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What are the proposed mechanisms by which ECT might modulate seizure susceptibility? 


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Electroconvulsive therapy (ECT) may modulate seizure susceptibility through various mechanisms. One proposed mechanism involves the induction of generalized seizures during ECT sessions, leading to the observation of central-positive complexes (CPCs) with specific characteristics. These CPCs exhibit consistent peak amplitude scalp topology and are correlated with gamma band oscillations, suggesting a link to thalamocortical networks and generalized epilepsy syndromes. Additionally, ECT's impact on GABAergic neurotransmission and excitation/inhibition (E/I) balance could influence seizure susceptibility, as seen in studies using C. elegans models. Furthermore, recent insights from epigenetic studies suggest that ECT can dynamically alter gene expression through epigenetic mechanisms, potentially affecting seizure thresholds. These combined findings highlight the multifaceted ways in which ECT may modulate seizure susceptibility.

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The OGT-1/EEL-1 complex in C. elegans modulates seizure susceptibility by regulating GABAergic neuron function, leading to an imbalance in excitation and inhibition, impacting sensitivity to electroshock.
ECT may modulate seizure susceptibility through thalamocortical mechanisms, as evidenced by central-positive complexes (CPCs) with consistent characteristics and source localization in the thalamus and cingulate cortex.
ECT may modulate seizure susceptibility through anticonvulsant mechanisms, altering factors that influence convulsant activity, as suggested by neurobiological theories and electrophysiological findings in the reviewed literature.
The proposed mechanisms by which ECT might modulate seizure susceptibility include the innate immune system and neurogenesis, as highlighted in pre-clinical studies.

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