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Siegel GJ, Agranoff BW, Albers RW, et al., editors. Basic Neurochemistry: Molecular, Cellular and Medical Aspects. 6th edition. Philadelphia: Lippincott-Raven; 1999.

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Basic Neurochemistry: Molecular, Cellular and Medical Aspects. 6th edition.

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Cerebral Metabolic Rate in Various Physiological States

and .

Correspondence to Donald D. Clarke, Chemistry Department, Fordham University, Bronx, New York 10458.

Cerebral metabolic rate is determined locally by functional activity in discrete regions

In organs such as heart or skeletal muscle that perform mechanical work, increased functional activity clearly is associated with increased metabolic rate. In nervous tissues outside the central nervous system, electrical activity is an almost quantitative indicator of the degree of functional activity; and in structures such as sympathetic ganglia and postganglionic axons, increased electrical activity produced by electrical stimulation definitely is associated with increased utilization of oxygen. Within the central nervous system, local energy metabolism also is correlated closely with the level of local functional activity. Studies using the [14C]deoxyglucose method have demonstrated pronounced changes in glucose utilization associated with altered functional activity in discrete regions of the central nervous system specifically related to that function [21]. For example, diminished visual or auditory input depresses glucose utilization in all components of the central visual or auditory pathways, respectively (Fig. 31-4). Focal seizures increase glucose utilization in discrete components of the motor pathways, such as the motor cortex and the basal ganglia (Fig. 31-5).

Figure 31-5. Local glucose utilization during penicillin-induced focal seizures.

Figure 31-5

Local glucose utilization during penicillin-induced focal seizures. Penicillin was applied to the hand and face area of the left motor cortex of a rhesus monkey. The left side of the brain is on the left in each of the autoradiograms in the figure. Numbers (more...)

Convulsive activity, induced or spontaneous, often has been employed as a method of increasing electrical activity of the brain (see Chap. 37). Davies and Remond [13] used the oxygen electrode technique in the cerebral cortex of cat and found increases in oxygen consumption during electrically induced or drug-induced convulsions. Because the increased oxygen consumption either coincided with or followed the onset of convulsions, it was concluded that the elevation in metabolic rate was the consequence of the increased functional activity produced by the convulsive state (see Chaps. 37 and 54).

Metabolic rate and nerve conduction are related directly

The [14C]deoxyglucose method has defined the nature and mechanisms of the relationship between energy metabolism and functional activity in nervous tissues. Studies in the superior cervical ganglion of the rat have shown almost a direct relationship between glucose utilization in the ganglion and spike frequency in the afferent fibers from the cervical sympathetic trunk [31]. A spike results from the passage of a finite current of Na+ into the cell and of K+ out of the cell, ion currents that degrade the ionic gradients responsible for the resting membrane potential. Such degradation can be expected to stimulate Na,K-ATPase activity to restore the ionic gradients to normal, and such ATPase activity in turn would stimulate energy metabolism. Indeed, Mata et al. [32] have found that, in the posterior pituitary in vitro, stimulation of glucose utilization due to either electrical stimulation or opening of Na+ channels in the excitable membrane by veratridine is blocked by ouabain, a specific inhibitor of Na,K-ATPase activity (see Chap. 5). Most, if not all, of the stimulated energy metabolism associated with increased functional activity is confined to the axonal terminals rather than to the cell bodies in a functionally activated pathway (Fig. 31-6) [33]. Astrocytes also contribute to the increased metabolism [34].

Figure 31-6. Effects of electrical stimulation of sciatic nerve on glucose utilization in the terminal zones in the dorsal horn of the spinal cord and in the cell bodies in the dorsal root ganglion.

Figure 31-6

Effects of electrical stimulation of sciatic nerve on glucose utilization in the terminal zones in the dorsal horn of the spinal cord and in the cell bodies in the dorsal root ganglion. (From [33].)

It is difficult to define metabolic equivalents of consciousness, mental work and sleep

Mental work. Convincing correlations between cerebral metabolic rate and mental activity have been obtained in humans in a variety of pathological states of altered consciousness [35]. Regardless of the cause of the disorder, graded reductions in cerebral oxygen consumption are accompanied by parallel graded reductions in the degree of mental alertness, all the way to profound coma (Table 31-7). It is difficult to define or even to conceive of the physical equivalent of mental work. A common view equates concentrated mental effort with mental work, and it is fashionable to attribute a high demand for mental effort to the process of problem solving in mathematics. Nevertheless, there appears to be no increased energy utilization by the brain during such processes. From resting levels, total cerebral blood flow and oxygen consumption remain unchanged during the exertion of the mental effort required to solve complex arithmetical problems [35]. It may be that the assumptions that relate mathematical reasoning to mental work are erroneous, but it seems more likely that the areas that participate in the processes of such reasoning represent too small a fraction of the brain for changes in their functional and metabolic activities to be reflected in the energy metabolism of the brain as a whole.

Table 31-7. Relationship Between Level of Consciousness and Cerebral Metabolic Ratea.

Table 31-7

Relationship Between Level of Consciousness and Cerebral Metabolic Ratea.

Sleep. Physiological sleep is a naturally occurring, periodic, reversible state of unconsciousness; and the EEG pattern in deep, slow-wave sleep is characterized by high-voltage, slow rhythms very similar to those often seen in pathological comatose states. As found in the pathological comatose states, cerebral glucose metabolism is depressed more or less uniformly throughout the brain of rhesus monkeys in stages 2 to 4 of normal sleep studied by the [14C]deoxyglucose method [36]. There are no comparable data available for the state of paradoxical sleep, also termed REM sleep, or for normal sleep in humans. During the stages of sleep as studied by PET scanning in humans, regional blood flow measurements suggest selective deactivation in certain regions of association cortex during slow-wave sleep and selective activation in other regions during REM sleep [37]. Regional metabolic measurements show activation in the same regions in association with rapid eye movements during REM sleep as with saccadic eye movements during wakefulness [38].

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Copyright © 1999, American Society for Neurochemistry.
Bookshelf ID: NBK27977

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