How we taste sweet and bitter food decoded

Scientists have discovered how cells transmit taste information to the brain for sweet, bitter and savoury flavours.
A team of investigators discovered how ATP or Adenosine-5-triphosphate � the body's main fuel source - is released as the neurotransmitter from sweet, bitter, and umami, or savoury, taste bud cells.
The CALHM1 channel protein, which spans a taste bud cell's outer membrane to allow ions and molecules in and out, releases ATP to make a neural taste connection.
The other two taste types, sour and salt, use different mechanisms to send taste information to the brain.
Kevin Foskett, professor of Physiology at the Perelman School of Medicine, University of Pennsylvania, and colleagues from the Monell Chemical Senses Center, the Feinstein Institute for Medical Research, and others found how ATP release is key to this sensory information path.

They found that the calcium homeostasis modulator 1 (CALHM1) protein, recently identified by the Foskett lab as a novel ion channel, is indispensable for taste via release of ATP.

"This is an example of a bona fide ATP ion channel with a clear physiological function. Now we can connect the molecular dots of sweet and other tastes to the brain," Foskett said.
Taste buds have specialised cells that express G-protein coupled receptors (GPCRs) that bind to taste molecules and initiate a complex chain of molecular events, the final step of which Foskett and collaborators show is the opening of a pore in the cell membrane formed by CALHM1.

ATP molecules leave the cell through this pore to alert nearby neurons to continue the signal to the taste centers of the brain. CALHM1 is expressed specifically in sweet, bitter, and umami taste bud cells.
Mice in which CALHM1 proteins are absent, developed by Feinstein's Philippe Marambaud, have severely impaired perceptions of sweet, bitter and umami compounds; whereas, their recognition of sour and salty tastes remains mostly normal.
The CALHM1 deficiency affects taste perception without interfering with taste cell development or overall function.
Using the CALHM1 knockout mice, team members from Monell and Feinstein tested how their taste was affected.

"The mice are very unusual. Control mice, like humans, lick avidly for sucrose and other sweeteners, and avoid bitter compounds. However, the mice without CALHM1 treat sweeteners and bitter compounds as if they were water. They can't taste them at all," said Monell's Michael Tordoff.
The team concluded that CALHM1 is an ATP-release channel required for sweet, bitter, and umami taste perception.
The study was published in journal Nature.