TY - JOUR
T1 - LPS sensitizes TRPV1 via activation of TLR4 in trigeminal sensory neurons
AU - Diogenes, A.
AU - Ferraz, C. C.R.
AU - Akopian, A. N.
AU - Henry, M. A.
AU - Hargreaves, K. M.
PY - 2011/6
Y1 - 2011/6
N2 - Recent studies have demonstrated that the lipopolysaccharide (LPS) receptor (TLR4) is expressed in TRPV1 containing trigeminal sensory neurons. In this study, we evaluated whether LPS activates trigeminal neurons, and sensitizes TRPV1 responses via TLR4. To test this novel hypothesis, we first demonstrated that LPS binds to receptors in trigeminal neurons using competitive binding. Second, we demonstrated that LPS evoked aconcentration-dependent increase in intracellular calcium accumulation (Ca2+)i and inward currents. Third, LPS significantly sensitized TRPV1 to capsaicin measured by (Ca 2+)i, release of calcitonin gene-related peptide, and inward currents. Importantly, a selective TLR4 antagonist blocked these effects. Analysis of these data, collectively, demonstrates that LPS is capable of directly activating trigeminal neurons, and sensitizing TRPV1 via a TLR4-mediated mechanism. These findings are consistent with the hypothesis that trigeminal neurons are capable of detecting pathogenic bacterial components leading to sensitization of TRPV1, possibly contributing to the inflammatory pain often observed in bacterial infections.
AB - Recent studies have demonstrated that the lipopolysaccharide (LPS) receptor (TLR4) is expressed in TRPV1 containing trigeminal sensory neurons. In this study, we evaluated whether LPS activates trigeminal neurons, and sensitizes TRPV1 responses via TLR4. To test this novel hypothesis, we first demonstrated that LPS binds to receptors in trigeminal neurons using competitive binding. Second, we demonstrated that LPS evoked aconcentration-dependent increase in intracellular calcium accumulation (Ca2+)i and inward currents. Third, LPS significantly sensitized TRPV1 to capsaicin measured by (Ca 2+)i, release of calcitonin gene-related peptide, and inward currents. Importantly, a selective TLR4 antagonist blocked these effects. Analysis of these data, collectively, demonstrates that LPS is capable of directly activating trigeminal neurons, and sensitizing TRPV1 via a TLR4-mediated mechanism. These findings are consistent with the hypothesis that trigeminal neurons are capable of detecting pathogenic bacterial components leading to sensitization of TRPV1, possibly contributing to the inflammatory pain often observed in bacterial infections.
KW - endotoxin
KW - neuropeptides/transmitters
KW - neuroscience/neurobiology
KW - pain
KW - pharmacology
UR - http://www.scopus.com/inward/record.url?scp=79956058346&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=79956058346&partnerID=8YFLogxK
U2 - 10.1177/0022034511400225
DO - 10.1177/0022034511400225
M3 - Article
C2 - 21393555
AN - SCOPUS:79956058346
SN - 0022-0345
VL - 90
SP - 759
EP - 764
JO - Journal of dental research
JF - Journal of dental research
IS - 6
ER -