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. 2011 Mar 28;7:20. doi: 10.1186/1744-8069-7-20

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

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