rotein expression in Nav1.7 embryonic null mice – mechanisms of compensation

Mice and humans who have lost the expression of functional sodium channel Nav1.7 are pain-free, but otherwise normal. This is the result of a loss of neurotransmitter release such as glutamate and Substance P from primary sensory neurons. The sensory neurons are otherwise normal apart from loss of neurotransmitter release. Adult gene deletion results in a loss of neuronal excitability with some analgesia that is not linked to opioid activity. Drugs that block Nav1.7 have lethal effects through action on the autonomic nervous system and the heart. But the embryonic null humans and mice are fine. Therefore there must be compensation for the embryonic loss of Nav1.7. This experiment compares the protein components of wild type normal mice and Nav1.7 embryonic deletion mice in order to identify compensatory mechanisms.