I'm looking at melanopsin, a photo pigment in the human eye. One of its actions is to trigger suprachiasmatic nuclei SCN to suppress melatonin release. I'm interested in learning what is the exact mechanism that actually suppresses melatonin release. Is it another hormone or some way of modulating the pineal gland function?
1$\begingroup$ Is this not answered within your own previous question? biology.stackexchange.com/questions/3614/… "melatonin release is suppressed by blue light with peak suppression occuring at 420-480nanometer range. This light is registered by Melanopsin, a photopigment in the eye. Melanopsin signals the Suprachiasmatic Nucleus, the master clock of the human body. Suprachiasmatic nucleus makes a decision to suppress melatonin release in response to blue light observed." $\endgroup$– rg255Apr 23, 2013 at 15:07
$\begingroup$ So you're interested in the nature of the signal between melanopsin and the SCN? $\endgroup$– blepApr 23, 2013 at 16:08
$\begingroup$ To clarify: I know that SCN makes a decision to suppress melatonin. What interests me is what takes place during the actual process of suppression. What physically ensures that pineal gland stops producing melatonin. Is it another hormone that is released? $\endgroup$– Alex StoneApr 24, 2013 at 3:26
From Kalsbeek et al 1999 Neuroscience (link 1, link 2)
"retina-mediated photic activation of suprachiasmatic nucleus neurons induces the release of GABA from efferent suprachiasmatic nucleus nerve terminals, resulting in an inhibition of melatonin release by the pineal gland."
So it appears that GABA is key. When the retina is stimulated by light it results in activation of the neurons within the SCN which then release GABA. There is much more detail within the article and this is not my field so you may get more from reading that rather than my summary attempts.
Take a look at this (especially page 938): Coordination of circadian timing in mammals by Steven M. Reppert & David R. Weaver Nature 418, 935-941 (29 August 2002) | doi:10.1038/nature00965
Sodium-dependent action potentials provide the primary means by which the SCN transmit circadian outputs to other brain areas and are essential to its role as a pacemaker1.
Signalling molecules from SCN efferents include neurotransmit- ters and secreted factors. An output role for secreted factors comes from the results of SCN transplant studies that suggest that the alternating activity of SCN-derived ‘inhibitory’ and ‘activating’ factors drives locomotor activity rhythms (and hence rest/activity and sleep/wake cycles) in rodents
There was also a mention of per/cry gene expression.
1$\begingroup$ Welcome to Biology SE. It would be helpful if you could summarize the findings in your own words: you cannot count on everyone having access to the journal, or the link even working in the future. $\endgroup$– blepApr 23, 2013 at 19:08
$\begingroup$ Sure, will do :-) $\endgroup$– ahhsadApr 23, 2013 at 19:09
$\begingroup$ Thanks for a great article! It does not explicitly state how the pineal gland is affected though. $\endgroup$ Apr 24, 2013 at 3:42