Cortical Plasticity Induced by Spike-Triggered Microstimulation in Primate Somatosensory Cortex

Electrical stimulation of the nervous system for therapeutic purposes, such as deep brain stimulation in the treatment of Parkinson’s disease, has been used for decades. Recently, increased attention has focused on using microstimulation to restore functions as diverse as somatosensation and memory. However, how microstimulation changes the neural substrate is still not fully understood. Microstimulation may cause cortical changes that could either compete with or complement natural neural processes, and could result in neuroplastic changes rendering the region dysfunctional or even epileptic. As part of our efforts to produce neuroprosthetic devices and to further study the effects of microstimulation on the cortex, we stimulated and recorded from microelectrode arrays in the hand area of the primary somatosensory cortex (area 1) in two awake macaque monkeys. We applied a simple neuroprosthetic microstimulation protocol to a pair of electrodes in the area 1 array, using either random pulses or pulses time-locked to the recorded spiking activity of a reference neuron. This setup was replicated using a computer model of the thalamocortical system, which consisted of 1980 spiking neurons distributed among six cortical layers and two thalamic nuclei. Experimentally, we found that spike-triggered microstimulation induced cortical plasticity, as shown by increased unit-pair mutual information, while random microstimulation did not. In addition, there was an increased response to touch following spike-triggered microstimulation, along with decreased neural variability. The computer model successfully reproduced both qualitative and quantitative aspects of the experimental findings. The physiological findings of this study suggest that even simple microstimulation protocols can be used to increase somatosensory information flow.     

Die Brutzeiten einiger Gänsearten und ihrer Bastarde in identischen Bedingungen

Zusammenfassung An Hand von 229 Brutbeginn-Daten von freilebenden Gänsen, die während der Jahre 1956–1966 in Seewiesen (Obb.) (48°N, 11°11E) brüteten, wurden die mittleren Brutbeginn-Daten von 5 Gänsearten und von Artbastarden bestimmt. Es zeigte sich, daß die untersuchten Arten unter diesen Bedingungen in derselben Reihenfolge brüteten, wie ihre Artgenossen in freier Wildbahn. Die mittleren Brutbeginn-Termine wurden allerdings um so mehr vorverlegt, je später die Art normalerweise brütet (Abb. 1). , die mit artfremden verpaart waren, brüteten zur selben Zeit wie ihre Artgenossen, die mit artgleichen verpaart waren (Abb. 1). GraugansxSchneegans-Bastard-, die mit Schneegantern verpaart waren, begannen meist nach den Graugänsen, aber stets vor den Schneegänsen zu brüten (Abb. 1, 2). Das intermediäre Brüten dieser wird als starkes Argument für die Richtigkeit der Hypothese gewertet, nach welcher die artspezifisch verschiedenen Brutzeiten wenigstens zum Teil genetisch bedingt sind. In der Diskussion wird die Frage kritisch erörtert, wie weit schon allein die Tatsache, daß die verschiedenen Arten über Generationen hinweg in derselben Reihenfolge wie ihre wildlebenden Artgenossen zu brüten beginnen, als Beweis für derartige genetische Unterschiede angesehen werden kann.

---

Summary In 229 cases onset of breeding was recorded from free-living geese of 5 species and of some hybrids of these species, kept in Seewiesen/Obb. (48° N, 11° 11E) from 1956 to 1966. It was found that the species under these conditions bred in the same seasonal sequence as did wild birds. The mean breeding times, however, were found to be advanced in relation to the onset of breeding in the wild (Fig. 1). This was especially evident in the case of late-breeding species. paired with of another species came into breeding condition at the same time as paired with of the same species (Fig. 1). GraylegxSnowgoose hybrid paired with Snowgoose in most cases started to breed later than Greyleg geese but always earlier than the mean breeding time for Snowgeese (Fig. 1, 2). This intermediate breeding time is taken as a strong argument for the hypothesis that the species specific differences in breeding times are, at least in part, genetic in origin. The question as to the extent to which the differences in breeding times alone, persisting for generations in the same sequence as those of wild birds, can be attributed to genetic differences between the species, is critically discussed.

     

Volume-sensitive taurine efflux from mammary tissue is not obliged to utilize volume-activated anion channels

Cell-swelling, induced by a hyposmotic shock, activates the release of taurine from lactating rat mammary tissue expiants. The degree of stimulation of taurine efflux was dependent upon the extent of cell-swelling. Volume-sensitive taurine release was attenuated by the anion transport inhibitors NPPB, DIOA, DIDS, niflumate, flufenamate, mefenamate and diiodosalicylate but not by salicylate. Cell-swelling, following a hyposmotic challenge, did not increase the unidirectional efflux of radiolabelled I^– or D-asparate from mammary tissue expiants. The results suggest that although mammary tissue expresses a volume-sensitive amino acid transport system which is inhibited by anion transport blockers the pathway has no identity with volume-activated anion channels.     

