Quote:
Originally Posted by N1
I think the two DSOs I looked at really are unsuitable for a proper test (too bright), and rather that looking for detail, a better measure could be "detected" vs. "not detected" as astro744 suggests, and doing that for a range of targets.
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Hi Mirko,
Indeed the targets of Omega Centauri and M22 are far too
bright to make some subjective analysis of dark adaptation.
Arguably, better choices are those on the verge of you perceiving
them or not, even after several hours of adaptation.
Quote:
I suppose if the exit pupil experiment did show a difference (all other factors being the same) between "pupil dilated to match exit pupil" and "fully dark adapted", that difference would be (almost) entirely due to said biochemical component of the process.
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It is important to keep in mind that pupil dilation, which is a muscular action,
is not the primary mechanism for photosensitivity when the eye is dark
adapted.
The article you cited itself explains it when it describes the function
of the molecular compound known as rhodopsin that acts as a biological pigment.
If you ever read generalized accounts of the chain of events
that take place at the molecular level when a photoreceptor neuron
cell triggers, I think we could all be excused for finding it complex
and seemingly convoluted.
If the mechanism had been designed by an engineer working at a modern
camera company, they would probably take him or her away on the
assumption they had lost their marbles.
Nevertheless it works and is testimony to what a few hundred million
years of evolution can produce.
Suffice to say that rhodopsin absorbs green-blue light and its levels
increases as you dark adapt. The build-up of rhodopsin as you
dark adapt takes place over tens of minutes.
When rhodopsin absorbs photons, a complex set of chemical events take place at the molecular level.
For example, see here -
http://en.wikipedia.org/wiki/Rhodopsin
Way down at the molecular level not just the photoreceptor neurons
in your eye but all neural cells use molecules such as sodium, potassium
and calcium to operate. In neurons they exist as charged ions to
create membrane potentials.
Though the build-up of rhodopsin takes place at the tens of minutes
scale, the actual chemical reaction times of when it is doing its job can
take place at the femtosecond and nanosecond scale.
So just as we are all aware that dietary intake of elements such
as potassium and sodium are essential to the human body for
brain and other nerve function, it is not surprising that they will
play a part in dark adaption. Vitamin A for example is essential
for the production of rhodopsin.
There have been studies into how dark adaptation tends to deteriorate
as most of us as we get older.
See
http://www.ncbi.nlm.nih.gov/pubmed/10748929
It is also important to remember that the visual system is not just about the
eye but also about the brain where a great deal of the processing takes place.
Many of us turn to metaphors such as digital cameras and CCD's to try and
understand how the human visual system works, but in my own reading
I have come to appreciate that that can be a mistake. For example, many
of us appreciate how colour works in a man-made digital camera and extrapolate to
that the human visual system works in a similar way. As it turns out, they
have little in common.
The take home message is that dark adaptation is not just about pupil
dilation which is a muscular action at the millimetre scale but is
greatly to do with what is happening at the atomic level with the
molecular biochemistry within your eye nerve cells.