A mutation in the voltagegated Ca2 channel that caused the p
-A mutation in the voltage-gated Ca2+ channel that caused the protein to mis-localize to dendritic membranes instead of axon terminals will (INCREASE or DECREASE) synaptic transmission. Why?
Solution
The voltage gated calcium channels are highly critical in maintaining nerve impulse transmission from one neuron to another. The calcium ions are released from the dendritic extensions of one neuron by pinching off of the membrane with calcium ions accumulated in it. This vesicle then fuses with the axon segments of next neuron after the synaptic complex. The infusion of these calcium vesicles help in modulation of ionic concentration in the post-synaptic neuron.
Thus, any mutation resulting in re-distribution of these calcium channels can directly affect the function of a cell. In context of neuronal synaptic transmission, failure of optimum localization of calcium channels can lead to mis-management of flow of bio-chemical information across two neurons. If a mutation results in mis-localization of voltage gated calcium channels from axon termini to dendritic termini will result in failure of impulse transmission across the synapse. This will hold particular importance for myelinated neurons because unlike non-myelinated neurons, the membrane localization of voltage gated ion channels significantly alters the rate and mode of transmission of biochemical information.
Thus, according to this explanation, it can be deciphered that a mutation in the voltage-gated Ca2+ channel that caused the protein to mis-localize to dendritic membranes instead of axon terminals will decrease synaptic transmission
