NEUROPHYSIOLOGY

Author: GARCÍA MARTÍNEZ CAROLINA.
Year: 2003.
University: MIGUEL HERNÁNDEZ DE ELCHE.
Place of defense: MEDICINA.
Place of preparation: INSTITUTO BIOLOGÍA MOLECULAR Y CELULAR.

Summary: The receiver vanilloides 1 (TRPV1) performs an essential role in signal transduction nociceptive thermal and chemical weapons. Antagonists TRPV1 are compounds useful to reveal the contribution of this receptor in pain, and therefore as potential analgesics. This paper addresses the combinatorial strategy for identifying blockers not petídicos of this receptor. We identified two compounds that were selective blockers effectively micromolar by a mechanism not competitive. The administration of these compounds slowed the nocicepción thermal and reduced the pain and inflammation caused by neurogenic injection of capsaicin and mustard oil. These blockers can be considered as much as seeded for their development as inflammatory analgesics in pain. Additionally, in order to accelerate the process of identifying the molecular details of the union to the recipient and the future design of rational antagonist, are conducted studies estructura-función on TRPV1. Waste acídicos located in the region of the pore, or loop P are important for blocking and permeability properties, including amino acids D646 and E636. Junco with results obtained by other mutations in being region, and based on the crystal structure of the potassium channel KcsA, there is a structural model of the pore region of TRPV1.

Author: BENAVIDES PUERTA M. AMPARO.
Year: 2003.
University: MIGUEL HERNÁNDEZ DE ELCHE.
Place of defense: MEDICINA.
Place of preparation: INSTITUTO DE NEUROCIENCIAS.

Summary: The ion intracellular calcium acts as a signal regulating many cellular functions, such as the release of neurotransmitters, gene expression or cell death. Excessive increases in the concentration of intracellular calcium, can trigger various pathological process leading to cell death. Therefore cells have developed a number of mechanisms that allow them to regulate the concentration of intracellular calcium, including; reservoirs that release intracellular calcium or capture and molecules tamponadoras calcium. In excitable cells, calcium channel-dependent voltage (CCDV) are the main route for regulating the flow of calcium ions inside the cell. The electrophysiological and pharmacological studies have shown the existence of different types of CCDV high threshold activation: L, N, P / Q and R. Such channels are complex multiprotéicos formed by the combination of several subunits. The subunit alpha1 is the main trainer subunit of ion channel. To date we have identified at least 7 genes different codificanla subunit alpha1: Cav1.1, Cav1.2, Cav1.3 and Cav1.4 belonging to CCDV type L, Cav2.1 (channel type Q / Q), Cav2. 2 (channel N-type) and Cav2.3 (channel type R). Among the various roles played by calcium influx through the CCDV in cells cromafines, we are particularly interested in regulating gene expression, and in particular on the transcriptional regulation of their own CCDV. Through the RT-PCR determine the existence of different types of subunits alpha1 the CCDV in cells cromafines cattle: Cav1.1, Cav1.2, Cav1.3, Cav2.1, Cav2.2 and Cav2.3. The comparative study of the cells in culture and intact adrenal medulla shows that there are major differences in the pattern of expression of these subunits. Moreover, the study carried out on transcriptional regulation of the CCDV shows that the inflow of calcium through the CCDV is capable of regulating both the level of transcription and stability RNAm some of the subunits alpha1-channels calcium, suggesting that the cell has self-regulatory mechanisms to facilitate the maintenance of cellular homeostasis.

Author: GONZÁLEZ GARCÍA CARMEN M..
Year: 2003.
University: ROVIRA I VIRGILI.
Place of defense: MEDICINA.
Place of preparation: FACULTAT DE MEDICINA I CIÈNCIES DE LA SALUT.

Summary: Doctoral Thesis This is the result of 4 years of work in the field of synaptic plasticity, particularly in the loss of neural connections. The loss of neural connections is a process that occurs in different life situations of agencies, among them aging and certain neurodegenerative diseases. This process also takes place in a physiological during postnatal development. During postnatal development there is a short period where it triggered an orderly mechanisms for consolidating certain synapses and elimination of others to get configure selective neural circuits mature, leaving finally cells postsinápticas inervadas by a single axon. This study attempts to clarify the system or systems involved in this loss of nerve connections that take place outside the physiological in the joints neuromuscular -sinapsis between a motor neuron and a cell muscular-. At birth, the muscle cells are inervadas for more than a terminal nerve from different motor neurons. These nerve endings redundant will be progressively eliminated until the situation monoinvervación, normal situation in the joints neuromuscular mature. This thesis has tried to test the hypothesis that the process of disengagement synaptic postnatal depends on the activation of a cascade of signal transduction proteins that begins with the activation of receptor-trombita PAR-1, this latter component postsináptico of the neuromuscular junction (in the muscle cell), and the subsequent activity of a protein kinase C, specifically the theta isoform.

Author: MUÑOZ CUEVAS FRANCISCO JAVIER.
Year: 2003.
University: COMPLUTENSE DE MADRID.
Place of defense: FACULTAD DE MEDICINA.
Place of preparation: FACULTAD MEDICINA.

Summary: En esta tesis hemos estudiado la implicación de las plasticidades a corto plazo de los potenciales de acción sobre la depresión sináptica a corto plazo.Este tipo de plasticidad sináptica ha sido involucrada en la regulación de distintos procesos cognitivos como la habituación , la coordinación motora o la synchronization populations neuronales.Para check the role of changes in action potentials on depression in the short term, we have made records electrofisiologicos extracellular and intracellular in hippocampal slices in vitro using stimulations tetánicas to 10HZ (600pulsos). In these experiments we found that at least a significant portion of the synaptic depression in the short term due to failures in inducing potentials acción.Estos failures are caused by an increase in the threshold for firing in the axones and the dependent hyperpolarisation activity of the membrana.Los changes on the eve shooting are due to the inactivation cumulative sodium channel, while the hyperpolarisation the membrane seems to be mediated by activation of the bomb Na + / K + -ATPasa.Además of these effects synaptic depression, repetitive stimulation to 10hz also produces an increase in the induction of the action potentials that allows fibers auementar its safety factor for several pulsos.En short, these arguments demonstrate that, ademá of known mechanisms that regulate synaptic plasticity classical, there are other processes operating at levels prior to the release of neurotransmitter.