Publications by authors named "Rocio Diez-Arazola"
Article Synopsis
- * Neurons without FBXO41 maintain normal structure but show impaired synaptic transmission, with excitatory neurons releasing fewer synaptic vesicles and inhibitory neurons having decreased functional properties.
- * During brain development, FBXO41 loss results in reduced size and cellularity in specific brain regions and delays in neuronal migration and activity, indicating its importance in early brain function.
Neuropeptides and neurotrophic factors secreted from dense core vesicles (DCVs) control many brain functions, but the calcium sensors that trigger their secretion remain unknown. Here, we show that in mouse hippocampal neurons, DCV fusion is strongly and equally reduced in synaptotagmin-1 (Syt1)- or Syt7-deficient neurons, but combined Syt1/Syt7 deficiency did not reduce fusion further. Cross-rescue, expression of Syt1 in Syt7-deficient neurons, or vice versa, completely restored fusion.
View Article and Find Full Text PDFRegulated secretion is controlled by Ca sensors with different affinities and subcellular distributions. Inactivation of (synaptotagmin-1), the main Ca sensor for synchronous neurotransmission in many neurons, enhances asynchronous and spontaneous release rates, suggesting that Syt1 inhibits other sensors with higher Ca affinities and/or lower cooperativities. Such sensors could include Doc2a and Doc2b, which have been implicated in spontaneous and asynchronous neurotransmitter release and compete with Syt1 for binding SNARE complexes.
View Article and Find Full Text PDFArticle Synopsis
- * Synaptotagmin proteins mainly handle synchronous release, while double C2 domain proteins (Doc2) serve as Ca2+ sensors for spontaneous release, showing higher Ca2+ sensitivity.
- * Doc2 proteins compete with synaptotagmin-1 by binding to SNARE complexes, indicating a broader mechanism where different proteins regulate vesicle fusion based on their actions with SNAREs.