An Integrated Surface Seismic/Seismic Profile Case Study: Simonette Area, Alberta

On the basis of conventional surface seismic data, the 13-15-63-25W5M exploratory well was drilled into a low-relief Leduc Formation reef (Devonian Wood-bend Group) in the Simonette area, west-central Alberta, Canada. The well was expected to intersect the crest of the reef and encounter about 50-60 m of pay; unfortunately it was drilled into a flank position and abandoned. The decision to abandon the well, as opposed to whipstocking in the direction of the reef crest, was made after the acquisition and interpretive processing of both near-and far-offset (252 and 524 m, respectively) vertical seismic profile (VSP) data, and after the reanalysis of existing surface seismic data

General features of the retinal connectome determine the computation of motion anticipation

Motion anticipation allows the visual system to compensate for the slow speed of phototransduction so that a moving object can be accurately located. This correction is already present in the signal that ganglion cells send from the retina but the biophysical mechanisms underlying this computation are not known. Here we demonstrate that motion anticipation is computed autonomously within the dendritic tree of each ganglion cell and relies on feedforward inhibition. The passive and non-linear interaction of excitatory and inhibitory synapses enables the somatic voltage to encode the actual position of a moving object instead of its delayed representation. General rather than specific features of the retinal connectome govern this computation: an excess of inhibitory inputs over excitatory, with both being randomly distributed, allows tracking of all directions of motion, while the average distance between inputs determines the object velocities that can be compensated for

Ca2+ Extrusion by NCX Is Compromised in Olfactory Sensory Neurons of OMP−/− Mice

The role of olfactory marker protein (OMP), a hallmark of mature olfactory sensory neurons (OSNs), has been poorly understood since its discovery. The electrophysiological and behavioral phenotypes of OMP knockout mice indicated that OMP influences olfactory signal transduction. However, the mechanism by which this occurs remained unknown.We used intact olfactory epithelium obtained from WT and OMP(-/-) mice to monitor the Ca(2+) dynamics induced by the activation of cyclic nucleotide-gated channels, voltage-operated Ca(2+) channels, or Ca(2+) stores in single dendritic knobs of OSNs. Our data suggested that OMP could act to modulate the Ca(2+)-homeostasis in these neurons by influencing the activity of the plasma membrane Na(+)/Ca(2+)-exchanger (NCX). Immunohistochemistry verifies colocalization of NCX1 and OMP in the cilia and knobs of OSNs. To test the role of NCX activity, we compared the kinetics of Ca(2+) elevation by stimulating the reverse mode of NCX in both WT and OMP(-/-) mice. The resulting Ca(2+) responses indicate that OMP facilitates NCX activity and allows rapid Ca(2+) extrusion from OSN knobs. To address the mechanism by which OMP influences NCX activity in OSNs we studied protein-peptide interactions in real-time using surface plasmon resonance technology. We demonstrate the direct interaction of the XIP regulatory-peptide of NCX with calmodulin (CaM).Since CaM also binds to the Bex protein, an interacting protein partner of OMP, these observations strongly suggest that OMP can influence CaM efficacy and thus alters NCX activity by a series of protein-protein interactions

Cholinergic modulation of hippocampal CA1 pyramidal neuron intrinsic excitability

Bibliography: p. 176-212Some pages are in colour.Cholinergic stimulation in the hippocampus increases neuronal excitability that contributes to rhythmic activity and seizures. In this dissertation, I used the whole-cell patch clamp techniques in hippocampal CA 1 pyramidal neurons to study the current underlying the cholinergic-dependent plateau potential (PP). When combined with muscarinic stimulation, depolarizing command potentials to evoke Ca²⁺ influx elicited a prolonged inward tail current (Itail). Itail had an extrapolated reversal potential of -20 m V and was abolished by chelating [Ca²⁺]i with BAPTA or removal of [Na+]0 Soluble guanylate cyclase (sGC) inhibitors depressed Itail whereas blocking cGMP specific phosphodiesterase enhanced Itail. Cyclic-nucleotide gated (CNG) channel blockers reversibly depressed Itail, but PKG inhibition had no effect. Thus, I propose that Ca²⁺ influx combined with muscarinic stimulation activates sGC and increases cGMP levels, leading to CNG channel activation and generation of the PP. R-type Ca²⁺ spikes are important in generating dendritic Ca²⁺ transients and burst firing. I show that R-type Ca²⁺ spikes are enhanced by activation of Ml/M3 muscarinic receptors. This enhancement requires increased [Ca²⁺]i and the activation of a Ca²⁺/calmodulin-dependent protein kinase II pathway. Enhanced R-type Ca²⁺ spikes could repetitively fire at theta frequencies (~5-10 Hz) and could contribute to spike generated DAPs and PPs. Blocking R-type Ca²⁺ channels depressed carbachol-induced field potential theta oscillations, implying that enhanced R-type Ca²⁺ spikes play a role in theta current generation. The sensitivity of the PP to the antiepiletic topiramate was investigated. In current clamp, PPs were depressed by therapeutic concentrations of topiramate. Conversely, ItailS evoked in voltage clamp were not depressed but significantly longer voltage steps were required to elicit Itail indicating that the Ca²⁺entry trigger for evoking PPs was depressed. Topiramate had no effect on Ca²⁺ spikes in control conditions, however Ca²⁺ spikes after muscarinic stimulation were reduced. Carbachol enhances R-type Ca²⁺ spikes; therefore, the effect of topiramate was tested on R-type Ca²⁺ channels. Carbachol-enhanced R-type Ca²⁺ spikes were depressed by topiramate. Topiramate also depressed currents mediated by Cav2.3 Ca²⁺ channels expressed in tsA-201 cells. Thus, I have found that topiramate reduces seizure activity in hippocampal neurons through a novel inhibitory action of R-type CA²⁺channels

