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Intrathecal interferon-gamma facilitates the spinal nociceptive flexor reflex in the rat
1Department of Laboratory Medical Science and Technology, Karolinska Institute, Huddinge, Sweden.
Insights
Intrathecal interferon-gamma (IFN-gamma) enhances spinal reflexes, potentially causing hyperalgesia. This effect is partly mediated by the nitric oxide pathway, suggesting IFN-gamma
Area of Science:
- Neuroscience
- Immunology
- Pain Research
Background:
- Cytokines, such as interferon-gamma (IFN-gamma), play a role in central nervous system (CNS) inflammation.
- The role of IFN-gamma in spinal nociception and pain modulation requires further elucidation.
Purpose of the Study:
- To investigate the effect of intrathecal (i.t.) interferon-gamma (IFN-gamma) on spinal nociceptive reflexes.
- To explore the underlying mechanisms, including the involvement of the nitric oxide (NO) pathway.
Main Methods:
- Intrathecal injections of IFN-gamma were administered to decerebrate, spinalized, unanesthetized rats.
- The spinal nociceptive flexor reflex was measured.
- The effect of a nitric oxide synthase inhibitor (nitro-L-arginine-ester) on IFN-gamma-induced reflex changes was assessed.
Main Results:
- IFN-gamma induced a transient, intense facilitation followed by a prolonged facilitation of the flexor reflex (lasting approximately 40 minutes).
- The facilitatory effects of IFN-gamma were partially and fully blocked by pretreatment with a nitric oxide synthase inhibitor.
- The inhibitor did not affect spinal cord blood flow, indicating a specific action on the NO pathway.
Conclusions:
- Spinal administration of IFN-gamma causes significant and prolonged facilitation of the flexor reflex, suggesting a hyperalgesic action.
- The facilitatory effect of IFN-gamma is mediated, at least in part, by the L-arginine-nitric oxide pathway.
- CNS-released IFN-gamma may contribute to pain and hyperalgesia in inflammatory conditions characterized by increased cytokine production.
Abstract:
The effect of intrathecal (i.t.) injection of the cytokine interferon-gamma) (IFN-gamma) on the spinal nociceptive flexor reflex was examined in decerebrate, spinalized, unanesthetized rats. IFN-gamma elicited an initial intense, brief facilitation of the flexor reflex followed by a sustained reflex facilitation lasting 40 +/- 5 min (range 20-65 min). The initial and prolonged reflex facilitations by IFN-gamma were partially and totally blocked, respectively, by i.t. pretreatment with nitro-L-arginine-ester, an inhibitor of nitric oxide synthase, at doses which did not influence spinal cord blood flow. Spinal application of IFN-gamma produced powerful and prolonged facilitation of the flexor reflex, possibly reflecting a hyperalgesic action of this cytokine. The facilitatory effect of IFN-gamma was mediated, at least in part, by the activation of the L-arginine-nitric oxide pathway. Thus, IFN-gamma released in the CNS may participate in eliciting pain and hyperalgesia in infectious or neuroinflammatory diseases where there is increased production of this cytokine.
