After much time getting side-tracked by articles that aren't accessible to all, I finally found something I'm willing to present for the journal club format and can volunteer to kick it off.
shruth, I haven't looked at your paper yet, but why don't we add it to the queue since it's outside your area of expertise and you indicate it will take some time to understand. I'm sure any article will present difficulties to those who are outside any given field, so I propose that I begin with one that at least is sufficiently within my field that I can provide guidance in how to read and interpret it so those unfamiliar with reading journal articles can get more gently eased into the process.
This is the article I've found:
http://www.pnas.org/cgi/content/full/102/5/1761
Messager S, Chatzidaki EE, Ma D, Hendrick AG, Zahn D, Dixon J, Thresher RR, Malinge I, Lomet D, Carlton MB, Colledge WH, Caraty A, Aparicio SA. Kisspeptin directly stimulates gonadotropin-releasing hormone release via G protein-coupled receptor 54. Proc Natl Acad Sci U S A. 2005 Feb 1;102(5):1761-6.
The abstract:
We have recently described a molecular gatekeeper of the hypothalamic-pituitary-gonadal axis with the observation that G protein-coupled receptor 54 (GPR54) is required in mice and men for the pubertal onset of pulsatile luteinizing hormone (LH) and follicle-stimulating hormone (FSH) secretion to occur. In the present study, we investigate the possible central mode of action of GPR54 and kisspeptin ligand. First, we show that GPR54 transcripts are colocalized with gonadotropin-releasing hormone (GnRH) neurons in the mouse hypothalamus, suggesting that kisspeptin, the GPR54 ligand, may act directly on these neurons. Next, we show that GnRH neurons seem anatomically normal in gpr54-/- mice, and that they show projections to the median eminence, which demonstrates that the hypogonadism in gpr54-/- mice is not due to an abnormal migration of GnRH neurons (as occurs with KAL1 mutations), but that it is more likely due to a lack of GnRH release or absence of GnRH neuron stimulation. We also show that levels of kisspeptin injected i.p., which stimulate robust LH and FSH release in wild-type mice, have no effect in gpr54-/- mice, and therefore that kisspeptin acts directly and uniquely by means of GPR54 signaling for this function. Finally, we demonstrate by direct measurement, that the central administration of kisspeptin intracerebroventricularly in sheep produces a dramatic release of GnRH into the cerebrospinal fluid, with a parallel rise in serum LH, demonstrating that a key action of kisspeptin on the hypothalamo-pituitary-gonadal axis occurs directly at the level of GnRH release. The localization and GnRH release effects of kisspeptin thus define GPR54 as a major control point in the reproductive axis and suggest kisspeptin to be a neurohormonal effector.
So, I'll give everyone a week to get ahold of the article who wishes to participate and read it over. On Saturday, Jan 28, I'll open the thread for it (this gives me the weekend to focus on the initial discussion) and some relevant background material, and kick off the topic. When I open the thread, I'll post an introduction to the topic, a little bit about why this is an interesting topic to me, and provide some background to help folks understand the content. I thought a PNAS article would be a good one to kick off the topic, because those are usually very thorough, and give a good example of high-quality, cutting-edge science.
