| Id |
Subject |
Object |
Predicate |
Lexical cue |
| TextSentencer_T1 |
0-101 |
Sentence |
denotes |
Activation of spinal glucagon-like peptide-1 receptors specifically suppresses pain hypersensitivity. |
| T1 |
0-101 |
Sentence |
denotes |
Activation of spinal glucagon-like peptide-1 receptors specifically suppresses pain hypersensitivity. |
| TextSentencer_T2 |
102-286 |
Sentence |
denotes |
This study aims to identify the inhibitory role of the spinal glucagon like peptide-1 receptor (GLP-1R) signaling in pain hypersensitivity and its mechanism of action in rats and mice. |
| T2 |
102-286 |
Sentence |
denotes |
This study aims to identify the inhibitory role of the spinal glucagon like peptide-1 receptor (GLP-1R) signaling in pain hypersensitivity and its mechanism of action in rats and mice. |
| TextSentencer_T3 |
287-451 |
Sentence |
denotes |
First, GLP-1Rs were identified to be specifically expressed on microglial cells in the spinal dorsal horn, and profoundly upregulated after peripheral nerve injury. |
| T3 |
287-451 |
Sentence |
denotes |
First, GLP-1Rs were identified to be specifically expressed on microglial cells in the spinal dorsal horn, and profoundly upregulated after peripheral nerve injury. |
| TextSentencer_T4 |
452-692 |
Sentence |
denotes |
In addition, intrathecal GLP-1R agonists GLP-1(7-36) and exenatide potently alleviated formalin-, peripheral nerve injury-, bone cancer-, and diabetes-induced hypersensitivity states by 60-90%, without affecting acute nociceptive responses. |
| T4 |
452-692 |
Sentence |
denotes |
In addition, intrathecal GLP-1R agonists GLP-1(7-36) and exenatide potently alleviated formalin-, peripheral nerve injury-, bone cancer-, and diabetes-induced hypersensitivity states by 60-90%, without affecting acute nociceptive responses. |
| TextSentencer_T5 |
693-820 |
Sentence |
denotes |
The antihypersensitive effects of exenatide and GLP-1 were completely prevented by GLP-1R antagonism and GLP-1R gene knockdown. |
| T5 |
693-820 |
Sentence |
denotes |
The antihypersensitive effects of exenatide and GLP-1 were completely prevented by GLP-1R antagonism and GLP-1R gene knockdown. |
| TextSentencer_T6 |
821-920 |
Sentence |
denotes |
Furthermore, exenatide evoked β-endorphin release from both the spinal cord and cultured microglia. |
| T6 |
821-920 |
Sentence |
denotes |
Furthermore, exenatide evoked β-endorphin release from both the spinal cord and cultured microglia. |
| TextSentencer_T7 |
921-1074 |
Sentence |
denotes |
Exenatide antiallodynia was completely prevented by the microglial inhibitor minocycline, β-endorphin antiserum, and opioid receptor antagonist naloxone. |
| T7 |
921-1074 |
Sentence |
denotes |
Exenatide antiallodynia was completely prevented by the microglial inhibitor minocycline, β-endorphin antiserum, and opioid receptor antagonist naloxone. |
| TextSentencer_T8 |
1075-1219 |
Sentence |
denotes |
Our results illustrate a novel spinal dorsal horn microglial GLP-1R/β-endorphin inhibitory pathway in a variety of pain hypersensitivity states. |
| T8 |
1075-1219 |
Sentence |
denotes |
Our results illustrate a novel spinal dorsal horn microglial GLP-1R/β-endorphin inhibitory pathway in a variety of pain hypersensitivity states. |