Cerebral cortex
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Comparative Study
NMDA receptor blockade alters stress-induced dendritic remodeling in medial prefrontal cortex.
The development and relapse of many psychopathologies can be linked to both stress and prefrontal cortex dysfunction. Glucocorticoid stress hormones target medial prefrontal cortex (mPFC) and either chronic stress or chronic administration of glucocorticoids produces dendritic remodeling in prefrontal pyramidal neurons. Exposure to stress also causes an increase in the release of the excitatory amino acid glutamate, which binds to N-methyl-D-aspartate (NMDA) receptors, which are plentiful in mPFC. ⋯ Instead, CPP-injected stressed rats showed hypertrophy of apical dendrites compared with controls. These results suggest that NMDA activation is crucial for stress-induced dendritic atrophy in mPFC. Furthermore, NMDA receptor blockade uncovers a new pattern of stress-induced dendritic changes, suggesting that other neurohormonal changes in concert with NMDA receptor activation underlie the net dendritic retraction seen after chronic stress.
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Perception is not a simple reflection of sensory information but varies within and between individuals. This applies particularly to the perception of pain, which, in the brain, is associated with neuronal responses at different frequencies. Here, we show how these different neuronal responses subserve interindividual and intraindividual variations in the perception of identical painful stimuli. ⋯ In contrast, both pain-related theta and gamma responses provide different and complementary information on intraindividual variations in the pain experience. We conclude that theta responses reflect rather constant physiological and psychological traits of the individual, whereas gamma responses relate to short-term modulations of the individual's state. These findings reveal how neuronal responses at different frequencies differentially contribute to the translation of sensory information into a subjective percept.