Background　Transient potential receptor vanilloid 1（TRPV1）， a non-selective cation channel， which mainly locates on the sensory nerve fibers， mediates nociception input and integrates external stimuli as well， affects the release of neurotransmitters and activates intracellular proteases to regulate synaptic transmission and intracellular function such as cellular apoptosis. Local anesthetics induce TRPV1 activation and at high concentration lead to neurotoxicity， such as neuropathic pain and hyperalgesia， which may be related to the nerve injury.　Objective　To review the research progress regarding involvement of TRPV1 in the neurotoxicity induced by local anesthetics.　Content　The activation of TRPV1 can increase the concentration of local anesthetic in nerve fibers and strengthen the action of blockade， increase intracellular calcium， the release of glutamate and N-methyl-D-aspartate receptor （NMDAR） activation， and consequently， mediate local anesthetic neurotoxicity via calcium overload， oxidative stress and activation of apoptotic pathways， which cause neuronal apoptosis.　Trend　TRPV1 receptor plays a role in neurotoxicity induced by local anesthetics， whether targeting TRPV1 receptor regulation could prevent neurotoxicity induced by local anesthetics is worthy of further investigation.