Vti1a, short for Vesicle transport through interaction with t-SNAREs 1A, is a member of the N-ethylmaleimide-sensitive factor attachment protein receptor protein family. It is involved in cell signaling as a vesicular protein and mediates vesicle trafficking, playing crucial roles in neural development, autophagy, and unconventional extracellular transport of neurons. It also participates in regulating neurosecretory events, spontaneous synaptic transmission, and postsynaptic efficacy in neurons [1,4].

In gene knockout studies, loss of Vti1a and Vti1b in mice leads to death at birth with massive neurodegeneration in peripheral ganglia and defective axon tracts [3]. Vti1a/b-deficient neurons show severely impaired synaptic vesicle and dense-core vesicle secretion, with reduced levels of secretion-mediating proteins and impaired cargo trafficking at the Golgi [5]. Ablation of Vti1a/1b in mouse cortex causes neural progenitor pool depletion and cortical layer 5 malformation [6]. Knockdown of Vti1a reverses the phenotype of increased spontaneous neurotransmission in Syt11-knockout neurons, indicating Vti1a as the main target of Syt11 inhibition [2].

In conclusion, Vti1a is essential for multiple neural functions such as neurotransmission, neuronal development, and vesicle secretion. Studies using gene knockout mouse models have revealed its significant roles in these processes. Dysfunction of Vti1a may be associated with nervous system disorders like hepatic encephalopathy, amyotrophic lateral sclerosis, and glioma, highlighting its importance in understanding disease mechanisms [1].