La posture, composante statique du contrôle moteur permettant une position érigée du corps, repose sur une décharge tonique des motoneurones innervant nos muscles antigravitaires. La décharge prend la forme de « potentiel de plateau » au niveau de motoneurones matures chez de nombreux vertébrés. Pour déterminer une éventuelle concordance entre l'émergence des propriétés de plateau et le développement postural, notre travail a eu pour but d'étudier la maturation et la nature ionique des potentiels de plateau des motoneurones innervant le muscle triceps surae (extenseur de la cheville) chez le rat nouveau-né.La réalisation de ces travaux de thèse nous a permis de dégager un mécanisme fondamental dans la genèse des propriétés de plateau des motoneurones lombaires. Ce mécanisme dont le fondement repose sur l'activation d'un « ménage à trois » jouerait un rôle majeur dans le développement moteur chez le rat. Dans la mesure où les potentiels de plateau des motoneurones sont fortement perturbés à la suite d'une lésion médullaire, cette avancée scientifique permettra éventuellement de mieux comprendre l'origine de certains déficits sensori-moteurs (spasticité, hyperalgésie...) et le développement de nouvelles stratégies thérapeutiques. / Posture allowing an erect posture of the body relies on spiking activity of motoneurons innervating antigravitary muscle. Discharge could take the form of plateau potential on mature motoneurons of numerous vertebrates. To determine a possible concordance between the emergence of plateau potential and postural control development, we studied the maturation and ionic nature of plateau potential of motoneurons innervating triceps surae muscle of neonatal rat.The conclusion of our work allows us to propose a fundamental mechanism in the genesis of plateau potential on lumbar motoneurons. This mechanism based on a "ménage a trois" seems to play an important role in the neonatal motor development. This scientific advance could eventually lead to a better understanding of the origin of some sensori-motor impairments (spasticity, hyperalgesia...) and development of therapeutic strategies.

This Master’s Thesis concerns the technical problems and solutions in the Telia Mobile’s Golden Gate Architecture. The Golden Gate project will bridge service control from the IPnetwork to the circuit switched network. Connecting the different users of PSTN, GSM, W-LAN, and GPRS networks together will require solutions to many problems. Most of the problems have already been defined by Telia. Our task is to evaluate two parts of the Golden Gate architecture, namely the Interconnect- and Service Provider roles. The Interconnector provider connects networks of different technical standards and enables other network operators to reach Service Providers on the Internet or other IP-based networks. The role concerns mainly mapping between SS7 signaling and the Session Initiation Protocol (SIP), charging and billing. Via the Interconnector the Service Provider can connect different services to any network. We will describe the SIP-protocol in detail and then we will look into the mapping between SS7 and SIP. We will also propose a charging model. It is important to have a solution that supports roaming between the different networks, we will evaluate such a solution. Most of the protocols (INAP, ENUM, MAP and ISUP) that are involved in the Golden Gate architecture are not completely defined. There are many Internet Drafts that discuss the possible functionality of the protocols and the interworking between them. Many different Internet-workgroups are working with these issues. No one seems to have the right answers for the interconnection between the protocols involved. Since the IP-telephony will probably replace today’s telephony systems, it is important to ensure a suitable Quality of Service (QoS), security that guarantees privacy, and a fair billing function. These are the three major problems in the IP-telephony world. IP-Telephony or Voice over IP (VoIP) has been on the market for a long time, there are many 'free IP-call sites' that use VoIP, but the quality of the calls are not yet good enough to replace traditional telephony. Our task here is to make sure that the necessary quality of service is provided, and a reliable charging model is used.

Glutathione (GSH) is a small antioxidant in the body and exists in large quantities compared to other antioxidants. The GSH redox state (Eh) helps developmental processes, however, when the GSH Eh is disrupted, cells may undergo significantly poor developmental pathways, possibly leading to long-lasting damages. Similarly, NADPH and Thioredoxin redox states can have a major impact on cellular function, viability, and response to both endogenous and exogenous toxicants. Subcellular, compartmentalized redox environments during normal or perturbed situations, specifically in the cytosol, mitochondria, and nucleus, are not well understood. Here, using the P19 neurogenesis model of cellular differentiation, the kinetics of subcellular H2O2 availability and GSH/GSSG and NADPH/NADP+ redox shifts were evaluated following oxidant exposure. Additionally, modified mouse embryonic fibroblasts (MEFs) were used to observe redox changes and protective mechanisms when major antioxidative pathways are inhibited, mainly those involving the GSH/GSSG and Trxred/Trxox pathways. Overall, treated undifferentiated cells showed a greater degree and duration of both H2O2 availability and GSH/GSSG and NADPH/NADP+ disruption throughout all compartments than differentiated neurons. Pretreatment with an Nrf2 inducer prevented H2O2-induced effects in all compartments of undifferentiated cells. Additionally, MEF cells without either GSH or Trx showed a greater degree and duration of GSH/GSSG and Trxred/Trxox disruption throughout the cytosol and nucleus when compared to normal functioning cells. Disruption of redox-sensitive developmental pathways is likely stage-specific, where cells that are less differentiated and/or are actively differentiating are most affected. Undifferentiated cells are more susceptible to oxidant-induced redox dysregulation but are protected through prior Nrf2 induction, which appears to preserve developmental programs and diminish the potential for poor developmental outcomes. The GSH and Trx antioxidant pathways converge to protect the cell, while cells that are missing one pathway or the other may undergo damaging developmental outcomes.