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According to the review on pyridoxine-dependent epilepsy, what is the suggested mechanism for sudden cerebral suppression during pyridoxine infusion?

a. Increased GABA production
b. Shift in glutamate and GABA balance
c. Adverse kinetics of glutamate decarboxylase
d. Altered binding capacity of pyridoxal phosphate

1 Answer

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Final answer:

The shift in glutamate and GABA balance is a suggested mechanism for sudden cerebral suppression during pyridoxine infusion, which points to an alteration in neurotransmitter release and receptor activity, affecting excitatory/inhibitory balance in epilepsy.

Step-by-step explanation:

According to the review on pyridoxine-dependent epilepsy, the suggested mechanism for sudden cerebral suppression during pyridoxine infusion could relate to a shift in glutamate and GABA balance. Current research emphasizes the critical role of the balance between excitatory and inhibitory neurotransmission in the regulation of neural network activity. In the case of epilepsy and other neurological disorders, altered glutamate and GABA signaling can disrupt this balance. The mechanism involves changes in neurotransmitter release, receptor availability, and homeostatic regulation which may collectively contribute to increased neural excitability or suppression during epileptic events.

Studies show that during seizures, there is an alteration in the excitatory/inhibitory balance, with an initial increase in inhibition followed by increased excitation as the seizure progresses, and eventually, inhibition once again dominates at seizure termination. Describing the mechanism further, during pyridoxine infusion, pyridoxal phosphate might alter the binding capacity or affect neurotransmitter receptor activity, leading to the observed cerebral suppression through a rebalanced neurotransmitter environment.

The neuronal network remodeling, including loss of GABAergic interneurons and formation of new excitatory circuits, also plays a role in the regulation of seizure intensity and can influence the sudden changes in cerebral activity during treatment.

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