The mechanisms of plasticity between the lateral amygdala and the perirhinal cortex

• Main Author: Laing, Michael
• Published: University of Bristol 2013
• Subjects: 612.825
• Online Access: http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.617930

A key feature of memory is that experiences with emotional significance are better remembered than those which lack emotional significance (Cahill 1994, Roozendaal 2008). The amygdala which is located within the medial temporal lobe, projects to multiple brain regions and via these projections the amygdala has the capacity to modulate the activity of other brain regions (Kajiwara 2003, Roozendaal 2008). There are robust reciprocal connections between the amygdala and the perirhinal cortex and activation of the lateral amygdala has been demonstrated to enhance learning and memory (Roozendaal 2008) and synaptic plasticity (Perugini 2012) within the perirhinal cortex. However, the mechanisms by which the amygdala regulates perirhinal cortex plasticity are still largely unknown. By studying synaptic communication and plasticity between the lateral amygdala and the perirhinal cortex is it possible to determine how the amygdala modulates activity within the perirhinal cortex? Horizontal slices were taken from juvenile male Lister Hooded rats and recordings were made in layer 111111 of the perirhinal cortex. Two stimulation electrodes were placed on the slice, one in the lateral amygdala and the other in layer 111111 of the perirhinal cortex. Extracellular field recordings demonstrated that blockade of the ~-adrenoceptors prevented the induction of lateral-amygdala (LA-PRh) long-term potentiation specifically. However the chemical activation of ~-adrenoceptors , by bath application of the J3- adrenoceptor agonist isoprenaline, induced perirhinal cortex (PRh-PRh) long-term potentiation when coupled with basal stimulation. Application of isoprenaline induced only a transient potentiation of the LA-PRh response however this was converted to long-term potentiation when delivered with a subthreshold long-term potentiation protocol. Voltage clamp recordings demonstrated that long-term depression at both the PRh-PRh and LA-PRh is NMDA-R dependent and -adrenoceptor independent, sensitive to NR2A but not NR2B inhibition and the long-term depression is induced presynaptically.