Hippocampal noradrenergic activation is necessary for object recognition memory consolidation and can promote BDNF increase and memory persistence

• NE injection on hippocampus promotes OR memory persistence.
• NMDA infusion in LC shares the effect of NE into CA1.
• OR training consolidation is attended by an increase of hippocampal NE levels.
• OR training consolidation is attended by an increase of hippocampal BDNF.
• NTS–PGi–LC pathway activation mediates the increase of hippocampal NE and BDNF.

Previously we showed that activation of the Nucleus of the Solitary Tract (NTS)–Nucleus Paragigantocellularis (PGi)–Locus coeruleus (LC) pathway, which theoretically culminates with norepinephrine (NE) release in dorsal hippocampus (CA1 region) and basolateral amygdala (BLA) is necessary for the consolidation of object recognition (OR) memory. Here we show that, while the microinjection of the beta-noradrenergic receptor blocker timolol into CA1 impairs OR memory consolidation, the microinjection of norepinephrine (NE) promotes the persistence of this type of memory. Further, we show that OR consolidation is attended by an increase of norepinephrine (NE) levels and of the expression of brain derived neurotrophic factor (BDNF) in hippocampus, which are impaired by inactivation of the NTS–PGi–LC pathway by the infusion of muscimol into the NTS.