The PR headlines are breathless and consistent:

Researchers Identify Brain Circuit That Regulates Thirst

Brain’s On-Off Thirst Switch Identified

The paper is here.

Yuki Oka, Mingyu Ye & Charles S. Zuker Thirst driving and suppressing signals encoded by distinct neural populations in the brain Nature (2015) doi:10.1038/nature14108

The takeaway punch message from the Abstract:

These results reveal an innate brain circuit that can turn an animal’s water-drinking behaviour on and off, and probably functions as a centre for thirst control in the
mammalian brain.

Somebody like me immediately thinks to himself “subfornical neurons control drinking behavior? This is like the fifth lecture in Psych 105: Introduction to Physiological Psychology.”

Let’s do a little PubMed troll for “subfornical drinking“. Yeah, we’ve known since at least the 1970s that the subfornical control of drinking behavior is essential, robust and mediated by angiotensin II signalling. We know how this area responds to blood volemia and natremia and how the positioning relative to the third ventricle and the function of the circumventricular organ vis a vis the blood-brain barrier permits this rapid-response. We know the signalling works through AT1 receptor subtype to excite subfornical neuronal activity via electrophysiological recording techniques and genetic deletions. Cholinergic mechanisms have likewise been identified as critical components via pharmacological experiments. Mapping of activated neurons has been used to identify related circuitry. The targets of subfornical neurons are known and their involvement in drinking behavior has likewise been characterized. Extensively. We know that electrical stimulation of these neuronal populations activates drinking in water sated rats, for goodness sake! We know there are at least three subpopulations of SFO neurons involved and something about the neurochemical signalling complexity.

There are review articles that you can read if you want to get up to speed.

The new work by Oka and colleagues simply repeats the above-mentioned electro-stimulation experiment from 1983 using optogenetic stimulation. Apart from this, maybe, we have an advance* in that they identified ETV-1 vs VGAT (GABA transporter) markers of two distinct subpopulations of neurons which have opposite effects on the motivation to consume water.

That’s it.

This paper is best described as a very small, incremental advance in understanding of thirst and drinking behavior, albeit tarted up with the pizzaz of optogenetic techniques.

Yet it was published in Nature.

Someone really needs to introduce the editorial staff of Nature to PubMed.
*BTW, a Nature editor confirms this microscopic incremental advance is what is new about this paper.