my guess is that you have something along the lines of calcium carbide in those rocks

that's what statistically means. in the long run, in the absence of a selecting force to promote the stability of a beneficial trait, genetic drift will tend to disable neutral traits. this is especially true when 1) the genetic sequences underlying the trait need to be very precise for the trait to function properly (much more important in receptor/effector systems than in gross physical traits) and 2) the sequences are rather long. thus, we can assume that this receptor does not represent a neutral trait, especially because it directly involves a phenotype that is intimately tied to survival (breathing).

if you had read my entire comment, you would have noticed that I said the exact same thing. and not all neurotransmitters are bitter (ie basic), just most. the weird thing is that the neurotransmitters that we know contract the bronchioles (eg acetylcholine) are also predicted to be bitter compounds. strange stuff indeed.

Genetic drift would not explain why it developed in the first place, and would not be sufficient to keep a complicated receptor/effector system intact in a large, heterogeneous population such as ours for very long (in genetic terms). most people misunderstand the term.

/degree in genetics and genomics

i use reasoning in an abstract sense to mean "biological driving force." but you already knew that.

I wonder what might be the reasoning behind this system evolving/remaining intact in humans. I can't really think of an exogenous substance that we inhale naturally that would activate such a response and confer an advantage to us. My best guess would be that the natural ligand for these receptors is something that is produced locally in the lungs in scenarios where bronchiodilation is desired (ie sympathetic stimulation). as someone else pointed out, many of the common neuroreceptors are alkaloids, and would probably activate these receptors. From the abstract, it sounds like these receptors are Gq (IP3 and calcium) receptors, which is interesting because the "classic" receptors that dilate the smooth muscle in the lungs are Gs receptors that stimulate increased cAMP. In smooth muscle, more calcium generally leads to stronger, not weaker, contraction. cAMP leads to relaxation, explaining why epinephrine and albuterol have their effects.

didn't have time to read the whole paper. exam on this stuff tomorrow though, wonder if I can use this on an essay question?

/med student

talk about a crappy experimental setup. no way to control for all the things that could explain this result.

these kinds of hand-wavy experiments will continue to crop up as our ability to measure the brain outstrips our ability to understand.

it's way to easy to point an fMRI at a region "linked" to a particular behavior or type of thinking, and then wax poetic about what the increased activity may or may not mean. sad coming from a relatively respected lab.

there is a moderate amount of smooth muscle found in the venous system. from what I have been taught (only in my first year of medical school), these muscles are not under the same kind of highly-specific nervous system control that the muscle in arteries is under. ie, your body has a hard time selectively contracting/relaxing specific veins. these muscles are predominantly under hormonal control, meaning that their contraction is regulated at a body-wide level.

the vast majority of control over where blood flows in the body is at the level of arterioles, which are small arteries found before capillary beds.

not always, just when the correction is trivial and doesn't contribute to the understanding at hand. isn't hyperbole ("always") a more dangerous use of language? so much for respect.

to be completely accurate, arteries do indeed 'deliver' blood, as they are responsible for the distribution of the blood to the body. feel free to pop open oed, which I'm sure a doctor of your caliber has at the ready, if you doubt me.

additionally, the elastic quality of the major arteries allows for pumping of blood outside the heart, which more closely fits with your highly specific (but in the context of the discussion at hand, meaningless) definition of deliver. and let's not forget the smooth muscle around arteries which can contract, leading to yet another form of active 'delivery' of blood.

thanks for your career advice, doc. it has been taken to heart.

woah, you're totally right. my professor screwed that one up. we were taught that PDE5 cleaves both cAMP and cGMP, but it looks like only PDE1, 2, and 3 cleave both.

the downstream effects would be almost identical though. both cAMP and cGMP cause myosin light chain kinase to be phosphorylated by their respective kinases (PKA and PKG), leading to lower myosin activity and thus relaxation.

nice catch!

that's semantics.

in the context of what the poster was saying, i was pointing out that it is arteries that serve as conduits for blood that is flowing toward the penis (and all other tissues of the body), and veins are what serve as conduits for blood flowing away from the tissues.

thanks for your deep insight though.

/medical student

1) veins don't deliver blood, arteries do

2) the relaxation I was referring to was of the smooth muscle in the walls of the arteries leading to the penis

3) there isn't much regulation of bloodflow that takes place on the venous side (ie venous drainage is relatively constant). thus if you increase flow inward it will necessarily lead to pooling (ie erection)

the classic ED drugs all work by relaxing the arteries that flow toward the penis by inhibiting PDE5, a phosphodiesterase predominantly found in penis arteries. this increases cAMP levels, leaving to vasodilation and an erection. unfortunately these drugs aren't perfectly specific, and cause small amount of vasodilation throughout the body, along with a corresponding drop in blood pressure. this is why they tell you not to take the ED pills if you take other vasodilators like nitroglycerin.

if you could engineer a Gs (i was wrong in my earlier post when I said Gi, you want more cAMP not less) receptor that was light sensitive, and get it to express only in the penis artery smooth muscle.... and shine light through your skin to activate these receptors, it would work the same way.

obviously not an ideal way to treat a disorder. these light gated channels are probably only good for basic scientific research.

actually, it totally could work. erections occur because certain smooth muscle in the penis relaxes, allowing blood to flow in the right places. ED drugs block the degradation of a chemical that promotes this relaxation. a light gated receptor of the proper type (Gi) could be designed to do the same thing.

Please note that we have added a consequence for failure. Any contact with the chamber floor will result in an unsatisfactory mark on your official testing record, followed by death.