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The prefrontal cortex (PFC) is the most evolved area of the primate brain, subserving our highest order cognitive abilities. The research of Patricia Goldman-Rakic showed that parallel sensory processing streams continue into the PFC, where they interact through extensive interconnections.
Recent physiological research has shown that neuromodulators can rapidly alter the strength of dlPFC network firing on a timescale of seconds, through powerful influences on the open states of ion channels residing near network synapses, a process called Dynamic Network Connectivity (DNC) .
Understanding how neurmodulators influence dlPFC circuits is beginning to explain about how cognitive state and arousal state are coordinated. In deep sleep we may be unconscious due to the absence of actylcholine and norepinephrine (NE) release.
Exposure to even mild, uncontrollable stress causes a rapid loss of PFC function. Feedforward Ca2+-PKC and cAMP-PKA signaling rapidly opens K+ channels to disconnect dlPFC networks and reduce neuronal firing, i.e. Going To Hell In A Handbasket.
Many layer III dlPFC DNC proteins are genetically altered in schizophrenia, and/or have documented changes in expression.
The prefrontal cortex (PFC) is needed for top-down control of attention, behavior and emotion: inhibiting inappropriate impulses, controlling distractions, sustaining attention on “boring” but important information (e.g. math homework), and delaying gratification. All of these abilities can be impaired in people with Attention Deficit Hyperactivity Disorder (ADHD).
Prefrontal cortical functions weaken with advancing age in both animals and humans. There is an increase in Ca2+-cAMP signaling in PFC that correlates with cognitive deficits, and a selective loss of long, thin spines from the monkey dlPFC.

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