Following an injury, uninjured neighbouring neurons may die by secondary mechanisms; which underlies expanding of tissue damage in many neurodegenerative diseases and traumas. There are various mechanisms suggested to be responsible for this transneuronal degeneration from excitotoxicity to neuroinflammation. The aim of this study was to analyse metabolic changes in these indirectly affected nerve cells upon axotomy of a small population of neighbouring neurons in culture. Adult Primary sensory neurons of dorsal root ganglia were isolated from adult BALB/c mice, which were anesthetised by an IP injection of ketamin (100mg/kg) and killed by cervical transection. After enzymatic and mechanical dissociation, neurons were seeded in 96-well plates at 10000 cells / well density. After 24 hrs in incubation, outgrown axons of 50 neurons in each well was cut with a UV laser. As a sham procedure, in control wells laser beam was fired near neurons without damaging any extensions. Following another 24 hrs of incubation, preparations were transferred to a cell metabolism analyser and processed according to manufacturer’s instructions for a metabolic dependency assay. In the injury wells the dependency of cultured nerve cells to glutamine as an energy source rose from 6,8 to 39,01 % (p<0,05) and to glucose from 25,3 to 70 % (p<0,05). Fatty acid utilization also increased from 12,4 to 18,8%, albeit not significantly. The study has demonstrated that even when a small fraction of nerve cells was injured, a large population of neighbouring cells are affected secondarily. These findings are important in understanding secondary neural degeneration in nervous system pathologies.