Thirst 

Thirst is the craving for liquids, resulting in the basic instinct of humans or animals to drink. It is an essential mechanism involved in fluid balance. It arises from a lack of fluids and/or an increase in the concentration of certain osmolites such as salt. If the water volume of the body falls below a certain threshold, or the osmolite concentration becomes too high, the brain signals thirst.

Continuous dehydration can cause myriad problems, but is most often associated with neurological problems such as seizures, and renal problems.

Excessive thirst, known as polydipsia, along with excessive urination, known as polyuria, may be an indication of diabetes.

There are receptors and other systems in the body that detect a decreased volume or an increased osmolite concentration. They signal to the central nervous system, where central processing succeeds. Some sources1 therefore distinguish "extracellular thirst" from "intracellular thirst", where extracellular thirst is thirst generated by decreased volume and intracellular thirst is thirst generated by increased osmolite concentration. Nevertheless, the craving itself is something generated from central processing in the brain, no matter how it is detected.

Contents

Detection

There are many different receptors for sensing decreased volume or an increased osmolite concentration.

Decreased volume

Further reading: Hypovolemia

Hypovolemia leads to activation of the renin angiotensin system (RAS) and a decrease in atrial natriuretic peptide. These mechanisms, along their other functions, contribute to elicit thirst, by affecting the subfornical organ.2. For instance, angiotensin II, activated in RAS, is a powerful dipsogen (ie it stimulates thirst) which acts via the subfornical organ.

Increased osmolite concentration

Main article: Osmoreceptor

An increase in osmotic pressure, e.g. after eating a salty meal1 activates osmoreceptors. There are osmoreceptors already in the central nervous system, more specifically in the hypothalamus, notably in two circumventricular organs that lack an effective blood-brain barrier, the organum vasculosum of the lamina terminalis (OVLT) and the subfornical organ (SFO). However, although located in the same parts of the brain, these osmoreceptors that evoke thirst are distinct from the neighbouring osmoreceptors in the OVLT and SFO that evoke arginine vasopressin release to decrease fluid output.3

In addition, there are visceral osmoreceptors2. These project to the area postrema2 and nucleus tractus solitarius2 in the brain.

Salt craving

Because sodium is also lost from the plasma in hypovolemia, the body's need for salt proportionately increases in addition to thirst in such cases1. This is also a result of the renin-angiotensin system activation.

Senior citizens

For adults over age 50, the body’s thirst sensation diminishes and continues diminishing with age, causing many to suffer symptoms of dehydration.

Central processing

The area postrema and nucleus tractus solitarius signal, by 5-HT2, to lateral parabrachial nucleus2, which in turn signal to median preoptic nucleus. In addition, the area postrema and nucleus tractus solitarius also signal directly to subfornical organ.2

Thus, the median preoptic nucleus and subfornical organ receive signals of both decreased volume and increased osmolite concentration. They signal to higher integrative centers2, where ultimately the conscious craving arises. However, the true neuroscience of this conscious craving is not fully clear.

In addition to thirst, the organum vasculosum of the lamina terminalis and the subfornical organ contribute to fluid balance by vasopressin release.


See also

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References

  1. ^ a b c Carlson, N. R. (2005). Foundations of Physiological Psychology: Custom edition for SUNY Buffalo. Boston, MA: Pearson Custom Publishing.
  2. ^ a b c d e f g h i j k l M.J. McKinley and A.K. Johnson (2004). "The Physiological Regulation of Thirst and Fluid Intake". News in Physiological Sciences 19 (1): 1–6. doi:10.1152/nips.01470.2003. PMID 14739394, http://physiologyonline.physiology.org/cgi/content/full/19/1/1. Retrieved on 2 June 2006. 
  3. ^ Walter F., PhD. Boron. Medical Physiology: A Cellular And Molecular Approaoch. Elsevier/Saunders. ISBN 1-4160-2328-3.  Page 872