116 research outputs found

    Physical complexity and cognitive evolution

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    Our intuition tells us that there is a general trend in the evolution of nature, a trend towards greater complexity. However, there are several definitions of complexity and hence it is difficult to argue for or against the validity of this intuition. Christoph Adami has recently introduced a novel measure called physical complexity that assigns low complexity to both ordered and random systems and high complexity to those in between. Physical complexity measures the amount of information that an organism stores in its genome about the environment in which it evolves. The theory of physical complexity predicts that evolution increases the amount of ‘knowledge’ an organism accumulates about its niche. It might be fruitful to generalize Adami’s concept of complexity to the entire evolution (including the evolution of man). Physical complexity fits nicely into the philosophical framework of cognitive biology which considers biological evolution as a progressing process of accumulation of knowledge (as a gradual increase of epistemic complexity). According to this paradigm, evolution is a cognitive ‘ratchet’ that pushes the organisms unidirectionally towards higher complexity. Dynamic environment continually creates problems to be solved. To survive in the environment means to solve the problem, and the solution is an embodied knowledge. Cognitive biology (as well as the theory of physical complexity) uses the concepts of information and entropy and views the evolution from both the information-theoretical and thermodynamical perspective. Concerning humans as conscious beings, it seems necessary to postulate an emergence of a new kind of knowledge - a self-aware and self-referential knowledge. Appearence of selfreflection in evolution indicates that the human brain reached a new qualitative level in the epistemic complexity

    Neuroethics, reductionism and dualism

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    Is neuroscience on the road to showing that character, consciousness and sense of spirituality are in fact no more than ?features of the machine?

    Quantum stochasticity and neuronal computations

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    The nervous system probably cannot display macroscopic quantum (i.e. classically impossible) behaviours such as quantum entanglement, superposition or tunnelling (Koch and Hepp, Nature 440:611, 2006). However, in contrast to this quantum ‘mysticism’ there is an alternative way in which quantum events might influence the brain activity. The nervous system is a nonlinear system with many feedback loops at every level of its structural hierarchy. A conventional wisdom is that in macroscopic objects the quantum fluctuations are self-averaging and thus not important. Nevertheless this intuition might be misleading in the case of nonlinear complex systems. Because of a high sensitivity to initial conditions, in chaotic systems the microscopic fluctuations may be amplified upward and thereby affect the system's output. In this way stochastic quantum dynamics might sometimes alter the outcome of neuronal computations, not by generating classically impossible solutions, but by influencing the selection of many possible solutions (Satinover, Quantum Brain, Wiley & Sons, 2001). I am going to discuss recent theoretical proposals and experimental findings in quantum mechanics, complexity theory and computational neuroscience suggesting that biological evolution is able to take advantage of quantum-computational speed-up. I predict that the future research on quantum complex systems will provide us with novel interesting insights that might be relevant also for neurobiology and neurophilosophy

    Giant Depolarizing Potentials Trigger Transient Changes in the Intracellular Cl- Concentration in CA3 Pyramidal Neurons of the Immature Mouse Hippocampus

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    Giant depolarizing potentials (GDPs) represent a typical spontaneous activity pattern in the immature hippocampus. GDPs are mediated by GABAergic and glutamatergic synaptic inputs and their initiation requires an excitatory GABAergic action, which is typical for immature neurons due to their elevated intracellular Cl- concentration ([Cl-]i). Because GABAA receptors are ligand-gated Cl- channels, activation of these receptors can potentially influence [Cl-]i. However, whether the GABAergic activity during GDPs influences [Cl-]i is unclear. To address this question we performed whole-cell and gramicidin-perforated patch-clamp recordings from visually identified CA3 pyramidal neurons in immature hippocampal slices of mice at postnatal days 4–7. These experiments revealed that the [Cl-]i of CA3 neurons displays a considerable heterogeneity, ranging from 13 to 70 mM (average 38.1 ± 3.2 mM, n = 36). In accordance with this diverse [Cl-]i, GDPs induced either Cl--effluxes or Cl--influxes. In high [Cl-]i neurons with a negative Cl--driving force (DFCl) the [Cl-]i decreased after a GDP by 12.4 ± 3.4 mM (n = 10), while in low [Cl-]i neurons with a positive DFCl [Cl-]i increased by 4.4 ± 0.9 mM (n = 6). Inhibition of GDP activity by application of the AMPA receptor antagonist CNQX led to a [Cl-]i decrease to 24.7 ± 2.9 mM (n = 8). We conclude from these results, that Cl--fluxes via GABAA receptors during GDPs induced substantial [Cl-]i changes and that this activity-dependent ionic plasticity in neuronal [Cl-]i contributes to the functional consequences of GABAergic responses, emphasizing the concept that [Cl-]i is a state- and compartment-dependent parameter of individual cells

    Giant depolarizing potentials trigger transient changes in the intracellular Cl(-) concentration in CA3 pyramidal neurons of the immature mouse hippocampus

