Mitochondrial dysfunction and subsequent increases in Reactive Oxygen Species (ROS) production are assumed to be key factors in ageing, which is associated with a general decline in physiological functions including cognitive ones. However, the specific role of ROS in processes concerning the brain is still unclear. One hypothesis is that ROS contributes to age-related impairment in learning and memory. Indeed it has been demonstrated that ROS are necessary components of signal transduction during normal neurophysiological processes in synaptic plasticity. To investigate the role of ROS production as a function of respiratory chain proteins, we used conplastic mouse strains with stable mutations of mitochondrial genes associated with respiration. In these strains, we studied the influence of different ROS levels on cognitive functions by measurements of synaptic plasticity via long-term potentiation in parallel with ROS production in the brain of different mouse strains at different time points. Furthermore we tested in vivo behavior and learning by the open field and the water maze behavioral tests. As a result of our investigation, we found different effects of the mutated respiratory chain proteins on the analyzed parameters. While young and adult mice (3 and 6 months old) having a mutation in complex V showed similarities to the control mice in all used tests, the mutations in complexes I, III and IV seem to lead to altered ROS production and a reduction in synaptic plasticity in brain tissue. Since an altered ROS production is not expected for complex V mutations, our data strongly suggest an influence of ROS on synaptic plasticity.