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& Fitzgerald, R

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Research suggests that the function of the norepinephrine transporter may be enhanced in people with ADHD, leading to increased reuptake of norepinephrine, which reduces its concentration in the synaptic gap ( Epilepsy is fundamentally characterized by abnormal neuronal activity, primarily driven by an imbalance between excitatory and inhibitory neurotransmission, which leads to the pathological over-synchronization of neuronal networks ( V ) subunit 1 ( SCN1A ), which encodes the Na V 1.1 subunit, is predominantly expressed in GABAergic neurons ( SCN1A mutations as one of the most frequently implicated genetic alterations in epilepsy ( SCN1A knockout mice have demonstrated that the loss of Na V 1.1 function selectively reduces Na + current density in inhibitory interneurons, while sparing excitatory pyramidal neurons ( SCN1B encodes Na V 1, which shares similar clinical features with SCN1A ( SCN1B mutations may involve impaired Na V 1.1 function, ultimately leading to abnormal Na + channels (Wei et al., 2017)

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