Neural network formation throughout development and regeneration after injury depends on accuracy of axonal pathfinding, which is influenced by chemical and physical cues. Recently, there is growing evidence that local temperature fluctuations in the brain play a crucial role in axonal guidance. However, the precise mechanisms involved in this process are not completely understood. We hypothesize that spontaneous and trauma-induced axon growth is repelled by increasing nanoscale temperature gradients leading to growth inhibition and growth cone retraction. Transient receptor potential vanilloid 4 (TRPV4) is a thermosensitive calcium-permeable channel. It senses temperature changes within the physiological and inflammation-induced range. TRPV4’s activation leads to an increase in the intracellular concentration of Ca2+. Through a supramolecular complex containing cytoskeletal proteins and regulatory kinases, TRPV4-mediated Ca2+ changes act as a direct regulator of microtubules and actin. This makes it a target for the study of axonal actin reorganization events at the subcellular levels. However, the effects of local temperature variations on axonal plasticity could not be studied due to technical limitations.We are leveraging the power of quantum physics through cutting-edge technologies to create diamond-probe induced temperature gradients on the Micro- and Nano-scale, enabling the manipulation and measurement of temperature at the Nano-scale. We are investigating the dynamics of spontaneous axon growth during development and regenerative plasticity of axonal networks after trauma, using our diamond-color-centers with micro-probe structures.We are combining this with microfluidic devices as a powerful and highly innovative tool to study the molecular mechanisms of spontaneous and trauma-induced axon growth.