Since I began studying psychopathy, I have often wondered about an evolutionary basis for this dangerous disorder. Psychopathy is considered to be a developmental disorder (Blair, 2006), which means that through its normal course of development the brain experiences stresses or biochemical changes that are not conducive to proper neurological development. This idea is supported by suppositions from both behavioral psychology and neuroscience; firstly, in behavioral psychology, it is suspected that serious child abuse could be an underlying factor behind psychopathy (Kunitz et al., 1998), and secondly, in neuroscience, it has been noted that many with psychopathy show a significant underdevelopment of a number of regions in their brain (for a review see Pemment, 2012).
In the pivotal study by Ludmer, Dudai, and Rubin (2011), it was found that amygdala activation during a moment of perceptual insight (measured using fMRI analysis) could be used as a reliable indicator to predict the long term retention of memory items (pictures). One of the fascinating things about this study is that the pictures presented to the participants were neutral, i.e. non arousing or repulsive. This means that activity in the amygdala is fluctuating (higher fluctuations are aiding memory retention) without a direct emotional stimuli. This is what sets it apart from classical fear conditioning, because there is a clear absence of an aversive stimuli.
I’m wondering if high amygdalar activation simply prepares a set of neurons to make a doorway, which will become reinforced through LTP during reconsolidation; this begs the question of whether or not a different memory can hijack the doorway. If this is true, then it doesn’t matter what activates the amygdala, if any memory, in neural substrate form, is in the right place at the right time it can take advantage of the doorway.If the amygdala evolved to tag memories and aid memory retention through fear conditioning, I’m wondering if over an evolutionary timescale the brain was capable of generating high enough activity in the amygdala on its own, without a stimulus.