A significant goal in studies on learning and memory is to relate cellular plasticity to the modification of behaviour. The phenomenon of dual-process learning affords an ideal opportunity to explore the complexities inherent in establishing this relationship. Dual-process learning occurs when depression (habituation) and facilitation (sensitization) are expressed simultaneously within a neural network and compete to determine the behavioural outcome. A large body of literature is reviewed to define characteristics which are common across the neural networks that exhibit dual-process learning: depression occurs at loci early in the reflex pathway, upstream of the modulatory system necessary for the induction of facilitation. Consequently, depression not only competes directly with facilitation for the determination, of behavioural change (by serial and/or parallel expression), but depression also precludes the ongoing development and maintenance of sensitization (by serial induction). A mathematical model is presented to formally describe the nature of this competition and how this competition leads to the kinetics of dual-process learning. The tentacle withdrawal reflex of the snag Helix aspersa exhibits dual-process learning and was further investigated in this study. The neural circuit mediating tentacle withdrawal is described along with the nature and the location of plasticity which occurs within that circuit. In turn, plasticity at the cellular level is related, via the network level, to plasticity at the behavioural level. The data demonstrate the importance of localizing the sites of plasticity within a neural network in order to explain (1) how plasticity at a particular locus influences plasticity occurring elsewhere in the network and (2) how plasticity at different loci affect different aspects of behaviour.

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The gonad of the snail Helix aspersa is innervated by a branch of the intestinal nerve. Here it is demonstrated that nerve stimulation causes peristaltic contractions and the acceleration of cilia beating in the proximal part of the hermaphroditic duct. Acetylcholine and serotonin induced peristaltic contractions when applied without nerve stimulation. As well, serotonin induced the acceleration of cilia beating. The neuropeptide FMRFamide caused dilation of the hermaphroditic duct. Pharmacological blocking of acetylcholine and serotonin receptors with concurrent nerve stimulation induced a dilation similar to that caused by FMRFamide application. It is suggested that all three transmitters are released from intestinal nerve terminals to facilitate oocyte transport during ovulation. Nerve stimulation induced an increase in gamete transport rates. Because several candidate chemical messengers failed to induce ovulation when injected into the circulatory system, Helix aspersa appears to initiate ovulation differently from related species. Whereas Aplysia and Lymnaea use hormones, Helix apparently signals ovulation via the intestinal nerve.

