Research reportAmygdala modulates memory for changes in reward magnitude: Reversible post-training inactivation with lidocaine attenuates the response to a reduction in reward
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Post-training intra-basolateral complex of the amygdala infusions of clenbuterol enhance memory for conditioned place preference and increase ARC protein expression in dorsal hippocampal synaptic fractions
2021, Neurobiology of Learning and MemoryCitation Excerpt :However, we cannot rule out the possibility that training in the unpaired arm produces a negative experience due to the lack of reward availability. The BLA is known to modulate memory of reward reduction and is critical for a conditioned aversive response to a goal box after reward reduction (Salinas & White, 1998; Salinas, Introini-Collison, Dalmaz, & McGaugh, 1997; Salinas, Packard, & McGaugh, 1993). Ultimately, our data suggest that activation of BLA β-adrenoceptors may serve as a widespread mechanism for modulating synaptic plasticity in efferent brain regions to facilitate long-term memory consolidation of different aspects of memory.
The basolateral amygdala in reward learning and addiction
2015, Neuroscience and Biobehavioral ReviewsCitation Excerpt :These data shed light on the important role of reward history in appetitive behavior. Many years later, the McGaugh lab was the first to show that the amygdala mediates the responses to these shifts in reward magnitude (Salinas et al., 1993). The BLA is involved when the outcome of an action (e.g., maze run) differs in magnitude from that expected based on that action's reward history (Salinas et al., 1993).
Behavioral neuroscience of psychological pain
2015, Neuroscience and Biobehavioral ReviewsCitation Excerpt :This has been done using the iSNC paradigm, in the runway, with a 10-to-1 pellet downshift, and targeting the amygdala. In one experiment, Salinas et al. (1993) infused lidocaine in several amygdala locations immediately after the first downshift session. Lidocaine is a sodium-channel blocker that produces a reversible inactivation of neural activity.