, 2006). This is an important
lead since the prefrontal cortex is involved in extinction, a type of learning (Santini et al., 2004), but more research is needed to explore the complex relationship between stress, fear conditioning, extinction, and possible morphological remodeling that may well accompany each of these experiences. The prefrontal cortex, amygdala, and hippocampus are interconnected and influence each other via direct and indirect neural activity (Akirav and Richter-Levin, 1999, Ghashghaei and Barbas, 2002, McDonald, 1987, Mcdonald et al., 1996 and Petrovich et al., 2001). For example, inactivation of the amygdala blocks stress-induced impairment ABT-263 mw of hippocampal LTP and spatial memory (Kim et al., 2005) and stimulation of basolateral amygdala enhances dentate gyrus field potentials (Ikegaya et al., 1996), while stimulation of medial prefrontal cortex decreases responsiveness of central amygdala output neurons (Quirk et al., 2003). The processing of emotional memories with contextual information requires amygdala-hippocampal interactions (Phillips and LeDoux, 1992 and Richardson et al., 2004), whereas the prefrontal cortex, with its powerful influence on amygdala activity (Quirk et al., 2003), plays an important role in fear extinction (Milad and Quirk, 2002 and Morgan and LeDoux, 1995). Because
of these interactions, future studies need to address their possible role in the morphological and functional changes MK-1775 concentration produced by single and repeated stress. As reviewed above, pyramidal neurons in mPFC display profound behaviorally induced plasticity (i.e., shrinkage and loss of spines with stress), as well as the capacity to recover from stress (i.e., neuronal resilience). In addition, performance on tasks that require PFC is highly vulnerable to decline with age in humans, nonhuman primates, and rodents (reviewed in (Gallagher and Rapp, 1997), and recent data
from NHPs suggest that age-related decline in cognitive performance reliant on PFC may result from loss of a particular class of axospinous synapses on PFC pyramidal neurons (Dumitriu et al., 2010a). More specifically, the NHP data suggest a model in which Ketanserin large, stable synapses remain unaffected by age, while thin, highly plastic spines are selectively lost from pyramidal neurons within layer III of mPFC (Dumitriu et al., 2010a). The rat model of chronic stress has proven to be a highly valuable model for the analysis of the potential interactive effects of stress and aging on the vulnerable pyramidal neurons in mPFC. For example, is either the behaviorally induced plasticity, i.e., the response to chronic stress, or the capacity to recover from stress affected by aging? These questions were addressed through exposing young, middle-aged, and aged male rats to stress and recovery followed by detailed morphologic analyses of layer III pyramidal neurons in PL (see Figure 3).
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