Context
Traumatic experiences in early childhood are associated with increased risk for developing stress-related disorders, which are linked to structural brain abnormalities. However, it is unclear if these volumetric brain changes are present before disease onset or reflect the consequences of the disease progression.
Objective
To identify structural abnormalities in the nonhuman primate brain that may predict increased risk for stress-related neuropsychiatric disorders in humans.
Design
Rhesus monkeys were divided in two groups at birth: a group raised with their mothers and other juvenile and adult animals (mother-reared, MR), and a group raised with three age-matched monkeys only (peer-reared, PR). Anatomical brain images were acquired in juvenile male and female rhesus monkeys using magnetic resonance imaging.
Main Outcome Measures
Volumetric measures of the anterior cingulate cortex, medial prefrontal cortex, hippocampus, corpus callosum and cerebellar vermis were compared between MR (n=15) and PR animals (n=13).
Results
Compared to MR monkeys, we found an enlarged vermis, dorsomedial prefrontal and dorsal anterior cingulate cortex in PR monkeys but no differences in the corpus callosum and hippocampus.
Conclusions
Peer-rearing during infancy induces enlargements in stress-sensitive brain regions. These changes may be a structural phenotype for an increased risk to stress-related neuropsychiatric disorders in humans.
In the rat, both the medial and lateral prefrontal cortices (PFC; mPFC and 1PFC, respectively) have direct connections with limbic structures that are important in the expression of fear and anxiety. The present study investigated the behavioral effects of excitotoxic lesions of either the mPFC or the 1PFC on conditioned and unconditioned fear paradigms. In both unconditioned fear paradigms (open field, elevated plus-maze), lesions of the mPFC decreased anxiety. In fear conditioning, 1PFC lesions substantially increased freezing throughout the different phases of the experiment, whereas mPFC lesions increased freezing to contextual cues and showed reduced freezing to discrete cues. These results support the functional role of the PFC in mediating or modulating central states of fear and anxiety and suggest a functional dissociation between the 1PFC and mPFC in their role in fear and anxiety.In many animal species, the stress response is expressed both behaviorally, by fear and anxiety states characterized by cessation of ongoing behavior and increased reactivity to environmental stimuli, and physiologically, by alterations in cardiovascular function, changes in autonomic tone, and activation of the neuroendocrine axes. Several lines of evidence indicate that the prefrontal cortex (PFC) is involved in the control of stress and emotional behavior. The prefrontal cortex is defined as the cortex of the anterior pole of the mammalian brain, which predominantly receives projections from the mediodorsal thalamic nucleus. In the rat, the PFC has been divided into two distinct regions, a medial and a lateral PFC (mPFC and 1PFC, respectively), on the basis of functional and hodological criteria.Anatomical studies have shown that both the mPFC and the 1PFC have direct connections with limbic structures, such as the amygdala, the hypothalamus, the nucleus accumbens, and the hippocampus (Ferine
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