THE RELATIONSHIP BETWEEN VOLTAGE GATED AND LIGAND GATED ION CHANNELS - PERSPECTIVES ON NEUROPHYSIOLOGY
Updated: Sep 8
RESEARCH CONDUCTED AT KING'S INSTITUTE OF PSYCHIATRY DURING NEUROSCIENCE MSc 2013-2015
Epilepsy can be described as abnormal LIGAND GATED ION CHANNEL exchange.
At resting potential, when a neuron receives a stimulas potassium K+ and Sodium Na+ ions exchange via voltage gated ion channels across the cell membrane. Shortly after there is a refractory period where the voltage gated ion channels restabalise via the exchange of calcium Ca2+, magnesium Mg2+ and chloride Cl- via LIGAND gated ion channels. When more calcium is outside the cell (as can be seen as a high plasma concentration of calcium) the refractory period cannot return to resting potential. This can lead to epilepsy and epileptic seizures.
Interestingly, physiological conditions that promote high serum calcium levels can also give way to epilepsy:
1. Primary hyperparathyroidism eg. parathyroid tumour will raise PTH1 levels releasing calcium from bone leading to elevated Ca2+ levels in blood serum.
2. Secondary hyperparathyroidism. PTH2 is released from the parathyroid gland in an attempt to store the excess Ca2+ back into bone. In epilepsy this is seen as a co-existing condition, namely Type I Diabetes and Insulin-dependant Type II Diabetes. This is linked to the administration of insulin in diabetes which disturbs the Na+/ K+ voltage gated ion channels leading to disturbance in the LIGAND GATED ION channels causing a higher Ca2+ level outside of the cell. Achieving Resting potential is delayed with delayed refractory period leading to shock of the neurons and possible seizures due to abnormal electric conduction along the neuron.
NB. IF EPILEPSY IS DUE TO UNSTABLE LIGAND GATED ION CHANNELS, STABILITY OF THE MEMBRANES CAN BE ACHIEVED VIA ADMINISTRATION OF CALCIUM CARBONATE eg. CALCICHEW/AD-CAL D3.
BY DR KATY WIN
PUBLISHED ONLINE 7TH SEPTEMBER 2026 @ 14:30
UPDATED 8TH SEPTEMBER 2026 @ 22:11
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