Final Report Summary - RSSCEMSR (Role of Secondary Sensory Cortices in Emotional Memory Storage/Retrieval)
Emotional memories are the core of our personal life. During an emotional experience, sensory stimuli, like odors, sound and colors, acquire a positive or negative value through their association with rewards or punishments, a process called “emotional learning”. Although we know a great deal about how the brain analyses sensory information, we know relatively little about how sensory representations become linked with values. Our research project hypothesizes that sensory cortices, and in particular the higher order sensory cortices, may represent the sites where sensory and emotional processes converge, i.e. where sensory stimuli become linked to the emotional values acquired with the experience and/or where the affective value acquired by sensory stimuli is stored. We adopt a multidisciplinary approach made of the combination of behavioral, electrophysiological, immunohistochemical and confocal analyses. Through these different approaches we uncovered that higher order sensory cortices are necessary not only for the storage of aversive memories (Sacco and Sacchetti, 2010) but is also essential to store appetitive memories.
We found that the neural circuitry within the Te2 that processes and stores emotional memories varies on the basis of the affective-motivational charge of tones. Indeed, in the Te2 cortex, stimuli of different valences recruit layers II/III in a similar way and layers IV and V in a different manner. Moreover, concerning layer II/III, catFISH analysis revealed that following the presentation of two auditory cues previously paired with either pleasant or painful stimuli, a large percentage of cells responds to both experiences but also a small fraction of neurons responds exclusively to one of them. The latter type of neurons signals the valence rather than the salience or the motor responses associated with the stimuli, and reflects selective associative processes. Pharmacogenetic silencing of memory-activated neurons causes amnesia. We therefore propose that through these neurons, sensory cortices can be able drive the activity of “emotional” subcortical centers, like the amygdala, to distinguish between emotionally charged or neutral stimuli. To support this idea, we performed electrophysiological recording of Te2 and BLA during the retrieval of fearful emotional memories. We found that these structures show a synchronized activity within the theta frequencies at remote but not recent time points. More important, we found that Te2 drives BLA activity during this recall in the 3-7 Hz frequency band, and the blockade of Te2 activity causes amnesia.
Unraveling the neural substrates underlying emotional memory storage will have a remarkable importance in several disciplines. At a general level, our findings would indicate that the sensory cortex is not solely devoted to the analysis of physical properties of sensory stimuli, but also participates in emotional processes related to the perceived stimuli. Such a neural system that bridges the gap between sensation and action provides the substrates for ‘intermediary’ or ‘integrative’ processing. These areas of the brain enable identical stimuli to trigger different responses depending on past experience. Furthermore, the identification of neural sites involved in the storage of emotional memories may have a great impact in the clinical treatments of emotional disorders.
We found that the neural circuitry within the Te2 that processes and stores emotional memories varies on the basis of the affective-motivational charge of tones. Indeed, in the Te2 cortex, stimuli of different valences recruit layers II/III in a similar way and layers IV and V in a different manner. Moreover, concerning layer II/III, catFISH analysis revealed that following the presentation of two auditory cues previously paired with either pleasant or painful stimuli, a large percentage of cells responds to both experiences but also a small fraction of neurons responds exclusively to one of them. The latter type of neurons signals the valence rather than the salience or the motor responses associated with the stimuli, and reflects selective associative processes. Pharmacogenetic silencing of memory-activated neurons causes amnesia. We therefore propose that through these neurons, sensory cortices can be able drive the activity of “emotional” subcortical centers, like the amygdala, to distinguish between emotionally charged or neutral stimuli. To support this idea, we performed electrophysiological recording of Te2 and BLA during the retrieval of fearful emotional memories. We found that these structures show a synchronized activity within the theta frequencies at remote but not recent time points. More important, we found that Te2 drives BLA activity during this recall in the 3-7 Hz frequency band, and the blockade of Te2 activity causes amnesia.
Unraveling the neural substrates underlying emotional memory storage will have a remarkable importance in several disciplines. At a general level, our findings would indicate that the sensory cortex is not solely devoted to the analysis of physical properties of sensory stimuli, but also participates in emotional processes related to the perceived stimuli. Such a neural system that bridges the gap between sensation and action provides the substrates for ‘intermediary’ or ‘integrative’ processing. These areas of the brain enable identical stimuli to trigger different responses depending on past experience. Furthermore, the identification of neural sites involved in the storage of emotional memories may have a great impact in the clinical treatments of emotional disorders.