Biomedical subjects

R Stoop

Publications and source records attributed to R Stoop.

At least 19 recordsLinked to original sources

PubMed2004

Two-tone suppression and combination tone generation as computations performed by the Hopf cochlea.

Recent evidence suggests that the compressive nonlinearity responsible for the extreme dynamic range of the mammalian cochlea is implemented in the form of Hopf amplifiers. Whereas Helmholtz's original concept of the cochlea was that of a frequency analyzer, Hopf amplifiers can be stimulated not only by one, but also by neighboring frequencies. To reduce the resulting computational overhead, the mammalian cochlea is aided by two-tone suppression. We show that the laws governing two-tone suppression and the generation of combination tones naturally emerge from the Hopf-cochlea concept. Thus the Hopf concept of the cochlea reproduces not only local properties like the correct frequency response, but additionally accounts for more complex hearing phenomena that may be related to auditory signal computation.

Animals↗

PubMed2004

Fast spike pattern detection using the correlation integral.

Conventional approaches to detect patterns in neuronal firing are template based. As the pattern length increases, the number of trial patterns to be tested leads to strongly divergent computational costs. To remedy this problem, we propose a different statistical approach, based on the correlation integral. Applications of our method to model and neuronal data demonstrate its reliability, even in the presence of noise. Additionally, our investigation provides interesting insights into the nature of correlation-integral anomalies.

Action Potentials↗

PubMed2004

Essential auditory contrast-sharpening is preneuronal.

Contrast-sharpening is a fundamental feature of mammalian sensory perception. Whereas visual contrast-sharpening has been fully understood in terms of the retinal neuronal wiring [DeVries, S. H. & Baylor, D. A. (1993) Cell 72, Suppl., 139-149], a corresponding explanation of auditory contrast-sharpening is still lacking. Here, we show that the essentials of auditory contrast-sharpening can be explained by using cochlear biophysics. This finding indicates that the phenomenon is basically of preneuronal origin.

Acoustic Stimulation↗

PubMed2004

Limit cycles, noise, and chaos in hearing.

Based on insight obtained from a newly developed cochlea model, we argue that noise-driven limit cycles are the basic ingredient in the mammalian cochlea hearing process. For insect audition, we provide evidence in favor of the persistence of this principle. We emphasize the role of bifurcations for the emergence of broad-range sound perception, both in the frequency and amplitude domain, and indicate that this crucially depends on the correct coupling between limit cycles. We review the limit-cycle coupling universality, and outline how it can be used to encode information. Cortical noise is the microscopic basis for this encoding, whereas chaos emerges as the macroscopic expression of computation being done in the network. Large neuron firing variability is one possible consequence of the proposed mechanism that may apply to both vertebrate and insect hearing.

Animals↗

PubMed2004

Natural computation measured as a reduction of complexity.

We argue that the deeper nature of computation is to reduce the statistical obstruction against prediction. From this, we derive an explicit measure of computation for general, artificial as well as natural, systems (electronic circuits, neurons, mechanical devices, etc.). The applicability and usefulness of this concept is demonstrated using well-studied families of dynamical systems, as well as experimental time series from cortical neurons.

Action Potentials↗

PubMed2003

Essential Role of Couplings between Hearing Nonlinearities.

Hopf-type nonlinearities have been recently found to be the basic mechanism of the mammalian cochlear response. Physiology requires that these nonlinearities be coupled. By suitably implementing a biomorphic coupling scheme of cochlear nonlinearities, we obtain a simple cochlea model that faithfully reproduces measured basilar membrane response, validating the utility of the Hopf amplifier concept. Our results demonstrate that the correct coupling between nonlinearities is as important as the nonlinearities themselves.

Animals↗

PubMed2003

Scaling properties of simple limiter control.

"Simple limiter control" of chaotic systems is analytically and numerically investigated, proceeding from the one-dimensional case to higher dimensions. The properties of the control method are fully described by the one-parameter one-dimensional flat-top map family, implying that orbits are stabilized in exponential time, independent of the periodicity and without the need for targeting. Fine-tuning of the control is limited by superexponential scaling in the control space, where orbits of the uncontrolled system are obtained for a set of zero Lebesgue measure. In higher dimensions, simple limiter control is a highly efficient control method, provided that the proper limiter form and placement are chosen.

