"In order to compensate for those open gates, the bee's brain would be expected to cause those receptor gates to atrophy or something.  Such compensatory mechanisms could conceivably have a lasting effect long after the neonic was gone (as with human brains after childhood exposure to certain chemicals.."

Good thinking about compensatory effects, there is some evidence in the bumblebee paper Jim referenced in this thread  for that, and other studies supporting compensatory effects are referenced there too.  Perhaps we should discuss the bumblebee paper?

The bumblebee paper demonstrates very clearly what happens when neurons are chronically depolarized.  In that paper, the authors measured substantial mitochondrial depolarization. What that says to me is that the neurons are exhausting themselves trying to restore the resting membrane potential, which they cannot do since sodium is constantly leaking out.  So the proton gradients on the neuronal mitochondrial membranes are depleted because they are making ATP (via oxidative phosphorylation) faster than they can restore their proton gradients.  Next stop:  Dead neurons.

Christina


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