An Integrated Surface and Borehole Seismic Case Study: Fort St. John Graben Area, Alberta, Canada

The deltaic sandstones of the basal Kiskatinaw Formation (Stoddard Group, upper Mississippian) were preferentially deposited within structural lows in a regime characterized by faulting and structural subsidence. In the Fort St. John Graben area, northwest Alberta, Canada, these sandstone facies can form reservoirs where they are laterally sealed against the flanks of upthrown fault blocks. Exploration for basal Kiskatinaw reservoirs generally entails the acquisition and interpretation of surface seismic data prior to drilling. These data are used to map the grabens in which these sandstones were deposited, and the horst blocks which act as lateral seals. Subsequent to drilling, vertical seismic profile (VSP) surveys can be run. These data supplement the surface seismic and well log control in that: 1) VSP data can be directly correlated to surface seismic data. As a result, the surface seismic control can be accurately tied to the subsurface geology; 2) Multiples, identified on VSP data, can be deconvolved out of the surface seismic data; and 3) The subsurface, in the vicinity of the borehole, is more clearly resolved on the VSP data than on surface seismic control. On the Fort St. John Graben data set incorporated into this paper, faults which are not well resolved on the surface seismic data, are better delineated on VSP data. The interpretive processing of these data illustrate the use of the seismic profiling technique in the search for hydrocarbons in structurally complex areas

An Integrated Surface Seismic/Seismic Profile Case Study of the Leduc Formation Reef, Lanaway Field, Alberta, Canada

On the basis of conventional surface seismic data, an exploratory well (referred to as the VSP well) was drilled into the updip, raised rim of the Leduc Formation (Devonian Woodbend Group) reef complex at Lanaway Field, southeastern Alberta, Canada. The well was expected to encounter an anomalous late-stage accretionary buildup at the Leduc level. It was anticipated that the Leduc at the VSP well location would be up to 80 m higher than at adjacent rim well sites. To the consternation of the geophysicists, the envisioned accretionary growth was not present; the top of the Leduc in the VSP well was consistent with other rim wells and inconsistent with the seismic interpretation. Fortunately, however, the Leduc was structurally closed and the VSP well was completed as an oil producer (from both the Nisku and Leduc Formations). In order to resolve the apparent discrepancy between the interpreted surface seismic data and geology at the VSP well, a vertical seismic profile (VSP) was conducted at the well site. The interpretation of the VSP data was expected to elucidate the geological origin of the misinterpreted seismic anomaly. Towards this end, the VSP was relatively successful. These data confirmed that the original interpretation of the surface seismic data (with respect to the Nisku, Ireton, and Leduc top) was incorrect, and that the anomaly observed on the surface seismic line was not a processing artifact. It was ultimately attributed to several superposed effects: (1) anomalous structural relief at the pre-Cretaceous subcrop; (2) stratigraphic anomalies within the Winterburn Group; (3) multiple interference; and (4) tuning effects associated with the thinning of the Ireton along the seismic profile

Metaplasticity of Hypothalamic Synapses following In Vivo Challenge

SummaryNeural networks that regulate an organism's internal environment must sense perturbations, respond appropriately, and then reset. These adaptations should be reflected as changes in the efficacy of the synapses that drive the final output of these homeostatic networks. Here we show that hemorrhage, an in vivo challenge to fluid homeostasis, induces LTD at glutamate synapses onto hypothalamic magnocellular neurosecretory cells (MNCs). LTD requires the activation of postsynaptic α2-adrenoceptors and the production of endocannabinoids that act in a retrograde fashion to inhibit glutamate release. In addition, both hemorrhage and noradrenaline downregulate presynaptic group III mGluRs. This loss of mGluR function allows high-frequency activity to potentiate these synapses from their depressed state. These findings demonstrate that noradrenaline controls a form of metaplasticity that may underlie the resetting of homeostatic networks following a successful response to an acute physiological challenge