Journal Article↗

PubMed2003

Determination of group I metabotropic glutamate receptor subtypes involved in the frequency of epileptiform activity in vitro using mGluR1 and mGluR5 mutant mice.

In mouse hippocampal slices, bicuculline elicited spontaneous epileptiform bursts with a duration of 200-300 ms and with a frequency of five to six events per minute. Application of group I metabotropic glutamate receptor agonist (RS)-3,5-dihydroxyphenylglycine ((RS)-DHPG) increased the burst frequency up to 300% at concentrations of 50 to 100 microM, while it decreased the burst duration below 100 ms. In slices of subtype I mGluR1 or subtype I mGluR5 knockout mice, bicuculline elicited spontaneous epileptiform bursts with similar duration and frequency as those measured in wild-type mice but without the previous effects seen following application of DHPG at concentrations up to 100 microM. Likewise, in slices of wild-type mice, preincubation with mGluR1 antagonist, 1-aminoindan-1,5-dicarboxylic acid (AIDA) or mGluR5 receptor antagonist, 2-methyl-6-(phenylethynyl)-pyridine (MPEP) blocked in both cases completely the increase in frequency following DHPG application. These findings suggest an interactive mechanism between mGluR1 and mGluR5 receptors in the modulation of epileptiform bursting activity by DHPG that could indicate a common intracellular signaling mechanism or possibly direct interaction between these two receptors.

Action Potentials↗

PubMed2002

Phenotypic differences in murine chondrocyte cell lines derived from mature articular cartilage.

OBJECTIVE: To obtain well characterized immortalized murine chondrocyte cell lines. The cell lines were obtained from mature articular chondrocytes, instead of embryonal cells which are used in most other studies. METHODS: Pieces of articular cartilage were cut from murine patellae and femoral heads. Chondrocytes were isolated by digestion with collagenase. These cells were cultured in monolayer and immortalized by transfection of the SV40 large T antigen gene. To preserve the differentiated phenotype, the resulting clones were cultured in three-dimensional carriers, alginate beads. The phenotypes of the cells were characterized using the following parameters: Cell morphology (light microscopy), messenger RNA (RT-PCR) and protein (immunohistochemistry) levels of extracellular matrix molecules. Moreover, responsiveness to interleukin-1(IL-1) was determined by measuring production of proteoglycans ((35)S-sulfate incorporation) and of nitric oxide (Griess reaction). RESULTS: Sixteen clones were obtained, ten (P1 to P10) derived from patellar cartilage, and six (H1 to H6) from femoral head cartilage. In seven cell lines (P2, P5, H1, H3, H4, H5, H6) high production of type II collagen corresponded with high levels of mRNA of type II collagen (and prevalence of the IIB type) and with high IL-1-induced suppression of proteoglycan synthesis. Like intact murine articular cartilage, all cell lines produced type I and type X collagens, but mRNA levels of both types of collagen were never higher in the cell lines as compared with intact cartilage. CONCLUSION: Our results demonstrate that it is possible to immortalize mature murine articular chondrocytes. Each of the obtained chondrocyte cell lines appeared to have a stable phenotype. Both relatively differentiated and relatively dedifferentiated chondrocyte cell lines could be identified.

Animals↗

PubMed2001

Increased resistance to collagen-induced arthritis in CD44-deficient DBA/1 mice.

