Acetyl-L-carnitine in neuropathic pain: experimental data

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CNS Drugs. 2007;21 Suppl 1:31-8; discussion 45-6.

Acetyl-L-carnitine in neuropathic pain: experimental data.

Chiechio S, Copani A, Gereau RW 4th, tti F.

Department of Pharmaceutical Sciences, University of Catania,

Catania, Italy.

Acetyl-L-carnitine (ALC) has gained clinical interest for its

analgesic effect in different forms of neuropathies associated with

chronic pain, such as diabetic and HIV-related peripheral

neuropathies. The antinociceptive effect of ALC has been confirmed

in several experimental models of neuropathic pain, including

streptozotocin- and chemotherapy-induced neuropathy, and the sciatic

nerve chronic constriction injury model.

In these models, prophylactic administration of ALC has proven to be

effective in preventing the development of neuropathic pain. In

addition, ALC is known to produce a strong antinociceptive effect

when given after neuropathic pain has been established.

ALC can also improve the function of peripheral nerves by increasing

nerve conduction velocity, reducing sensory neuronal loss, and

promoting nerve regeneration.

Analgesia requires repeated administrations of ALC, suggesting that

the drug regulates neuroplasticity across the pain neuraxis. Recent

evidence indicates that ALC regulates processes that go beyond its

classical role in energy metabolism.

These processes involve the activation of muscarinic cholinergic

receptors in the forebrain, and an increased expression of type-2

metabotropic glutamate (mGlu2) receptors in dorsal root ganglia

neurons. Induction of mGlu2 receptors is mediated by acetylation

mechanisms that involve transcription factors of the nuclear factor

(NF)-kappaB family.