Table 8.
Comparison of the pharmacology of stimulus-induced rodent LTP and human secondary hyperalgesia or clinical pain
Target, action | Rodent LTP | Human models of secondary hyperalgesia | Human clinical pain | Comments | |
---|---|---|---|---|---|
QST: secondary hyperalgesia | Clinical response: pain report | ||||
Induction (Human postoperative pain) | |||||
μ-opioid receptor agonist | X | X | n.t. (area) X (thr/rating) |
controversial | |
NMDA receptor antagonist | X | X1 |
X (area) X (thr/rating) |
X | Ketamine also blocks OIH induction in rodents and humans |
α-adrenergic receptor antagonist | X | X |
X (area) n.t. (thr/rating) |
X | Acute spinal application of clonidine in humans |
NK1 receptor antagonist | X | 0 | n.t. | n.t. | Acute spinal application in rodents vs. chronic oral application in humans |
Modulation of α2δ VGCC subunit | 0 | X/0 | n.t. | X | Acute spinal application in rodents vs. chronic oral application in humans |
Maintenance (Human chronic neuropathic pain) | |||||
μ-opioid receptor agonist | X | X |
0 (area) X (thr/rating) |
X | |
NMDA receptor antagonist | 0 | X | X (area) X (thr/rating) | X | |
Modulation of α2δ VGCC Subunit | X | X | n.t. | n.t. | |
α-adrenergic receptor agonist/noradrenaline reuptake inhibitor | X | n.t. |
X (area) X (thr/rating) |
X | Clonidine (rodents) vs. venlafaxine (humans) |
X, induction/established state blocked by action at target
0, induction/established state not blocked action at target
n.t., not tested
QST, quantitative sensory testing
area, area of secondary hyperalgesia mapped using QST
thr/rating, threshold or rating of evoked pain as determined by QST
OIH, opioid-induced hyperalgesia
1, including action on LTP of human pain perception