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The emotional valence of a memory can be changed, and this probably involves a change in the connectivity between hippocampal and amygdalar memory traces.
In mice with mechanical hyperalgesia, reactivation of the sensitized pain pathways renders the hyperalgesic state labile and susceptible to being reversed.
A study by Krepleet al. shows that acid-sensitive ion channel 1A in the nucleus accumbens inhibits cocaine-related synaptic plasticity and cocaine-conditioned behaviour in rodents.
Pain-sensitive sensory neurons in the dorsal root ganglion release calcitonin gene-related peptide, which could over time have long-term consequences on metabolism and longevity by reducing pancreatic release of insulin.