The five tastes—sweet, salty, sour, bitter, and umami—allow us to perceive the chemical makeup of food. Taste receptor cells, specialized sensory cells located primarily on the tongue, convert chemical stimuli into signals the brain can interpret. Sour taste is unique among these sensations because it is a direct response to the presence of acidity, specifically the concentration of hydrogen ions, or protons \(\text{(H}^+)\), in food. The mechanism for sourness remained mysterious until recently, posing a significant challenge to taste researchers.
The Mechanism of Proton Sensing
Sourness is a chemical sensation caused by acids dissolving in saliva, which subsequently release hydrogen ions \(\text{(H}^+)\). The concentration of these free \(\text{H}^+\) ions determines the intensity of the sour taste we perceive. When an acidic substance is consumed, these positively charged ions interact with the taste receptor cells on the tongue’s surface. This interaction triggers signal transduction, where the chemical presence of the acid is converted into an electrical event.
For the cell to register the sour stimulus, the hydrogen ions must enter the taste receptor cell. The influx of these positive charges causes the cell’s internal voltage to become less negative, a process called depolarization. This electrical change then signals the cell to release neurotransmitters, which are chemical messengers. These neurotransmitters subsequently activate the gustatory nerve fibers, sending the “sour” message directly to the brain.
Identifying the OTOP1 Receptor
The specific molecular machinery responsible for this proton entry and signal initiation is the Otopetrin 1 (OTOP1) protein. OTOP1 is the primary sour taste receptor channel, a discovery that resolved a long-standing question in taste science. Its identification marked a significant advance in understanding how the body detects acidity.
The OTOP1 protein functions as a proton channel, forming a pore or pathway through the taste cell’s membrane. This channel is gated, opening in response to acidic conditions to allow a rapid influx of \(\text{H}^+\) ions into the cell. The resulting spike in positive charge inside the cell initiates the depolarization and subsequent release of neurotransmitters.
This receptor is expressed primarily on Type III taste receptor cells, which are the specialized cells known to respond to sour stimuli. Researchers confirmed OTOP1’s role using genetic manipulation, such as creating mice without a functional OTOP1 gene. These “knockout” mice showed a severely diminished or eliminated neural response to sour solutions, providing definitive evidence that OTOP1 is necessary and sufficient for sour taste perception. OTOP1 has also been implicated in sensing ammonium chloride, suggesting its role extends beyond just detecting traditional acids.
The Physiological Importance of Sour Taste
The ability to detect sourness serves as a biological and evolutionary safeguard for many animals, including humans. Sour taste acts primarily as a warning system against the ingestion of potentially harmful or spoiled food. Foods often become highly acidic as they spoil due to microbial fermentation, and the sharp, unpleasant taste of high acidity signals that the item may be unsafe to consume.
Sourness also helps regulate diet by signaling the presence of unripe fruits, which contain high concentrations of organic acids. The aversive nature of intensely sour flavors encourages an organism to wait for the fruit to ripen, which reduces acidity and increases sugar content. The sensation of sourness plays a role in preparing the body for digestion. Tasting acidic compounds stimulates the salivary glands, increasing the flow of saliva which aids in the initial breakdown of food and stimulates the efficient secretion of other digestive enzymes.