Randy wrote:

Can you  (or
anyone else), please now provide supportive evidence (from any study) for
the irreversibility of neurological effects from any of the neonics, from
which we can then begin polite discussion?

I changed the thread name.  This will be, I hope, the polite and open
minded thread.

James provided an open access paper

http://ncbi.nlm.nih.gov/pmc/articles/PMC4415021/

 which shows a bioaccumulation of neonics in the brain over time which
would tend to support irreversibility.  Beyond that what the paper says
about long term damage effects to the neurons is pretty alarming.

The amounts used are field relevant.  2 ppb of imidacloprid is roughly what
would be found in a field of canola that was UNTREATED with imidacloprid
(treated instead with thiamethoxam) but was picking up imidacloprid from
the previous years soil treatment with imidacloprid on potatoes.  Bees
weren't dying from the dosages given,  but having neurological effects.

Years ago Pham-Delegue showed neurological effects in honeybees at these
dosages (and not sustained), but much cruder set up (proboscis extension
test).

Here is a second paper.  Also open access (somehow came up from google
scholar,  apidologie papers are not usually open access for the first five
years):

http://scholar.google.ca/scholar_url?url=https://hal.archives-ouvertes.fr/hal-01003656/document&hl=en&sa=X&scisig=AAGBfm1-q9-68awzEoAXiCNRqIkLl6GCsA&nossl=1&oi=scholarr&ved=0CBsQgAMoADAAahUKEwiMr8yujuLIAhWFeD4KHcRjAg8

Neural effects of insecticides in the honey bee
Luc P. BELZUNCES, Sylvie TCHAMITCHIAN, Jean-Luc BRUNET

from that paper:

The mechanisms by which neonicotinoids
impair learning and memory performances may
be more complex than expected. The metabolism
of certain neonicotinoids in insects and
plants results in the appearance of metabolites
toxic to bees. In plants and in the honey bee,
imidacloprid is transformed into different
metabolites such as olefin and 5-hydroxyimidacloprid,
which are toxic to the bees and
are suspected to bind to the nicotinic acetylcholine
receptor (Nauen et al. 2001; Suchail et al.
2001, 2004). The metabolism of thiamethoxam
results in clothianidin, a metabolite as toxic as
thiamethoxam that has been registered as
insecticide (Nauen et al. 2003; Ford and Casida
2006; Benzidane et al. 2010). The toxicokinetics
of acetamiprid in bees is somewhat
different and leads to the appearance of 6-
chloronicotinic acid. This metabolite is toxic in
chronic exposure but not in acute exposure and
remains stable for at least 72 h, especially in the
head and the thorax (Suchail et al. 2001, 2004;

Pages 353-354 have a discussion about receptor binding sites and
dissociation constants that may be relevant to our discussion, but the work
is with leaf hoppers not bees.

Stan

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