The deletion of STOP/MAP6 protein in mice triggers highly altered mood and impaired cognitive performances

摘要: The microtubule-associated Stable Tubulie Only Polypeptide (STOP; also known as MAP6) protein plays a key role in neuron architecture and synaptic plasticity, the dysfunctions of which are thought to be implicated pathophysiology psychiatric diseases. deletion STOP mice leads severe disorders reminiscent several schizophrenia-like symptoms, associated with differential alterations serotonergic tone somas versus terminals. In knockout (KO) compared wild-type mice, serotonin (5-HT) markers found markedly accumulated raphe nuclei and, contrast, deeply depleted all projection areas. present study, we carefully examined whether 5-HT imbalance would lead behavioral consequences evocative mood and/or cognitive disorders. We showed that KO exhibited depression-like behavior, decreased anxiety-status validated paradigms. addition, although had preserved very short-term memory, they failed perform well other learning memory tasks. regional norepinephrine observed for 5-HT. As consequence, mutant were hypersensitive acute antidepressants different selectivity. Altogether, these data indicate caused deep performances might have crucial networks development.