The neuronal engram created during fear learning relies on both, plasticity of the neuronal network for its formation and the stability for persistence. The allocation of neurons to a specific engram depends on their excitability. Molecules regulating the excitation / inhibition balance (E/I balance) in the brain are therefore considered key players in engram formation. Nogo-A has been shown to influence the E/I balance, restrict activity-dependent functional and structural plasticity and modulate learning and memory formation. However, whether Nogo-A controls the memory engram formation and the mechanisms of this action is still unknown. Behavioural experiments were combined with histochemical analysis to address this hypothesis. Moreover, the cell type-specific role of Nogo-A was assessed comparing the full Nogo-A knockout (KO) to conditional KOs missing Nogo-A either in Parvalbumin (PV) expressing interneurons or in excitatory neurons in a contextual fear conditioning paradigm. Nogo-A KO in excitatory neurons shows an increased freezing time accompanied by a higher number of cFOS expressing neurons in the basolateral amygdala. An opposite trend was observed upon Nogo-A deletion in PV interneurons. The effect of a Nogo-A deletion on fear memory could only be observed in female mice, suggesting a sex- and cell type-specific effect of Nogo-A in this context. Nogo-A-loss-of-function in acute hippocampal slices shows an increased Ca2+-influx upon chemically induced long term potentiation indicating a higher neuronal excitability, supporting the results above. Current 2-Photon Ca2+-imaging experiments address whether the activity of Nogo-A on engram formation may be related to its ability to modulate neuronal network synchronization.