Abstract

The Nucleus of the Solitary Tract (NTS) receives gustatory and visceral information from afferent fibers in the vagus and projects to the Nucleus Paragigantocellularis (PGi), among several other brain region. PGi sends excitatory fibers, mostly glutamatergic, to the Locus Coeruleus (LC). In turn, LC sends noradrenergic projections to many areas of the brain, including hippocampus (HIPP) and amygdala. Here we show that the NTS–PGi–LC–HIPP pathway is required for the memory consolidation of object recognition (OR). The inhibition of NTS, PGi or LC by microinfusion of the GABAA receptor agonist, muscimol, into each of these structures up to 3h after object recognition memory training impairs its consolidation as assessed in a retention test 24h later. The posttraining microinfusion of the β-blocker, timolol into CA1 mimics this effect. Intra-CA1 NA microinfusion does not alter retention per se, but reverses the disruptive effect of muscimol given into NTS, PGi or LC. This effect of NA is shared by a microinfusion of NMDA into LC. These results support the idea that the NTS–PGi–LC–CA1 pathway contributes to memory consolidation through a β-noradrenergic mechanism in CA1.

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