Remote sensing as tool for development of landslide databases: The case of the Messina Province (Italy) geodatabase

Landslide geodatabases, including inventories and thematic data, today are fundamental tools for national and/or local authorities in susceptibility, hazard and risk management. A well organized landslide geo-database contains different kinds of data such as past information (landslide inventory maps), ancillary data and updated remote sensing (space-borne and ground based) data, which can be integrated in order to produce landslide susceptibility maps, updated landslide inventory maps and hazard and risk assessment maps. Italy is strongly affected by landslide phenomena which cause victims and significant economic damage to buildings and infrastructure, loss of productive soils and pasture lands. In particular, the Messina Province (southern Italy) represents an area where landslides are recurrent and characterized by high magnitude, due to several predisposing factors (e.g. morphology, land use, lithologies) and different triggering mechanisms (meteorological conditions, seismicity, active tectonics and volcanic activity). For this area, a geodatabase was created by using different monitoring techniques, including remote sensing (e.g. SAR satellite ERS1/2, ENVISAT, RADARSAT-1, TerraSAR-X, COSMO-SkyMed) data, and in situ measurements (e.g. GBInSAR, damage assessment). In this paper a complete landslide geodatabase of the Messina Province, designed following the requirements of the local and national Civil Protection authorities, is presented. This geo-database was used to produce maps (e.g. susceptibility, ground deformation velocities, damage assessment, risk zonation) which today are constantly used by the Civil Protection authorities to manage the landslide hazard of the Messina Province

Presynaptic Nicotinic α7 and Non-α7 Receptors Stimulate Endogenous GABA Release from Rat Hippocampal Synaptosomes through Two Mechanisms of Action

BACKGROUND: Although converging evidence has suggested that nicotinic acetylcholine receptors (nAChR) play a role in the modulation of GABA release in rat hippocampus, the specific involvement of different nAChR subtypes at presynaptic level is still a matter of debate. In the present work we investigated, using selective α7 and α4β2 nAChR agonists, the presence of different nAChR subtypes on hippocampal GABA nerve endings to assess to what extent and through which mechanisms they stimulate endogenous GABA release. METHODOLOGY/FINDINGS: All agonists elicited GABA overflow. Choline (Ch)-evoked GABA overflow was dependent to external Ca(2+), but unaltered in the presence of Cd(2+), tetrodotoxin (TTX), dihydro-β-erythroidine (DHβE) and 1-(4,4-Diphenyl-3-butenyl)-3-piperidinecarboxylic acid hydrochloride SKF 89976A. The effect of Ch was blocked by methyllycaconitine (MLA), α-bungarotoxin (α-BTX), dantrolene, thapsigargin and xestospongin C, suggesting that GABA release might be triggered by Ca(2+) entry into synaptosomes through the α7 nAChR channel with the involvement of calcium from intracellular stores. Additionally, 5-Iodo-A-85380 dihydrochloride (5IA85380) elicited GABA overflow, which was Ca(2+) dependent, blocked by Cd(2+), and significantly inhibited by TTX and DHβE, but unaffected by MLA, SKF 89976A, thapsigargin and xestospongin C and dantrolene. These findings confirm the involvement of α4β2 nAChR in 5IA85380-induced GABA release that seems to occur following membrane depolarization and opening calcium channels. CONCLUSIONS/SIGNIFICANCE: Rat hippocampal synaptosomes possess both α7 and α4β2 nAChR subtypes, which can modulate GABA release via two distinct mechanisms of action. The finding that GABA release evoked by the mixture of sub-maximal concentration of 5IA85380 plus sub-threshold concentrations of Ch was significantly larger than that elicited by the sum of the effects of the two agonists is compatible with the possibility that they coexist on the same nerve terminals. These findings would provide the basis for possible selective pharmacological strategies to treat neuronal disorders that involve the dysfunction of hippocampal cholinergic system

Time course of GABA release in response to different agonists.

<p>Stimulatory effects of Ch (1 mM; ▾) (A) and 5IA85380 (10 nM; ♦) (B). Values are from two experiments and represent mean ± SEM of eight replicate superfusion chambers per condition (basal or evoked release). **p<0.01, ***p<0.001 versus time 36.5; ^#p<0.05, ^##p<0.01 versus basal release (•). Two way ANOVA followed by Tukey-Kramer <i>post hoc</i> test.</p