The intracellular signaling pathway of octopamine upregulating immune resistance functions in Penaeus monodon

Octopamine (OA), a biogenic monoamine, is known to mediate several immune responses. This study analyzed the effects of OA on immunological regulation in the tiger shrimp Penaeus monodon. The immune parameters including total haemocyte count, differential haemocyte count, phenoloxidase activity, respiratory bursts, superoxide dismutase activity, and phagocytic activity and clearance efficiency in response to the pathogen, Photobacterium damselae, were determined when shrimp were individually injected with saline or OA at 100 or 1000 pmol shrimp−1. In addition, the intracellular second messengers in haemocyte such as Ca2+ and adenosine 3′,5′-cyclic monophosphate (cAMP) were examined in shrimp receiving saline or OA at 1 or 10 nmol shrimp−1. Results showed that all of the immune parameters significantly increased at 2–4 h in OA-injected shrimp except hyaline cells in 100 pmol shrimp−1-injected shrimp at 4 h, but phenoloxidase activity per granulocyte significantly decreased at 2–4 h. However, these had returned to saline control levels after receiving OA for 8 h except differential haemocyte count and phenoloxidase activity per granulocyte for 16 h. An injection of OA also significantly increased the survival rate of shrimp challenged with Pho. damselae. Shrimp receiving OA at 1 and 10 nmol shrimp−1 significantly increased the intracellular Ca2+ concentration ([Ca2+]i) at 30–60 min and 30 min, and cAMP concentration [cAMP]i) at 5–15 min and 15 min, respectively. However, [Ca2+]i at 50–60 min, and [cAMP]i at 30–60 min returned to saline control when the shrimp received OA at 10 nmol shrimp−1, and at 1 and 10 nmol shrimp−1, respectively. These results suggest that OA administration by injection at ≤1000 pmol shrimp−1 mediates transient upregulation of immunity together with the increased resistance of P. monodon to Pho. damselae, which are modulated through intracellular Ca2+ and cAMP second messenger pathways.