Arianna Maffei, Stony Brook University, New York

Amygdalocortical Plasticity and Hedonic Value of Sensory Stimuli

Sensory stimuli have a sensory identity and an intrinsic affective dimension, or hedonic value. A stimulus modality where this is intuitive is taste: when put in the mouth, a taste is not perceived only by its chemical composition, but it is considered either pleasurable, or aversive. The affective dimension of a stimulus can change, a pleasurable taste can become aversive if it is paired with a gastric malaise. This shift in hedonic values is learned, and can be studied in the laboratory using a behavioral training paradigm known as Conditioned Taste Aversion Learning (CTA). CTA learning is hypothesized to depend on changes in the functional connection between the basolateral amygdala (BLA) and the primary gustatory cortex (GC), as well as plasticity within GC. We have recently identified the postsynaptic targets of BLA afferents in GC and begun assessing the capacity and mechanisms for plasticity at this input. Here I will discuss our new data unveiling the effect of CTA learning on GC neuron excitability and the BLA-GC synapse. Our results indicate that CTA learning affect both excitatory and inhibitory drive onto GC neurons, with a net shift of the E/I balance toward excitation. In addition, CTA learning weakens BLA-GC synapses, suggesting that CTA learning may depend on Long Term Depression (LTD) of the BLA-GC synapse. Finally, I will show that synaptic plasticity at the BLA-GC input is sufficient for CTA learning. To do that, we substituted the gastric malaise typically paired with sucrose during CTA training with the phasic stimulation paradigm for LTD using optogenetic activation of BLA terminal fields in GC, and assessed CTA learning in rats. The pairing of sucrose and phasic-LTD activation of BLA afferents in GC was sufficient to induce a CTA. Our results demonstrate that CTA learning alters synaptic transmission in GC, and directly link CTA learning with LTD of BLA-GC synapses onto L2/3 EXC neurons. (Supported by NIH-NIDCD grant R01-DC013770 to A.M. and A.F.)

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