Since proteins are the molecular actors that mediate signal transduction, protein synthesis as well as protein Reversine degradation must be important for plasticity and memory. Indeed, regulated proteolysis plays a critical role in the remodeling of synapses. Regulated proteolysis is achieved by two major systems in eukaryotic cells: the proteasome and the lysosome. The lysosome degrades most membrane and endocytosed proteins. Owing to their large surface-to-volume ratio, the degradation of membrane proteins such as receptors by the endocytic/lysosomal pathway must be especially efficient and tightly regulated in neurons. Whereas several studies have implicated the proteasome in LTM in Aplysia, in the crab and in mammals, less is known about the implication of the lysosome in this process. It has been suggested that Neur is implicated in both the proteasome and the lysosome degradation pathways. Dbr is involved in protein degradation, and has been characterized as a component of the multivesicular bodies, an actor of the lysosome pathway. Subsequently, the MVB membrane becomes continuous with lysosomes leading to degradation of the receptor. Although we cannot rule out that dbr could be implicated in LTM via another pathway, we suggest that its function in LTM takes place through the lysosomal protein degradation pathway. The mucosal epithelium is of immense importance in host defense and immune surveillance, as it is the initial tissue encountered by the majority of infecting microorganisms. Vaginal epithelium provides a physical barrier, which recognizes commensal and pathogenic microbes, as well as regulating the influx of immune cells to prevent inflammatory tissue destruction. This specialized interaction between microbes, epithelial cells and local immune cells results in either a degree of mutualism between microbe and host, as in the case of commensal microbes, or a breach of the mucosal barrier and subsequent cell injury, as in the case of pathogenic microbes. Indeed, the integrity of the host immune system plays an important role in defining whether a microbe acts as a commensal colonizer or as an opportunistic pathogen. Of particular interest are ‘opportunistic’ microbes, which although normally commensal are capable of becoming pathogenic. The polymorphic fungus Candida albicans is one such opportunistic microbe, being a constituent of the normal vaginal microbiota but commonly causing mucosal disease in healthy women of fertile age. Recently, we identified a host mechanism in oral ECs that discriminates between the commensal and pathogenic states of C albicans, which is based on hypha recognition and fungal burdens. We demonstrated that epithelial innate immunity against C. albicans is initiated via NF-kB and a bi-phasic mitogen-activated protein kinase response. Activation of NF-kB and the first MAPK phase, constituting activation of the c-Jun transcription factor, is independent of morphology and is due to the recognition of fungal cell wall polysaccharides.