Pro-inflammatory cytokines do not affect basal or hypoxia-stimulated discharge of rat vagal paraganglia.
Vagal paraganglia are structurally similar to the carotid body and are chemosensitive to reduction in the . We hypothesized that they may also mediate communication between the immune system and the central nervous system via pro-inflammatory cytokines or endotoxin. In vitro experiments with isolated superior laryngeal nerve (SLN) paraganglia were performed to test this hypothesis. We exposed the cells to increasing concentrations of interleukin-1β, tumour necrosis factor-α or interleukin-6 (0.1, 0.3 and 1 ng ml(-1)) or bacterial lipopolysaccharide (LPS, 10 and 100 ng ml(-1)) during both normoxia ( ≈ 100 mmHg) and hypoxia ( < 40 mmHg) whilst single-fibre recordings were made from the main SLN trunk using a glass suction electrode. The results of these experiments confirmed previous findings that these cells respond strongly to changes in , significantly increasing their discharge rate in response to hypoxia (from 0.71 ± 0.23 to 10.95 ± 1.74 Hz, P < 0.0001). However, neither the cytokines nor LPS had any significant effect on the baseline discharge rate of the SLN units at any concentration. When compared with time-matched controls, the cytokines and LPS also had no effect on the peak hypoxic discharge rate of the SLN (P = 0.59 and 0.65, respectively). In conclusion, neither the basal nor the hypoxic discharge rate of the SLN paraganglia is modulated by the inflammatory mediators tested above, suggesting that these structures are not the afferent limb of an 'immune reflex'.[1]References
- Pro-inflammatory cytokines do not affect basal or hypoxia-stimulated discharge of rat vagal paraganglia. O'Connor, E.T., O'Halloran, K.D., Jones, J.F. Exp. Physiol. (2012) [Pubmed]
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