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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A pair of GABAli neurons (cerebral A interneuron [Cr-Aint], Arshavsky et al., 1993; Norekian and Satterlie, 1993) was shown to drive a prolonged afterdischarge in the network that controls the buccal cone appendages.
Neuronal hyperactivity has been well documented in electrophysiological studies in rodent SCI models and is characterized by increased evoked and spontaneous action potential frequencies, lowered thresholds for action potential generation, and prolonged afterdischarge activity [52-56].
Moreover, vanillin also induced a significant shortened epileptic afterdischarge duration (Wu et al., 1989).
For each mouse, the amplitude of the pulses for stimulating BLA was set as 60 [micro]A (1 s train containing 60 Hz unidirectional pulses) at the first time and increased by 20 [micro]A every 10 min until the duration of the afterdischarge (AD) recorded in the BLA was longer than 5 s; then this stimulating amplitude was used in the further kindling process in this mouse.