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Table 8 Comparison of the pharmacology of stimulus-induced rodent LTP and human secondary hyperalgesia or clinical pain

From: Long-term potentiation in spinal nociceptive pathways as a novel target for pain therapy

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

X 1

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)

  1. X, induction/established state blocked by action at target
  2. 0, induction/established state not blocked action at target
  3. n.t., not tested
  4. QST, quantitative sensory testing
  5. area, area of secondary hyperalgesia mapped using QST
  6. thr/rating, threshold or rating of evoked pain as determined by QST
  7. OIH, opioid-induced hyperalgesia
  8. 1, including action on LTP of human pain perception