negative regulation of sensory perception of sweet taste

Definition

Target type: biologicalprocess

Any process that stops, prevents or reduces the frequency, rate or extent of sensory perception of sweet taste. [GO_REF:0000058, GOC:mr, GOC:TermGenie, PMID:1716172]

Negative regulation of sensory perception of sweet taste involves a complex interplay of cellular and molecular mechanisms. It begins with the detection of sweet tastants by taste receptor cells (TRCs) located on the tongue. These TRCs express G protein-coupled receptors (GPCRs), primarily the heterodimer of T1R2 and T1R3, which bind to sweet molecules and initiate a signaling cascade. Upon binding, the T1R2/T1R3 receptor activates the G protein gustducin, leading to the production of the second messenger inositol trisphosphate (IP3). IP3 triggers the release of calcium ions (Ca2+) from intracellular stores, initiating a depolarization of the TRC membrane. This depolarization propagates to nearby neurons, sending a signal to the brain that is interpreted as sweetness.

However, constant exposure to sweet tastes would desensitize the system, leading to a diminished sweet perception. To counteract this, various mechanisms are involved in negative regulation of sweet taste perception:

1. **Desensitization of Taste Receptors:** Sweet taste receptors can undergo desensitization after prolonged exposure to sweet tastants. This occurs through several mechanisms:
* **Phosphorylation:** Receptor kinases can phosphorylate the T1R2/T1R3 receptor, leading to its internalization and degradation.
* **Endocytosis:** The receptors can be internalized through endocytosis and sequestered away from the cell surface, reducing their availability for ligand binding.
* **G protein uncoupling:** The G protein gustducin can be uncoupled from the activated receptor, preventing further signaling.

2. **Regulation of Intracellular Signaling:** The downstream signaling pathways can also be regulated to attenuate the sweet taste signal:
* **IP3 degradation:** Phosphatases can break down IP3, reducing its availability to activate Ca2+ release.
* **Calcium buffering:** Cellular mechanisms can buffer the increase in Ca2+ levels, preventing excessive depolarization of the TRC.
* **Activation of inhibitory pathways:** The signaling cascade can activate inhibitory pathways, such as the G protein-coupled receptor kinase (GRK) pathway, which can attenuate the sweet taste response.

3. **Adaptation at the Neuronal Level:** At the neuronal level, adaptation can occur to reduce the sensitivity to sweet stimuli:
* **Synaptic depression:** The release of neurotransmitters from taste neurons can be reduced through synaptic depression, diminishing the signal transmission to the brain.
* **Modulatory neurons:** Specialized neurons can release neurotransmitters that inhibit the transmission of sweet taste signals to the brain.

These negative regulatory mechanisms ensure that the sweet taste system remains responsive to changes in sweetness levels and prevents habituation to constant sweet stimuli. The fine-tuned balance between stimulatory and inhibitory pathways allows for the perception of a wide range of sweet tastes, from subtle sweetness to intense sweetness. '
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Proteins (1)

Compounds (4)