TESTING MACROEVOLUTIONARY HYPOTHESES WITH CLADISTIC ANALYSIS: EVIDENCE AGAINST RECTANGULAR EVOLUTION

The properties of cladistic data sets from small monophyletic groups (6–12 species) are investigated using computer simulations of macroevolution. Two evolutionary models are simulated: gradualism and the punctuated-equilibrium hypothesis. Under the conditions of our simulations these two models of evolution make consistently different predictions about the distribution of autapomorphies among species. When strict stasis is enforced, the punctuated-equilibrium hypothesis predicts that the most expected number of autapomorphies per species will be zero, no matter how many characters are used in the analysis. As the number of characters used in the analysis increases, the distribution of the number of autapomorphies per species becomes bimodal. Under gradualism, the distribution of autapomorphies remains unimodal under all conditions, but the number of species without autapomorphies can fall to zero. A survey of real cladograms of extant monophyletic groups from a wide range of taxa indicates that the predictions of the punctuated-equilibrium hypothesis about autapomorphies do not hold. This constitutes strong evidence against the punctuated-equilibrium hypothesis.     

The Role of Reactive Oxygen Species in Inflammatory Disease: Evaluation of Methodology

The production of reactive oxidants has been implicated in the pathology of a number of inflammatory conditions, including inflamed arthritic joints. Many assays for the detection of these oxidants in diseased states have been described, but there are a number of potential pitfalls in both experimental design and the interpretation of results obtained with these techniques. Here, we describe a number of commonly used assays to detect the production of reactive oxidants and critically discuss their usefulness and limitations. We focus on the role of xanthine oxidase in reactive oxidant production in inflammatory disease.     

Crystallographic aspects of sub-elementary cellulose fibrils occurring in the wall of rose cells culturedin vitro

Summary Quantities of disencrusted sub-elementary cellulose fibrils from the cell wall of rose cells culturedin vitro were prepared. Following an X-ray and electron diffraction analysis, these fibrils gave a cellulose diffraction pattern which presented only two strong equatorial diffraction spacings at 0.409 and 0.572 nm indicating that the fibrils have a crystalline structure resembling that of cellulose IV_I. This observation is best explained in terms of a lateral disorganization of the cellulose chains within the fibrils. This disorganization cannot be eliminated and is connected with the small width of the fibrils which contain from 12 to 25 cellulose chains only. In these fibrils, most of the cellulose chains are superficial and not locked with neighboring chains in a tight hydrogen bond system as in thicker cellulose microfibrils.     

Electron diffraction from the primary wall of cotton fibers

Summary Electron diffraction patterns have been obtained from selected areas of disencrusted microfibrils isolated from the primary cell wall of cotton fibers. The resultant fiber diagram has the same meridional repeat distance as a corresponding pattern of secondary wall microfibrils but differs markedly in the equatorial reflections. The primary wall diagram displays only two strong equatorial reflections centered at 0.570 nm and 0.416 nm. The similarity of these spacings with those of cellulose IV suggests that the crystalline structure of the primary wall cellulose is similar to that of cellulose IV_I and is best explained in term of native cellulose I crystals having good longitudinal coherence (i.e., coherence along the length of the microfibrils) but with poor lateral organization of the network of inter chain hydrogen bonds. Similar results were also obtained for other primary wall specimens.     

Kinetic analysis of the activation of transducin by photoexcited rhodopsin. Influence of the lateral diffusion of transducin and competition of guanosine diphosphate and guanosine triphosphate for the nucleotide site.

The activation of transducin (T) by photoexcited rhodopsin (R*) is kinetically dissected within the framework of Michaelis-Menten enzymology, taking transducin as substrate of the enzyme R*. The light scattering "release" signal (Vuong, T.M., M. Chabre, and L. Stryer, 1984, Nature (Lond.). 311:659-661) was used to monitor the kinetics of transducin activation at 20 degrees C. In addition, the influence of nonuniform distributions of R* on these activation kinetics is also explored. Sinusoidal patterns of R* were created with interference fringes from two crossed laser beams. Two characteristic times were extracted from the Michaelis-Menten analysis: t(form), the diffusion-related time needed to form the enzyme-substrate R*-transducin is 0.25 +/- 0.1 ms, and T(cat), the time taken by R* to perform the chemistry of catalysis on transducin is 1.2 +/- 0.2 ms, in the absence of added guanosine diphosphate (GDP) and at saturating levels of guanosine triphosphate (GTP). With t(form) being but 20% of the total activation time t(form) + t(cat), transducin activation by R* is not limited by lateral diffusion. This is further borne out by the observation that uniform and sinusoidal patterns of R* elicited release signals of indistinguishable kinetics. When (GDP) = (GTP) = 500 microM, t(cat) is lengthened twofold. As the in vivo GDP and GTP levels are comparable, the exchange of nucleotides may well be the rate-limiting process.