, the number of AChE-positive cells was reduced only by 12 ± 6%, compared to control levels. These findings suggest that fimbrial transections caused retrograde degeneration of cholinergic septo-hippocampal neurons, and that NGF treatment significantly attenuated this degeneration. The study also found that NGF treatment partially prevented the loss of large cell bodies in the septal area. The results indicate that NGF may promote the survival of cholinergic neurons after axonal injury. The findings have implications for Alzheimer's disease, as the selective loss of cholinergic neurons in the basal forebrain is a key feature of the disease. The study suggests that increasing NGF availability to cholinergic neurons may help prevent or reduce their degeneration.Nerve growth factor (NGF) promotes survival of septal cholinergic neurons after fimbrial transections in adult rats. The study investigated whether NGF could affect the survival of central cholinergic neurons following axonal transections. Unilateral fimbrial transections reduced the number of large cell bodies in the medial septal nucleus and the vertical limb of the diagonal band of Broca, as visualized by Nissl staining. Additionally, the number of AChE-positive cells in these areas was reduced after pretreatment with diisopropylfluorophosphate. However, in animals chronically treated with NGF, the number of AChE-positive cells was reduced only by 12 ± 6%, compared to control levels. These findings suggest that fimbrial transections caused retrograde degeneration of cholinergic septo-hippocampal neurons, and that NGF treatment significantly attenuated this degeneration. The study also found that NGF treatment partially prevented the loss of large cell bodies in the septal area. The results indicate that NGF may promote the survival of cholinergic neurons after axonal injury. The findings have implications for Alzheimer's disease, as the selective loss of cholinergic neurons in the basal forebrain is a key feature of the disease. The study suggests that increasing NGF availability to cholinergic neurons may help prevent or reduce their degeneration.