Cerebral cortex concepts

In general, quality is assessed by quantifiable traits that are more or less related to specific attributes of the product and the production process. Moreover, the assessment depends on the information delivered by the sensory organs. Information is filtered and evaluated by the brain depending on the specific information provided but also on the concept of understanding that already exists in the cerebral cortex (Singer, 2000). A mental representation of a sensory event can shape neural processes that underlie the formulation of the actual sensory experience. Thus, the subjective sensory experience is shaped by interactions between expectations and incoming sensory information. 

A particularly good example of how the working of the body is related to God s divine will is Boerhaave s discussion of the Aristotelian concept of sen-sorium commune in explaining the connection between the body and the mind as well as the connection of man to God. It is the place in the brain where all sense perception and impressions of the nerves come together and cause ideas, emotions, passions and voluntary motions. Boerhaave localised the sensorium commune in the place where all sensations originate, i.e. in all the points where the cerebral cortex and spinal marrow transfer into nerves. Boerhaave is very particular in stating that once the sensorium commune has set the body into motion it functions automatically, which means that for instance when someone decides to walk from Leiden to Amsterdam and back, the body will automatically do so. 

ACh is synthesized in the cerebral cortex as well as in all parts of the autonomic system. Intracellular ACh levels regulate the rate of synthesis, thus illustrating a negative feedback mechanism. One concept that may explain the manner of ACh release from storage vesicles is exocytosis, an opening in the vesicle membrane to the surrounding medium and subsequent resealing. 

If we may extrapolate from these results to the clinical situation, we conclude that maintenance of optimal intracellular T3 concentrations in the central nervous system requires T4 as a substrate and a series of adaptations in the metabolism of this prohormone and T3, which then compensates for the plasma hypothyroxinemia. To the extent that the compensatory changes described in the cerebral cortex of the hypothyroid rat do not occur in the human, a reduction of serum T4 in iodine deficient persons could present a significant threat to the thyroid status of the cerebral cortex, even if serum T3 remained at normal concentrations. There are no data with respect to the presence of a local T4 to T3 conversion system in the human central nervous system. However, the similarity of the responses of the pituitary-thyroid axis to hypothyroidism and iodine deficiency in the rat and man suggests that the Type 11 deiodinase is common to both species (28,43). Presumably then, the concepts regarding intracerebral thyroid hormone metabolism derived from those experiments in the rat are also relevant to man. 

This problem was addressed by refining analysis techniques to permit analysis of energy metabolites in small 20-80 mg brain samples (Schenker et al., 1966). This approach permitted analysis in cortex, subcortex, and cerebellum of ATP in symptomatic animals without inclusion in the kemicteric samples of normal tissue. Results showed a 13% depletion in the cerebellum of mildly symptomatic Gunn rats, and a 27% depletion of ATP in animals with advanced symptoms. Cortex and subcortex (nonstained) samples were unchanged. This supported the concept, based on symptomatology, and neuropathologic findings, that the toxicity of bilirubin in vivo is limited to the cerebral areas affected. 

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