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Knocking out P2X receptors reduces transmitter secretion in taste buds

Yijen A Huang1, Leslie M Stone, Elizabeth Pereira

  • 1Department of Physiology and Biophysics, Miller School of Medicine, University of Miami, Miami, Florida 33136, USA.

The Journal of Neuroscience : the Official Journal of the Society for Neuroscience
|September 24, 2011
PubMed

Insights

Taste cells lacking P2X2 and P2X3 receptors fail to release ATP, challenging prior assumptions. This suggests P2X2 receptors are crucial for taste-evoked ATP secretion via autocrine signaling.

Area of Science:

  • Neuroscience
  • Sensory Biology
  • Cellular Physiology

Background:

  • Adenosine triphosphate (ATP) is a key neurotransmitter in taste perception, activating P2X2 and P2X3 receptors on gustatory nerves.
  • Mice lacking P2X2 and P2X3 receptors (DKO mice) exhibit abolished taste behavior and neural responses, implying these receptors are essential.
  • It was previously assumed that ATP secretion remained normal in DKO mice, with only postsynaptic targets removed.

Purpose of the Study:

  • To investigate the assumption that ATP secretion is normal in P2X2 and P2X3 double knock-out (DKO) mice.
  • To determine the role of P2X2 and P2X3 receptors in the process of ATP release from taste receptor cells.
  • To identify potential mechanisms underlying altered ATP secretion in the absence of P2X2 and P2X3 receptors.

Main Methods:

  • Functional imaging and ATP biosensor cells were used to measure ATP release from taste cells.
  • Cell-free assays and KCl depolarization were employed to assess ATP secretion capacity.
  • Reverse transcriptase (RT)-PCR, immunostaining, and histochemistry analyzed protein expression (Pannexin1, TRPM5, NTPDase2, P2X4, P2X7) and ultrastructure.

Main Results:

  • Taste receptor cells from DKO mice failed to release ATP in response to tastant stimulation, despite normal calcium mobilization.
  • ATP release was successfully elicited in DKO cells via KCl depolarization, indicating functional ATP-release machinery.
  • Expression levels of key ATP secretion/degradation proteins (Pannexin1, TRPM5, NTPDase2) and P2X4/P2X7 were similar in DKO and wild-type (WT) mice.

Conclusions:

  • The study refutes the assumption that ATP secretion is normal in P2X2/P2X3 DKO mice; these cells cannot release ATP when stimulated by tastants.
  • P2X2 receptors, expressed in WT taste buds, appear to act as an autocrine signal, amplifying taste-evoked ATP secretion.
  • The findings highlight a critical role for P2X2 receptors in the presynaptic release of ATP, essential for taste signal transduction.

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