When we examined the potential molecular mechanisms that could be responsible for the changes in electrophysiological parameters that we observed in the studied models of depression and hypothyroidism, we considered the participation of synaptotagmin I, the main Ca2+ sensor, postsynaptic proteins, metabolic disturbances, changes in mitochondrial dynamics, neurotrophic factors, alterations in the intensity of oxidative stress, intracellular signaling pathways and the level of acetylcholine, a neurotransmitter involved in cognitive processes. This evidence concerns the gene SYT1 and hypothyroidism.