Central hyperventilatory action of the stress-related neurohormonal peptides, corticotropin-releasing factor and urotensin-I in the trout Oncorhynchus mykiss

The stress-related neurohormonal peptides corticotropin-releasing factor (CRF) and urotensin-I (U-I), an ortholog of mammalian urocortin 1, are widely distributed in the central nervous systems of teleost fish but little is known about their possible central neurotropic actions. In the present study, we investigated the effect of intracerebroventricular (ICV) injection of CRF and U-I (1–10 pmol) on ventilatory and cardiovascular variables in our established unanaesthetized trout model. CRF and U-I produced a significant dose-dependent and long-lasting increase in the ventilatory frequency (VF) and the ventilatory amplitude (VA). Consequently the net effect of these peptides was a hyperventilatory response since the total ventilation (VTOT) was significantly elevated. However, CRF evoked a significant hyperventilatory response 5–10 min sooner than that observed after ICV administration of U-I and the hyperventilatory effect of 10 pmol CRF was twofold higher than that of equimolar dose of U-I. Pre-treatment of the trout with the antagonist, alpha-helical CRF9–41, significantly reduced by about threefold the CRF-induced increase in VF, VA and VTOT. The most significant cardiovascular action of central CRF and U-I was to evoke a hypertensive response without changing the heart rate. Peripheral injection of CRF and U-I at doses of 5 and 50 pmol produced no change in VF, VA or VTOT. Only a transient hypertensive response without change in heart rate was observed after the injection of the highest dose of U-I. Our results demonstrate that in a teleost fish, CRF and U-I produce a potent hyperventilatory response only when injected centrally. The two endogenous stress-related neuropeptides may play an important stimulatory role acting as neurotransmitters and/or neuromodulators in the central control of ventilatory apparatus during stress.