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Burn‐injury Alters Brain Catecholamine Levels and β‐AR Signaling
Author(s) -
El Ayadi Amina,
Wang Ye,
Guillory Ashley,
Herndon David,
Finnerty Celeste
Publication year - 2015
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.29.1_supplement.727.17
Subject(s) - burn injury , total body surface area , catecholamine , prefrontal cortex , endocrinology , medicine , western blot , chemistry , surgery , biochemistry , cognition , psychiatry , gene
The prefrontal cortex is the most evolved brain region sensitive to the detrimental effects of stress exposure. Burn injury causes a dramatic increase in systemic catecholamines (CAs) levels accompanied by a post‐burn hypermetabolic response and chronic activation of beta adrenergic (β‐AR)‐mediated signaling. While many have addressed the systemic effects of burn‐ induced CAs, to our knowledge, no one has looked at the central effects of burn‐induced stress. In this study we are analyzing the effect of burn injury on CAs levels and β‐AR signaling in the prefrontal cortex. To this end, we used our rat burn scald model with a 60% total body surface area scald burn. Rats were burned according to established published procedures. The animals were sacrificed at 2,6, 24 hours and 1 week post‐burn. The brain immediately removed, dissected and stored at ‐80. We used 3‐CAT ELISA kit to determine CAs levels, catch point assay to determine cAMP levels, and PKA activity was measured using a kit. Western blot analysis was used to analyze the β‐AR expression and downstream signaling targets. We found that burn injury increases adrenaline levels at 2 and 6 hrs post‐burn while significantly decreasing noradrenaline levels at the same time points. PKA levels were significantly increased 7 days post‐burn. Levels of cAMP were not significant different. We analyzed the role of the β‐AR signaling following burn injury and found that β2‐AR levels were significantly increased 7 days. PKA levels were increased at 6hrs (P<0.001). The Gs levels were decreased at 6 hrs while the levels of Gi protein were initially decreased before increasing at 1 week post‐burn. These data show that burn injury alters brain CAs and subsequent β‐AR signaling activation possibly via both the canonical and the non‐canonical pathways.