Putative neuroprotective role of centrally administered corticotropin-releasing factor in low-temperature-exposed neonatal chicks

Corticotropin-releasing factor (CRF) modulates the activity of the hypothalamic–pituitary–adrenal axis, and has a key role in mediating neuroendocrine effects that occur in response to stressful stimuli. We have recently shown that exposure of neonatal chicks to low-temperature resulted in increased oxidative damage to the brain and i.c.v. injection of CRF increased homeothermy that was associated with tissue specific enhancement of mitochondrial fatty acid oxidation enzyme activities. These observations prompted an investigation into the potential role of CRF in a state of oxidative damage in the brain and other vital organs in low-temperature-exposed chicks. In the first experiment, neonatal chicks (Gallus gallus) were given i.c.v. injection of CRF (42 pmol) or saline and were then exposed to low-temperature (20 °C) for 3 h. Malondialdehyde (MDA) levels were measured in the plasma, brain, heart and skeletal muscle. In the second experiment, to confirm the modulatory role of CRF in the brain oxidative damage, as observed in the first experiment, neonatal chicks were given the i.c.v. injection of CRF (42 pmol), astressin (6 nmol, CRF receptor antagonist), or CRF (42 pmol) plus astressin (6 nmol) in combination, and were then exposed to low-temperature (20 °C) for 3 h. CRF significantly decreased the weight gain and feed consumption of chicks that were recovered by astressin. In the plasma, significantly higher MDA levels were observed in i.c.v. CRF chicks exposed to low-temperature, but this pattern was not observed in the brain, heart and skeletal muscle. Brain MDA levels in i.c.v. CRF chicks were decreased as compared with that of i.c.v. saline chicks on low-temperature exposure while i.c.v. astressin increased the MDA levels. In conclusion, CRF plays a putative neuroprotective role in the brain of low-temperature-exposed neonatal chicks.