Crinoids have remarkable regenerative capacities. After traumatic or self-induced amputation they can replace one or several arms through a complex sequence of morphogenetic events which lead quickly to the complete reconstruction of the lost part. These phenomena are well known in their general aspects and a comprehensive description of arm regeneration was previously provided (Candia Carnevali et al., Recent Trends in Regeneration Research. Plenum Press, New York, '89). However, there is a considerable gap in knowledge of the early regenerative phases which are particularly significant for the following development. The aim of the present work is to describe and interpret the different aspects of these early stages of arm regeneration in Antedon mediterranea. According to our results the regenerative development ofAntedon arm seems to consist of an epimorphic

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Crinoid echinoderms can completely and rapidly regenerate arms lost following self-induced or traumatic amputation. Arm regeneration in these animals therefore provides a valuable experimental model for studying all aspects of regenerative processes, particularly with respect to the nervous system and its specific contribution to regenerative phenomena. Taking into account the primary role of the nervous system in regeneration in other invertebrates, we have investigated the specific involvement of neural factors, viz. the monoamine neurotransmitters dopamine and serotonin, in arm regeneration of Antedon mediterranea. In the present work, the presence of classical monoamines has been revealed by employing specific immunocytochemical and histofluorescence tests in association with biochemical detection by means of high pressure liquid chromatography. The distribution pattern of these neurohumoral molecules at standard regenerative stages has been compared with that of normal non-regenerating arms. Results indicate that both dopamine and serotonin dramatically change in both their distribution and concentration during the repair and regenerative processes. Their remarkably enhanced pattern during regeneration and widespread presence at the level of both nervous and non-nervous tissues indicates that they are important neural growth-promoting factors in crinoid arm regeneration.& k w d :

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Somatostatin (SRIF) exerts a modulatory function on neuronal transmission in the CNS. It has been proposed that a reduction of calcium currents is the major determinant of the inhibitory activity of this peptide on synaptic transmission. Because the neurotoxicity induced by activation of the NMDA subtype of glutamate receptor is mediated through excessive Ca2+ influx, we investigated whether SRIF counteracted NMDA‐induced neuronal cell death. Neurons from embryonic rat cerebral cortex were cultured for 7–10 days and then exposed to 0.5 and 1 mM NMDA for 24 h. The neuronal viability, as assessed by the colorimetric method, decreased by 40 and 60%, respectively, compared with the control condition. Morphological and biochemical evidence indicated that cell death occurred by necrosis and not through an apoptotic mechanism. SRIF (0.5–10 µM), simultaneously applied with excitatory amino acid, significantly reduced in a dose‐dependent manner the neurotoxic effect of NMDA but not that of KA (0.25–0.5 mM). GABA (10 µM) partially protected neurons to a similar extent from NMDA‐ or KA‐induced toxicity. SRIF type 2 receptor agonists, octreotide (SMS 201‐995; 10 µM) and vapreotide (RC 160; 10 µM), did not influence the NMDA‐dependent neurotoxicity. The intracellular mechanism involved in SRIF neuroprotection was investigated. Pertussin toxin (300 ng/ml), a G protein blocker, antagonized the protective effect of SRIF on NMDA neurotoxicity. Furthermore, the neuroprotective effect of SRIF was mimicked by dibutyryl‐cyclic GMP (10 µM), a cyclic GMP analogue, whereas 8‐(4‐chlorphenylthio)‐cyclic AMP (10 µM), a cyclic AMP analogue, was ineffective. The cyclic GMP content was increased in a dose‐dependent manner by SRIF (2.5–10 µM). Finally, both specific (Rp‐8‐bromoguanosine 3′,5′‐monophosphate, 10 µM) and nonspecific [1‐(5 isoquinolinylsulfonyl)‐2‐methylpiperazine (H7), 10 µM] cyclic GMP‐dependent protein kinase (cGMP‐PK) inhibitors did not interfere with NMDA toxicity but substantially reduced SRIF neuroprotection. Our data suggest a selective neuroprotective role of SRIF versus NMDA‐induced nonapoptotic neuronal death in cortical cells. This effect is likely mediated by cGMP‐PK presumably by regulation of the intracellular Ca2+ level.