Air-Exposure- and Reoxygenation-Stimulated Expressions of Caspase-3 and Induction of Apoptosis in the Central Nervous System of the Crab Erimacrus isenbeckii

Air exposure stress during live transport and subsequent reoxygenation are factors in the development of molecular/pathological and compensatory/adaptive responses. They affect the physiological functions and survival of economically important invertebrate species, in particular, crustaceans. In this study, we consider the effects of anoxia and subsequent reoxygenation on the physiological responses, signaling pathways involved in stress, and cell apoptosis in the central nervous system (CNS) of the horsehair crab, <i>Erimacrus isenbeckii</i>. The results showed that 1 day of air exposure stress and 1 subsequent day of reoxygenation cause the immunoreactivity of tyrosine hydroxylase (TH) and neuropeptide Y (NPY) to change, suggesting that these changes may be associated with adaptive responses, which are presumably employed to avoid oxidative damage and provide the initial mechanism for survival. Caspase-3 immunoreactive neurons increased eight-fold in the brain and 7.2-fold in the VNC after 1 day of reoxygenation, and the TUNEL-positive cell percentage rose from 0% (control) to 8.4% in the brain and from 1.7% (control) to 13% in the VNC. The results of our study provide evidence that anoxia and reoxygenation can activate caspase-3 and facilitate apoptosis in the CNS of crabs. These results provide evidence that even short-term air exposure stress followed by reoxygenation can trigger significant apoptotic cell death in crustacean neural tissue, which is important for developing better live transport practices.