Ontogenesis and functional morphology of the digestive system of the freshwater prawn, Macrobrachium amazonicum (Decapoda: Palaemonidae)

The appropriate feeding regime for larvae and post-larvae of crustacean decapods is essential for successful larval culture. Reports on the development and morphology of the mouthparts and foregut of these crustaceans have aided in the selection of appropriate larval foodstuffs and consequently increased larval survival and growth rate during development. In the present study, the functional morphology of foregut and mouthparts was investigated in larvae and post-larvae of the freshwater prawn M. amazonicum (Heller, 1862). From observations gathered on both the outer and inner feeding apparati the first stage larvae have obligatory lecithotrophy and feeding behaviour is initiated after molting to the second stage. The foregut of the larvae undergoes diverse morphological changes during larval development and the larval foregut of this species is primarily a mixing organ due to the absence of gastric mills and similar structures. After metamorphosis into post-larvae, drastic morphological changes occur in the foregut and mouthparts to adapt the animals to feed on the greater diversity of foods that are available in their new benthic habitat.

Stimulatory effects of adenosine on prolactin secretion in the pituitary gland of the rat

We investigated the effects of adenosine on prolactin (PRL) secretion from rat anterior pituitaries incubated in vitro. The administration of 5-N- methylcarboxamidoadenosine (MECA), an analog agonist that preferentially activates A2 receptors, induced a dose-dependent (1 nM to 1 µM) increase in the levels of PRL released, an effect abolished by 1,3-dipropyl-7-methylxanthine, an antagonist of A2 adenosine receptors. In addition, the basal levels of PRL secretion were decreased by the blockade of cyclooxygenase or lipoxygenase pathways, with indomethacin and nordihydroguaiaretic acid (NDGA), respectively. The stimulatory effects of MECA on PRL secretion persisted even after the addition of indomethacin, but not of NDGA, to the medium. MECA was unable to stimulate PRL secretion in the presence of dopamine, the strongest inhibitor of PRL release that works by inducing a decrease in adenylyl cyclase activity. Furthermore, the addition of adenosine (10 nM) mimicked the effects of MECA on PRL secretion, an effect that persisted regardless of the presence of LiCl (5 mM). The basal secretion of PRL was significatively reduced by LiCl, and restored by the concomitant addition of both LiCl and myo-inositol. These results indicate that PRL secretion is under a multifactorial regulatory mechanism, with the participation of different enzymes, including adenylyl cyclase, inositol-1-phosphatase, cyclooxygenase, and lipoxygenase. However, the increase in PRL secretion observed in the lactotroph in response to A2 adenosine receptor activation probably was mediated by mechanisms involving regulation of adenylyl cyclase, independent of membrane phosphoinositide synthesis or cyclooxygenase activity and partially dependent on lipoxygenase arachidonic acid-derived substances.