Tizanidine primarily works by acting as an α2-adrenergic agonist. This means it binds to α2-adrenoreceptors in the central nervous system, specifically in the spinal cord and brainstem.
This binding reduces the release of excitatory neurotransmitters, like norepinephrine and glutamate. This reduction leads to decreased nerve impulse transmission in the spinal cord. The result is muscle relaxation.
The exact effects depend on the receptor subtype involved. α2A-adrenoreceptors are believed to play a more significant role in mediating tizanidine’s muscle relaxant effects than α2B or α2C subtypes.
| Α2A | Primary mediator of muscle relaxation |
| Α2B | Contributes to overall effect, but less significant than α2A |
| Α2C | Minor contribution to tizanidine’s effects |
This mechanism differs from that of other muscle relaxants, making tizanidine a unique option for treating muscle spasticity. Its selective action on central nervous system receptors minimizes peripheral side effects common with some other classes of muscle relaxants.
Therefore, understanding this targeted action at the α2-adrenergic receptors is key to comprehending tizanidine’s therapeutic benefits and potential side effects.
