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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Nurses can benefit from including a post-discharge follow-up telephone call to bridge the gap between discharge and the patient's first after-discharge encounter with a healthcare provider.
Further, phenytoin also reduces the influx of calcium ions during depolarization.[2] At the synapse, phenytoin decreases post-tetanic potentiation and repetitive after-discharge.[1,9] Further, hydantoins have an effect on the cerebellum, activating inhibitory pathways that extend to the cerebral cortex.[1,3,5,9] Thus, phenytoin and other hydantoins block the initiation of electrical discharge by altering cellular depolarization.