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Afterdischarge

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Afterdischarge 

the ability of neurons to rhythmically discharge impulses for a relatively long time after cessation of the stimulus. Usually, the stronger the stimulus and the longer its action on the receptors, the longer the afterdischarge. A short-term afterdischarge is produced by successive depolarization of the membrane of the neuron after prolonged rhythmic stimulation. A prolonged afterdischarge depends on the circulation of nerve impulses in the closed neuronal circuits of the reflex center.



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Evidence consistent with a pain-generating mechanism following injury include (1) the existence of hyperactivity in the spinal cord and thalamus of patients with SCI [43,58-59], (2) effectiveness of local anesthetics in alleviating pain when delivered to the injured cord [41,60], and (3) sensitization and prolonged afterdischarges of spinal sensory neurons following SCI [25,31,42,61-62].
Additionally, due to the afterdischarge effect noted by Mandell, this pattern progressively increases the body's tolerance for higher levels of energy.
Rats were stimulated daily and seizure class (Racine scale) and afterdischarge duration (ADD) were determined following each stimulation.
 
 
 
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