Saturday, February 10, 2007

 

Neuronal Fatigue

Neuronal Fatigue

Not only does neurophysiological partitioning siphon off available ATP to other more important circuits within the CNS, dysponetic processing secondary to subluxation can also reduce intracellular energy reserves of neurons, with a consequent decrement in neuronal performance, such as a reduction in action potential amplitude or a reduction in maximum frequency of activation. When a neuron transmits more frequently or more continuously than appropriate to its physical design, and is required to repolarize its membrane and resynthesize transmitter more rapidly than its capacity, fatigue may occur as it does at any cell. The possible sites of this fatigue lie within the mechanisms for polarizing the membrane and for synthesizing transmitter substance.

Continued activation of circuits in the neocortex, limbic system, thalamus, hypothalamus or reticular activating system as a consequence of dysponetic processing (secondary to subluxation) can generate fatigue of neurons in any CNS area. Any circumstances that diminish or impair restorative processes within the organism, such as sleep deficits, debilitating active dis-ease, injury or drugs, facilitate the development of neuronal fatigue.

When energy reserves (ATP) within a neuron are reduced sufficiently, the energy available for repolarizing the membrane after each transmission of an action potential is reduced, with resultant impairment of the repolarization process. Impaired and inefficient neuronal performance results. A lengthened repolarization time reduces the maximum frequency of transmission of action potentials and an incompletely repolarized membrane would reduce the magnitude of the action potential.

Declining ATP resources within a neuron also reduces the energy at hand for synthesizing neurotransmitters and receptor function. The result is a reduction in the excitatory or inhibitory effect of the neuron.


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