Synaptotagmin 11 (Syt11) is a gene that plays a pivotal role in neuronal vesicular trafficking and exocytosis [1]. It is associated with pathways like clathrin-mediated endocytosis, Rho GTPase signaling, and cell motility-related functions [1]. Syt11 has been implicated in various neurological diseases, highlighting its overall biological importance. Genetic models, especially mouse models, have been crucial for studying its functions.

In Syt11-knockout (KO) hippocampal neurons, there is an increased frequency of miniature excitatory post-synaptic currents, indicating that Syt11 suppresses spontaneous neurotransmission [2]. Syt11-KO mice also exhibit deficits in presynaptic GABAB receptors (GBRs) and Cav2.2 channels, reduced neurotransmitter release, and decreased GBR-mediated presynaptic inhibition, suggesting its role in the assembly and stable expression of GBR/Cav2.2 complexes [3]. Syt11 deficiency in dopamine neurons in early adolescence leads to persistent social deficits and other schizophrenia-like behaviors in mice via dopamine over-transmission [4]. In microglia-specific Syt11-conditional-knockout (cKO) mice, Syt11-cKO results in microglial activation and elevated mRNA levels of certain cytokines [5].

In conclusion, Syt11 is essential for neuronal functions such as regulating spontaneous neurotransmission, facilitating the assembly of presynaptic signaling complexes, and modulating dopamine transmission. It also plays a role in microglial immune responses. Mouse KO and CKO models have significantly contributed to understanding its role in neurological diseases like schizophrenia and Parkinson's disease.