Читать книгу Canine and Feline Epilepsy - Luisa De Risio - Страница 46

Decrease in synaptic efficacy results in milder postsynaptic excitation, and consequently diminished amplification and spread of the seizure discharge. One mechanism limiting synaptic transmission during a sustained seizure discharge is the depletion of synaptic vesicles containing neurotransmitter. Staley et al. (1998) investigated the effects of synaptic depletion in vitro using a model of CA3 electrographic seizure discharges produced by hyperkalaemia. CA3 discharges consist of recurrent neuronal depolarizations with bursts of action-potential firing separated by period of electrographic silence. Staley et al. found that the duration of the seizure burst was proportional to the duration of the silent period preceding the burst, consistent with the hypothesis that the seizure burst duration depended on the renewed availability of immediately releasable glutamate. If glutamate-containing synaptic vesicles are replaced at a steady rate, longer inter-burst periods allow a greater resupply of immediately releasable glutamate, and an increased duration of the subsequent electro-graphic seizure discharge. Inter-burst intervals of 2–3 s or longer were necessary to achieve the longest burst durations (up to 420 ms). Thus, as the seizure discharge develops, it consumes the supply of readily releasable glutamate needed to sustain the seizure, potentially acting as a governor on excitatory drive. As the glutamate reservoir is replenished continuously, however, additional control mechanisms are necessary to prevent re-initiation of seizure activity.