β-Adrenoceptors and synaptic plasticity in the perirhinal cortex

Experiences with a high degree of emotional salience are better remembered than events that have little emotional context and the amygdala is thought to play an important role in this enhancement of memory. Visual recognition memory relies on synaptic plasticity in the perirhinal cortex but little is known about the mechanisms that may underlie emotional enhancement of this form of memory. There is good evidence that noradrenaline acting via β-adrenoceptors (β-ADRs) can enhance memory consolidation. In the present study we examine the role of β-ADRs in synaptic plasticity at the amygdala–perirhinal pathway (LA–PRh) and compare this to mechanisms of intra-perirhinal (PRh–PRh) synaptic plasticity. We demonstrate that activity-dependent PRh–PRh long-term potentiation (LTP) does not rely on β1- or β2-ADRs and that LA–PRh LTP relies on β1-ADRs but not β2-ADRs. We further demonstrate that application of the β-ADR agonist isoprenaline produces lasting PRh–PRh potentiation but only transient potentiation at the LA–PRh input. However, at the LA–PRh input, combining stimulation that is subthreshold for LTP induction with isoprenaline results in long-lasting potentiation. Isoprenaline-induced and isoprenaline plus subthreshold stimulation-induced potentiation in the PRh–PRh and LA–PRh inputs, respectively were both dependent on activation of NMDARs (N-methyl-D-aspartate receptors), voltage-gated calcium channels and PKA (protein kinase A). Understanding the mechanisms of amygdala–perirhinal cortex plasticity will allow a greater understanding of how emotionally-charged events are remembered.