Brain structure prefrontal cortex

The prefrontal cortex (PFC) is the anterior part of the frontal lobes of the brain. It lies in front of the motor and premotor areas. The PFC is divided into the lateral, orbitofrontal, and medial prefrontal areas (Barbas and Pandya, 1987, 1989). Comprehensive reviews of this structure and functions of the PFC have been published in various forms (Fuster, 1997 Goldman-Rakic, 1987 Miller and Cohen, 2001 Passingham, 1993 Tanji and Hoshi, 2008). The PFC possesses a wealth of anatomical connectivity with multiple cortical and subcortical areas, and is involved in broad aspects of behavioral control. The PFC has been implicated in complex cognitive behaviors, social behaviors, and personality expression. Recent studies of this area have revealed its role in the control of a much broader spectrum of functions, such as cross-modal and cross-temporal association of information, in the executive control of behavior, and in the top-down control of neural networks involving the cortical and subcortical areas. Among them, the executive control of action was a term coined to capture various aspects of PFC function. 

These results are consistent with the morphological findings reported in postmortem brains of patients with schizophrenia (i.e., decrease number of spines in prefrontal cortex (Garey et al., 1998 Glantz and Lewis, 2000 Rosoklija et al., 2000 Kolluri et al., 2005), and thus could be related to the deficit in synaptic connectivity assumed to underlie the disease (structural misconnectivity), leading to cognitive deficits. 

Thus, a GSH deficit has consequences consistent with the concept of functional disconnectivity, as hypofunction of NMDA-R and alteration of dopamine signaling have been observed. When imposed on animals during development, a GSH deficit induces also a structural disconnectivity, as revealed by the decrease in dendritic spines and parvalbumin-immunoreactivity of inhibitory intemeurons in the prefrontal cortex Finally, a transient GSH deficit during brain development causes deficits in visual recognition and olfactory integration. 

Brain glucose utilization decreases when alertness and cognitive performance are impaired by sleep deprivation, especially in the prefrontal cortex, a region involved in alertness, attention, and higher order cognitive processes and in the thalamus, a subcortical structure involved in alertness and attention. 

Phenylalanine and related metabolites inhibit activity of 3-hydroxy-3-methylglutaryl coenzyme-A (HMG-CoA) reductase (Fig. 9.2). This aizyme is critical for proper synthesis of cholesterol in phenylalanine-sensitive oligodendrocytes located in the frontal brain, especially in the prefrontal cortex. Locally synthesized cholesterol makes up approximately 30 % of all myelin lipids of the brain tissue. The function of cholesterol is not only structural but is also required for proper neuronal signal transmission [50]. Inhibition of HMG-CoA reductase by phaiylalanine is partially reversible in some individuals. This explains the improvement in myelination observed in MRl scans of poorly controlled patients who have returned to diet and have lowered their blood phenylalanine concentrations. The reduction in phenylalanine allows for proper myelin production in the phenylalanine-sensitive oligodendrocyte population [50,57,58] (Fig. 9.3). 

Figure 5. Positron emission tomography shows the brain areas activated and deactivated during REM sleep when compared to waking. In the forebrain, more activated areas are principally limbic structures, while the posterior cingulate cortex, part of the prefrontal and parietal cortex, are deactivated. Modified from Hobson et al. (1998). Reprinted from NeuroReport with permission.

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