Joe Guillaume Pelletier

Prefrontal Control of the Amygdala

Accumulating evidence indicates that phobic and posttraumatic anxiety disorders likely result from a failure to extinguish fear memories. Extinction normally depends on a new learning that competes with the original fear memory and is driven by medial prefrontal cortex (mPFC) projections to the amygdala. Although mPFC stimulation was reported to inhibit the central medial (CEm) amygdala neurons that mediate fear responses via their brainstem and hypothalamic projections, it is unclear how this inhibition is generated. Because the mPFC has very sparse projections to CEm output neurons, the mPFC-evoked inhibition of the CEm is likely indirect. Thus, this study tested whether it resulted from a feedforward inhibition of basolateral amygdala (BLA) neurons that normally relay sensory inputs to the CEm. However, our results indicate that mPFC inputs excite rather than inhibit BLA neurons, implying that the inhibition of CEm cells is mediated by an active gating mechanism downstream of the BLA.

Amygdala oscillations and the consolidation of emotional memories

The amygdala receives multi-modal sensory inputs and projects to virtually all levels of the central nervous system. Via these widespread projections, the amygdala facilitates consolidation of emotionally arousing memories. How the amygdala promotes synaptic plasticity elsewhere in the brain remains unknown, however. Recent work indicates that amygdala neurons show theta activity during emotional arousal, and various types of oscillations during sleep. These synchronized neuronal events could promote synaptic plasticity by facilitating interactions between neocortical storage sites and temporal lobe structures involved in declarative memory.

Emotional enhancement of memory via amygdala- driven facilitation of rhinal interactions

Emotions generally facilitate memory, an effect mediated by the basolateral amygdala (BLA). To study the underlying mechanisms, we recorded BLA, perirhinal and entorhinal neurons during an appetitive trace-conditioning task. We focused on the rhinal cortices because they constitute the interface between the hippocampus, a mediator of memory consolidation, and the neocortex, the storage site of declarative memories. We found that, after unexpected rewards, BLA activity increased impulse transmission from perirhinal to entorhinal neurons and that this effect decayed as the association between conditioned stimuli and rewards was learned. At this late phase of learning, the BLA effect occurred when the animals were anticipating the reward. By enhancing the processing of sensory cues, the BLA-mediated facilitation of rhinal interactions may explain how the amygdala promotes memory formation in emotional conditions.

Role of amygdala oscillations in the consolidation of emotional memories.

Much evidence indicates that emotional arousal generally improves memory and that the amygdala is responsible for this effect. The available data suggest that stress hormones and neuromodulators released in emotionally arousing conditions alter the activity of basolateral amygdala (BLA) neurons in the hours after the learning episode. In turn, these changes would facilitate synaptic plasticity elsewhere in the brain; however, the biological mechanisms underlying the facilitation of memory consolidation by the BLA remain unknown. This article focuses on data suggesting that synchronized oscillatory BLA activity promotes synaptic plasticity by facilitating interactions between neocortical and temporal lobe areas involved in declarative memory.