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MUC1 est une mucine membranaire dont l'expression est augmentée et altérée dans le cancer et l'ischémie rénale. La transition épithélium-mésenchyme (TEM) est un processus dynamique de plasticité cellulaire impliqué dans la progression métastatique et la réparation tissulaire. Nos travaux montraient l'implication de MUC1 dans la plasticité épithéliale rénale à travers l'action de MUC1 dans des lignées cancéreuses rénales et dans des modèles murin et humain de régénération rénale. Dans le carcinome rénal, nous démontrions que (i) MUC1 et SNAIL, facteur de transcription de la TEM, étaient surexprimés dans une série de carcinomes sarcomatoïdes, (ii) SNAIL augmentait indirectement l'expression MUC1, (iii) la surexpression de MUC1 induisait la TEM, (iv) le domaine C-terminal de MUC1 (MUC1-C) augmentait l'interaction de la beta-caténine avec le promoteur de SNAIL favorisant l'activité transcriptionnelle de SNAIL, et (v) le blocage de la localisation nucléaire de MUC1-C diminuait l'activation de la voie Wnt /beta caténine et celle de SNAIL. Au total, nos résultats démontraient que MUC1 est un acteur de la TEM rénale associé au cancer et apparaît comme une nouvelle cible thérapeutique.Dans la régénération rénale, nous montrions que (i) la régénération rénale s'accompagnait d'une plasticité épithéliale transitoire compatible avec une TEM dans un modèle murin et sur des biopsies de greffon humain, (ii) MUC1 était induite au cours de la TEM associée à la régénération, (iii) l'absence de MUC1 (souris Ko Muc1)s'associait à des lésions tubulaires rénales plus sévères, et (iv) l'induction de MUC1 était inversement corrélée au degré de fibrose rénale. Au total, nos résultats suggèrent un rôle de néphroprotection conféré par MUC1 aux cellules épithéliales rénales au cours de la régénération. / MUC1 is overexpressed in renal carcinoma and ischemia. The epithelial-mesenchymal transition (EMT) is a dynamic process consisted of cellular plasticity involved in tumoral progression and tissue repair. Our work showed the involvement of MUC1 in renal epithelial plasticity through the action of MUC1 in renal cancer cell lines and in mouse and human kidney regeneration models.MUC1 is overexpressed in human carcinomas. The transcription factor SNAIL can activate epithelial-mesenchymal transition (EMT) in cancer cells. In this study, in renal carcinoma, we demonstrate that (i) MUC1 and SNAIL were overexpressed in human sarcomatoid carcinomas, (ii) SNAIL increased indirectly MUC1 expression, (iii) MUC1 overexpression induced EMT, (iv) MUC1 C-terminal domain (MUC1-C) and beta-catenin increased SNAIL transcriptional activity by interaction with its promoter and (v) blocking MUC1-C nuclear localization decreased Wnt/beta-catenin signaling pathway activation and SNAIL expression. Altogether, our findings demonstrate that MUC1 is an actor in EMT and appears as a new therapeutic target.In renal regeneration, we demonstrated that (i) regeneration was characterized by a transient EMT in mouse model and human biopsies allograft, (ii) MUC1 was induced during EMT-regeneration associated, (iii) the lack of MUC1 (Muc1 KO mouse) was associated with more severe renal tubular damage, and (iv) MUC1 induction was inversely correlated with renal fibrosis. Altogether, our results suggest MUC1 mitigates renal ischemic damage through EMT activation during regeneration.

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In this thesis I examined factors limiting population success of apple snails (Pomacea spp.) in Florida wetlands. First, I examined effects of summertime hydropattern in replicated wetlands on reproduction and juvenile growth. Annual reproductive effort of Florida apple snails (Pomacea paludosa) and the invasive apple snail P. maculata under was not affected by deeper water in the summer. When juvenile P. paludosa were forced to grow in reportedly favorable and relatively deeper summertime depths survival was high between treatments and growth was unaffected. In the other chapter I examined interactions between the two snails with a series of observations and experiments. I examined historical data on the assemblages and found that P. paludosa were locally extinguished in one of the wetlands within six years of invasion by P. maculata. Two field experiments gave conflicting results about the importance of interspecific inhibition of P. paludosa by the invasive snail, but in either case resource reduction could not be demonstrated. Lab exposure to P. maculata chemical cues strongly inhibited P. paludosa growth, although P. paludosa did not behaviorally avoid mucus of P. maculata. In mesocosms Pomacea paludosa growth was reduced with increasing exposure to adult P. maculata waterborne cues, and the results suggest that contact with mucus at a low exposure may even have a greater inhibiting effect. This interspecific direct chemical growth inhibition was novel for gastropods, but could be more generally important, and its potential impacts to P. paludosa populations should be explored further. / Includes bibliography. / Thesis (M.S.)--Florida Atlantic University, 2020. / FAU Electronic Theses and Dissertations Collection

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Planorbella trivolvis, a snail routinely found in catfish ponds, is an intermediate host in the life cycle of Bolbophorus damnificus, a digenetic trematode responsible for mortalities in catfish. This research generated information on the life cycle and the population dynamics of P. trivolvis in catfish ponds which could be implemented to control P. trivolvis. Research indicated that: P trivolvis is present year-round; survives overwintering at water temperatures of 5°C; reproduces year-round; is found in vegetation, sediment and water in ponds year-round; lays eggs two months post-hatch; and has a life span of at least one year. Planorbella trivolvis infected with Bolbophorus spp. were found in 0.8% of the snails examined; found in juvenile snails (4 mm), and could shed 3,200 cercariae/day, and shed these cercariae for up to 21 days. This data indicated that constant snail monitoring and persistent snail control is imperative to control P. trivolvis in catfish ponds.