OBJECTIVE: To study the role of CD44, the principal hyaluronan (HA) receptor, in experimental arthritis. METHODS: We generated CD44 gene deficiency in arthritis-susceptible DBA/1LacJ mice to study the role of CD44 directly in collagen-induced arthritis (CIA). Wild-type and CD44-deficient mice were immunized with chicken type II collagen, and the onset and severity of CIA were monitored up to day 64. The immune status of immunized mice was determined at the end of the experiments. Cell transfer experiments were performed to monitor lymphocyte traffic to the inflamed joints. RESULTS: Mice homozygous for the CD44 mutation developed normally and showed no phenotypic defects. Although they showed a normal response to immunization with type II collagen and had Th1/Th2 ratios comparable with those in wild-type animals, CD44-deficient mice exhibited significant reductions in both the incidence and severity of CIA. This was accompanied by altered serum levels of HA, reduced expression of L-selectin, and a delayed entry of intravenously injected CD44-deficient donor lymphocytes into the arthritic joints of recipient mice. CONCLUSION: While CD44 is not essential for morphogenesis and autoimmunity, this cell surface receptor seems to play an important role in the development of arthritis, most likely by directing leukocyte traffic to the site of inflammation.

Animals↗

PubMed2001

Expression of type X collagen in young and old C57Bl/6 and Balb/c mice. Relation with articular cartilage degeneration.

OBJECTIVE: To investigate whether the development of osteoarthritic lesions in the knee joints of mice is associated with increased immunostaining of type X collagen. METHODS: Sections of total knee joints in combination with immunohistochemistry were used to study the distribution of type X collagen in the cartilage of young and old mice of two mouse strains, Balb/c and C57Bl/6, known to develop osteoarthritic lesions at different locations. Expression of type X collagen and PTH/PTHrP-receptor mRNA were studied by RT-PCR. RESULTS: Young adult Balb/c and C57Bl/6 mice both expressed type X collagen in the non-calcified cartilage of the tibia-femoral joint. Old mice of both strains had a strongly increased deposition of type X collagen in the patella-femoral but not in the tibia-femoral joint. The locations in the murine knee joints prone to develop osteoarthritis (OA) did not preferentially express increased amounts of type X collagen. Thus, whereas increased type X was observed in both strains in the patella-femoral joints, only Balb/c mice preferentially developed osteoarthritic lesions in these joints. Also cartilage degeneration was usually seen only in the lateral compartment of the knee joints of C57Bl/6 mice but this was not accompanied by increased type X collagen immunostaining. Increased deposition of type X collagen was not associated with elevated levels of type X collagen mRNA or with decreased levels of PTH/PTHrP-receptor mRNA. CONCLUSION: Type X collagen expression and spontaneous OA in mice are not necessarily related since OA prone locations in the murine knee joint do not preferentially express type X collagen.

Age Factors↗

PubMed2001

Type II collagen degradation in articular cartilage fibrillation after anterior cruciate ligament transection in rats.

OBJECTIVE: To investigate the kinetics of early cartilage changes in mechanically induced osteoarthritis (OA) and the association of these changes with damage to the type II collagen network. METHODS: Experimental OA was induced by anterior cruciate ligament transsection in the rat knee joint (ACLT-OA). Animals were sacrificed after 2, 7, 14, 28 and 70 days. Knee joints were evaluated using routine histology and immunohistochemistry for denatured (unwound) type II collagen to detect collagen damage. An antibody recognizing the collagenase cleavage site in type II collagen was used to study the role of collagenase in this process. RESULTS: The first changes of the articular cartilage after anterior cruciate ligament transection occurred in the superficial zone. These changes included loss of superficial chondrocytes, swelling of the remaining chondrocytes and superficial fibrillation. The swelling of the chondrocytes did not result from a change towards the hypertrophic phenotype, since these cells did not stain for type X collagen. A marked increase in denatured type II collagen staining was present in the fibrillated areas. Staining of the collagenase cleavage site showed the same distribution as denatured collagen but was clearly less intense. Collagen damage could never be detected before fibrillation occurred and was not present in non-fibrillated areas. CONCLUSIONS: These results indicate that in this model cartilage degeneration starts at the articular surface and that this degeneration is associated with a localized expression of type II collagen degradation products.

Animals↗

PubMed2000

Optimized chaos control with simple limiters.

We present an elementary derivation of chaos control with simple limiters using the logistic map and the Henon map as examples. This derivation provides conditions for optimal stabilization of unstable periodic orbits of a chaotic attractor.

