Leptin dependent changes in the expression of tropomyosin receptor kinase B protein in nucleus of the solitary tract to acute intermittent hypoxia

• After acute IH TrkB protein expression was elevated in caudal medial NTS.
• IH decreased synaptophysin, but did not alter BDNF and GAP-43 protein expression.
• IH in leptin deficient rats did not alter protein expression of TrkB, BDNF and GAP43.
• Decreased synaptophysin to IH was not changed in leptin deficient rats.

To investigate the possibility that leptin exerts an effect in NTS by inducing changes in the expression of pre- and/or post-synaptic proteins, experiments were done in Sprague–Dawley wild-type rats (WT) rats and leptin-deficient rats (LepΔ151/Δ151; KILO rat) exposed to 8 h of continuous intermittent hypoxia (IH) or normoxia. Protein was extracted from the caudal medial NTS and analyzed by western blot for the expression of brain-derived neurotrophic factor (BDNF), tropomyosin receptor kinase B (TrkB), synaptophysin, synaptopodin and growth-associated protein-43 (GAP-43). In WT rats, BDNF and GAP 43 protein expression levels were not altered after IH or normoxia, although there was a trend towards an increase in BDNF expression. On the other hand, after IH, protein expression of both isoforms of the BDNF receptor TrkB (gp95 and gp145) was higher. Furthermore, synaptophysin protein expression was lower compared to normoxic WT rats. In the KILO rat, no changes were observed in the protein expression of BDNF, TrkB, or GAP 43 after IH when compared to KILO normoxic controls. However, synaptophysin was lower in the IH exposed KILO rat compared to normoxic controls, as found in the WT rat. Expression of synaptopodin was not detected in NTS in either IH or normoxic animals of all groups. These results suggest that leptin released during IH may contribute to neurotrophic changes occurring within NTS and that these changes may be associated with altered chemoreceptor reflex function.