Adaptive evolution of voltage-gated sodium channels: stories from electric fish, desert mice, and scorpions

Professor Harold Zakon, School of Biological Sciences at the University of Texas, Austin

Seminar: Friday 2nd August 2013, 1:00pm
Lecture Theatre D, Carnegie Wing, Bute Building

I am delighted to announce a seminar to be delivered by Harold Zakon who will visit St Andrews on 2nd August. Harold is currently on sabbatical at the University of Cambridge, the recipient of a Parke-Davis Fellowship to work with Simon Laughlin and Clare Baker. Harold is perhaps most famous for his outstanding work on the neurobiology and behaviour of weakly electric fish and he will spend about half of his seminar telling us a recent story to emerge from his lab (topic 1, below). However, he will also tell us about his new and fascinating work on mice from the Sonoran desert that are resistant to the toxins of scorpions on which they predate (topic 2, below).

Harold is keen to meet as many kindred spirits as possible during his visit. If you would like to chat with him please let me know (kts1) and I’ll try to make a suitable arrangement.

Keith Sillar

1) Electric fish are green: energy conservation and ion channel recycling in electric fish.

Na channels are cycled into and out of the electric organ membranes in a circadian rhythm to regulate amount of Na current and thus the amplitude of the EOD. The amplitude of the EOD is greater at night when the fish are active and less in the day due to pulling back on Na channels. This saves fish about 30-60% of the energy they would spend on the EOD.

2) Evolution of resistance to scorpion toxins by a desert mouse: how a mouse converts a painful peptide into an analgesic.

We have been studying a Na channel in a mouse that lives in the Sonoran desert and preys on scorpions. This mouse is resistant to scorpion stings. In fact, it actually has evolved a sodium channel in its pain receptors that it blocked by toxin peptides (scorpion peptides activate, not block Na channels) and thereby has converted a peptide that is painful to one that acts as an analgesic.