Journal Article↗

PubMed2000

Modulation of epileptiform discharges in the rat limbic system in vitro by noradrenergic agents.

Application of bicuculline (20 microm) in a horizontal slice preparation of the rat limbic system induced epileptiform discharges ('bursts') that spread from the hippocampus to the entorhinal cortex (EC) and the basolateral amygdala (BLA). These bursts were time locked, with the CA3-CA2 regions discharging first at a 0.1+/-0. 008Hz (n=30 slices) frequency, followed after 27+/-3 ms by the superficial layers of the EC and after 44.3+/-3 ms by the BLA. Application of 50 microM noradrenaline (NA) for 4 min reduced the burst frequency to 40% of its initial value. Pharmacological study of NA action on burst frequency revealed that it consisted of a beta adrenoreceptor-mediated increase and an alpha(2) adrenoreceptor-mediated decrease of epileptiform bursting frequency.

Adrenergic Agonists↗

PubMed2000

Differences in type II collagen degradation between peripheral and central cartilage of rat stifle joints after cranial cruciate ligament transection.

OBJECTIVE: Type II collagen degradation is thought to be the key process in cartilage degradation during the development of osteoarthritis (OA). In this study, we investigated the kinetics of type II collagen degradation during surgically induced OA. METHODS: Experimental OA was induced in male Wistar rats by transecting the cranial (anterior) cruciate ligament (CCL). Hematoxylin and eosin staining was used to study overall cartilage degradation, while immunostained sections were used to demonstrate denatured type II collagen (Col2-3/4m antibody) and the collagenase cleavage site in type II collagen (Col2-3/ 4Cshort antibody). RESULTS: During the first 3-4 weeks, cartilage destruction, associated with chondrocyte death, proteoglycan depletion, and a marked increase in the collagenase cleavage neoepitope, was mainly located at the margins of the cartilage. From weeks 3-4, the central part of the cartilage showed increased surface fibrillation and apparent chondrocyte death. In these areas, increased denatured type II collagen staining but little cleavage-site staining was present. CONCLUSION: These results indicate that cartilage degradation after CCL transection in the rat consists of 2 phases. An early phase located at the cartilage margins and a late phase located at the central part of the cartilage. In the early phase, collagenase-dependent cartilage damage occurred. During the late phase, the level of type II collagen denaturation increased.

Animals↗

PubMed2000

Generic origins of irregular spiking in neocortical networks.

We identify generic sources of complex and irregular spiking in biological neural networks. For the network description, we operate on a mathematically exact mesoscopic approach. Starting from experimental data, we determine exact properties of noise-driven, binary neuron interaction and extrapolate from there to properties of more complex types of interaction. Our approach fills a gap between approaches that start from detailed biophysically motivated simulations but fail to make mathematically exact global predictions, and approaches that are able to make exact statements but only on levels of description that are remote from biology. As a consequence of the approach, a novel coding scheme emerges, shedding new light on local information processing in biological neural networks.

Action Potentials↗

PubMed2000

When pyramidal neurons lock, when they respond chaotically, and when they like to synchronize.

We give an overview on the locking properties of perturbed regularly firing pyramidal neurons, as a function of perturbation strength, self-spiking frequency and perturbation frequency. For inhibitory perturbations, instead of locking chaotic response emerges for a whole range of parameters. This suggests that global synchronization on the set of inhibitory connections may easily be achieved.

Action Potentials↗

PubMed2000

Noise-driven neocortical interaction: a simple generation mechanism for complex neuron spiking.

We discuss a generic scenario along which complex spiking behavior evolves in biologically realistic neural networks. Our nonlinear dynamics approach is based directly on rat neocortical in vitro recordings. Using this experimental data, we obtain a full overview on the possible spiking behaviors of pyramidal neurons that are engaged in binary interactions. Universality arguments imply that the observed spiking behaviors are largely independent from the specific properties of individual neurons; theoretical arguments and numerical experiments indicate that they should be observable in in vivo neocortical neuron networks.

Animals↗