Thanks Ghislain for an interesting read!

Here is my interpretation of this article, for what it is worth and for those who are interested.  I have tried to simplify it for laypeople (I’m used to reading this stuff).  I give some direct quotes and interpret them, and for the rest I just summarize the text. If you have any other technical questions, please contact me.   The authors employ time-tested and very standard neurophysiological methods to the problem. The main novelty is that they figured out a way to test whole sections of honeybee brain, when previously only individual cells were observed. (I haven’t verified their claim about this however)

“Although sublethal levels of neonicotinoids are known to disrupt honeybee learning and behaviour, the neurophysiological basis of these effects has not been shown.”

CW:  They are saying no one has figured out how it works at the neuron level.

“…we show that the neonicotinoids imidacloprid and clothianidin, and the organophosphate miticide coumaphos oxon, cause a depolarization block of neuronal firing and inhibit nicotinic responses.”

CW:  The neonics and organophosphates lock the receptors in the “on” position so that they can’t respond properly to natural signals (acetylcholine).

“These effects are observed at concentrations that are encountered by foraging honeybees and within the hive, and are additive with combined application.”

CW:  Concentration at “field dose” was tested…this is a questionable concern when looking at isolated tissues since the effect there is cumulative, so…I don’t know why the authors would bother with that comment…..but as the neonics are irreversibly bound to the receptors, upon continued exposure, the effect gets worse.  (This is all that matters here as it’s an isolated neuro prep)

They say their results show how cognitive behavior is affected as a result of this exposure.  It’s because the neurons are blocked….permanently.

They then cite many studies showing that honeybee cognitive and neuro impairment has been shown to be a result of sublethal neonic exposure.  They say this effect could be made worse by the additional use of organophosphates like coumaphos (miticide used by some beekeepers).  How these compounds interact at the target site has not been studied…this means, what happens to the receptor when it’s exposed to both of these chemicals at the same time?

They point out that neonics turn on ACh receptors, whereas organophosphates disable the enzyme acetylcholinesterase (this is supposed to break down the ACh in the synapses so that overstimulation of receptors doesn’t happen.  When the enzyme is not available, acetylcholine hangs around in the synapse and continuously stimulates the receptors, to the same effect that neonics have when they block the receptor in the “open” position).

They have developed a method for testing these compounds in whole brain tissue.  That is a big advance over previous work that could only measure responses in isolated neurons, because the entire synapse is necessary when looking at the two pesticide classes and the interaction that they are interested in here.  Acetylcholinesterase is found in the synaptic cleft (the space between neurons) and the nACh receptor is found in the second (AKA postsynaptic) neuron.

They used concentrations they found in the literature that duplicated “field concentrations” of neonics…but because the effect of these compounds is cumulative as they are irreversible, this fact doesn’t much matter.  Meaning, it doesn’t matter if they got the concentrations “right” or not.  This experiment was just to determine what happens when the neurons are exposed to neonics and organophosphates, and at the level of the neuron, “field relevant concentrations” aren’t….relevant!!!

Clothianidin is more potent than imidacloprid.

What happens is that instead of action potentials (the normal way many neurons respond and communicate) the neuron membrane just depolarizes and stays depolarized.  This is what they call a “block” because it is dysfunctional.

Then they tested normal ACh responses in their prep.  They found differences consistent with the presence of receptor subtypes.  These are well-known in other animals so it’s no surprise to find subtypes in our honeybee.

When they added neonics to the bath, the ACh responses were inhibited.

If the neurons are exposed to both coumaphos and a neonic, the inhibition is additive (worse).

They conclude:

“The effects of cholinergic pesticides on KCs are expected to lead to significant impairment of all cognitive functions that depend on this higher-order brain region, including multisensory integration, associative learning and memory, and spatial orientation. Consistent with this, sublethal exposure of honeybees to neonicotinoids significantly impairs olfactory learning in laboratory-based studies, and adversely affects navigation and foraging behaviour in the field.” (see their paper for cited references)

In my assessment, this is a well-conducted study.  The criticism that the neurons should be treated with “field-level concentrations” is specious and shows a complete lack of understanding of this type of experiment.  The question was:  What happens to the neurons when these chemicals get into the synapses?  That’s what they tested and they did a good job of it.

Nature Communications is a respected journal that usually gets good reviewers.  They didn’t fail us on this one.

Christina

             ***********************************************
The BEE-L mailing list is powered by L-Soft's renowned
LISTSERV(R) list management software.  For more information, go to:
http://www.lsoft.com/LISTSERV-powered.html