Gliotransmission modulates baseline mechanical nociception.
Foley, Jeannine C.
McIver, Sally R.
Haydon, Philip G.
Abstract: Pain is a physiological and adaptive process which occurs to
protect organisms from tissue damage and extended injury. Pain sensation beyond
injury, however, is a pathological process which is poorly understood. Experimental
models of neuropathic pain demonstrate that reactive astrocytes contribute to reduced
nociceptive thresho... read morelds. Astrocytes release "gliotransmitters" such as D-serine,
glutamate, and ATP, which is extracellularly hydrolyzed to adenosine. Adenosine 1
receptor activation in the spinal cord has anti-nociceptive effects on baseline pain
threshold, but the source of the endogenous ligand (adenosine) in the spinal cord is
unknown. In this study we used a transgenic mouse model in which SNARE-mediated
gliotransmission was selectively attenuated (called dnSNARE mice) to investigate the
role of astrocytes in mediating baseline nociception and the development of
neuropathic pain. Under baseline conditions, immunostaining in the dorsal horn of the
spinal cord showed astrocyte-specific transgene expression in dnSNARE mice, and no
difference in expression levels of the astrocyte marker GFAP and the microglia marker
Iba1 relative to wild-type mice. The Von Frey filament test was used to probe
sensitivity to baseline mechanical pain thresholds and allodynia following the spared
nerve injury model of neuropathic pain. DnSNARE mice exhibit a reduced nociceptive
threshold in response to mechanical stimulation compared to wild-type mice under
baseline conditions, but nociceptive thresholds following spared nerve injury were
similar between dnSNARE and wild-types. This study is the first to provide evidence
that gliotransmission contributes to basal mechanical nociception.
Keywords: Adenosine, Astrocyte, Gliotransmission, Pain.
Springer Open.read less
- Foley, Jeannine, Sally R. McIver, and Philip G. Haydon. "Gliotransmission modulates baseline mechanical nociception." Molecular Pain 7, no. 1 (12, 2011): 1-5.