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    Giant depolarizing potentials (GDPs) represent a typical spontaneous activity pattern in the immature hippocampus. GDPs are mediated by GABAergic and glutamatergic synaptic inputs and their initiation requires an excitatory GABAergic action, which is typical for immature neurons due to their elevated intracellular Cl(-) concentration ([Cl(-)](i)). Because GABA(A) receptors are ligand gated Cl(-) channels, activation of these receptors can potentially influence [Cl(-)](i). However, whether the GABAergic activity during GDPs influences [Cl(-)](i) is unclear. To address this question we performed whole-cell and gramicidin-perforated patch-clamp recordings from visually identified CA3 pyramidal neurons in immature hippocampal slices of mice at postnatal days 4-7. These experiments revealed that the [Cl(-)](i) of CA3 neurons displays a considerable heterogeneity, ranging from 13 to 70 mM (average 38.1 ± 3.2 mM, n = 36). In accordance with this diverse [Cl(-)] (i), GDPs induced either Cl(-)-effluxes or Cl(-)-influxes. In high [Cl(-)](i) neurons with a negative Cl(-)-driving force (DF(Cl)) the [Cl(-)](i) decreased after a GDP by 12.4 ± 3.4 mM (n = 10), while in low [Cl(-)](i) neurons with a positive DF(Cl) [Cl(-)](i) increased by 4.4 ± 0.9 mM (n = 6). Inhibition of GDP activity by application of the AMPA receptor antagonist CNQX led to a [Cl(-)](i) decrease to 24.7 ± 2.9 mM (n = 8). We conclude from these results, that Cl(-)-fluxes via GABA(A) receptors during GDPs induced substantial [Cl(-)](i) changes and that this activity dependent ionic plasticity in neuronal [Cl(-)](i) contributes to the functional consequences o

    Functional and structural properties of dentate granule cells with hilar basal dendrites in mouse entorhino-hippocampal slice cultures

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    During postnatal development hippocampal dentate granule cells (GCs) often extend dendrites from the basal pole of their cell bodies into the hilar region. These so-called hilar basal dendrites (hBD) usually regress with maturation. However, hBDs may persist in a subset of mature GCs under certain conditions (both physiological and pathological). The functional role of these hBD-GCs remains not well understood. Here, we have studied hBD-GCs in mature (≥18 days in vitro) mouse entorhino-hippocampal slice cultures under control conditions and have compared their basic functional properties (basic intrinsic and synaptic properties) and structural properties (dendritic arborisation and spine densities) to those of neighboring GCs without hBDs in the same set of cultures. Except for the presence of hBDs, we did not detect major differences between the two GC populations. Furthermore, paired recordings of neighboring GCs with and without hBDs did not reveal evidence for a heavy aberrant GC-to-GC connectivity. Taken together, our data suggest that in control cultures the presence of hBDs on GCs is neither sufficient to predict alterations in the basic functional and structural properties of these GCs nor indicative of a heavy GC-to-GC connectivity between neighboring GCs

    Effects of Functional Oils and Monensin Alone or in Combination on Feedlot Cattle Growth and Carcass Composition (Progress Report)

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    This report represents the first trial of a study consisting of a commercial mixture of functional oils (Essential, Oligo Basics USA LLC, Wilmington, DE) used alone and in combination with Monensin to evaluate the effects on steers performance when fed a high concentrate diet. One hundred and twenty steers, average initial weight 322 kg, were divided into five treatments with four pens per treatment and six steers per pen. The treatments were Control (C), Monensin (223 mg/hd/d) (M), Monensin (223 mg/hd/d) + Essential (250 mg/kg DMI) (ME), Essential Low (250 mg/kg DMI) (EL), and Essential High (500 mg/kg DMI) (EH). All steers were fed the same diet on an ad libitum basis, treatments M and EL for 172 days and treatments C, ME, and EH for 179 days. Steers were harvested at an average weight of 617 kg. Results to date suggest that cattle provided functional oils in their diet perform equally as well in the feedyard and in carcass composition as cattle provided a more traditional ionophore in their diet

    Layer-specific changes of KCC2 and NKCC1 in the mouse dentate gyrus after entorhinal denervation

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    The cation-chloride cotransporters KCC2 and NKCC1 regulate the intracellular Cl− concentration and cell volume of neurons and/or glia. The Cl− extruder KCC2 is expressed at higher levels than the Cl− transporter NKCC1 in mature compared to immature neurons, accounting for the developmental shift from high to low Cl− concentration and from depolarizing to hyperpolarizing currents through GABA-A receptors. Previous studies have shown that KCC2 expression is downregulated following central nervous system injury, returning neurons to a more excitable state, which can be pathological or adaptive. Here, we show that deafferentation of the dendritic segments of granule cells in the outer (oml) and middle (mml) molecular layer of the dentate gyrus via entorhinal denervation in vivo leads to cell-type- and layer-specific changes in the expression of KCC2 and NKCC1. Microarray analysis validated by reverse transcription-quantitative polymerase chain reaction revealed a significant decrease in Kcc2 mRNA in the granule cell layer 7 days post-lesion. In contrast, Nkcc1 mRNA was upregulated in the oml/mml at this time point. Immunostaining revealed a selective reduction in KCC2 protein expression in the denervated dendrites of granule cells and an increase in NKCC1 expression in reactive astrocytes in the oml/mml. The NKCC1 upregulation is likely related to the increased activity of astrocytes and/or microglia in the deafferented region, while the transient KCC2 downregulation in granule cells may be associated with denervation-induced spine loss, potentially also serving a homeostatic role via boosting GABAergic depolarization. Furthermore, the delayed KCC2 recovery might be involved in the subsequent compensatory spinogenesis

    UML Support for Reliability Evaluation

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    Abstract. Today's software systems are developed and targeted for satisfying sometimes very critical functions. Reliability is considered to be one of the most important nonfunctional quality attribute of such software systems. The aim of reliability estimation in early stages of software development process -analysis and design -should reduce the future costs for possible failure repairing through increasing the reliability before the construction of the software system. Because, the Unified Modeling Language (UML) becomes the standard for software system's specification, the last works done in architecture based reliability estimation and assessment use UML as the base for software architecture specification. In this paper, we discuss the existing approaches with critical overview and outline the directions for future research
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