Publications by authors named "Bjoern Ludwar"

Hyaluronic acid (HA) contributes to extracellular matrix viscosity and fiber regeneration. HA role in resistance training (RT) performance adaptations is unclear. RT men performed power training (nonfunctional overreaching (NFOR) or normal training (CG)) over 7.

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Some synapses show two forms of short-term plasticity, homosynaptic facilitation, and a plasticity in which the efficacy of transmission is modified by subthreshold changes in the holding potential of the presynaptic neuron. In a previous study we demonstrated a further interactive effect. We showed that depolarizing changes in the presynaptic holding potential can increase the rate at which facilitation occurs.

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In a type of short-term plasticity that is observed in a number of systems, synaptic transmission is potentiated by depolarizing changes in the membrane potential of the presynaptic neuron before spike initiation. This digital-analog form of plasticity is graded. The more depolarized the neuron, the greater the increase in the efficacy of synaptic transmission.

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Background: Inexpensive screening tools are needed to identify individuals predisposed to developing diabetes mellitus (DM). Such early identification coupled with an effective intervention could help many people avoid the substantial health costs of this disease. We investigated the hypothesis that fluctuating asymmetry (FA) in fingerprints is an indicator of type 2 diabetes mellitus (T2DM).

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It has been suggested that changes in intracellular calcium mediate the induction of a number of important forms of synaptic plasticity (e.g., homosynaptic facilitation).

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Complex behaviors often require coordinated movements of dissimilar motor structures. The underlying neural mechanisms are poorly understood. We investigated cycle-by-cycle coordination of two dissimilar feeding structures in Aplysia californica: the external lips and the internal radula.

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We study a form of short-term synaptic plasticity that was originally described as a graded potentiating effect of holding potential on spike-mediated synaptic transmission (Shimahara and Tauc, 1975). This form of plasticity has recently generated considerable interest, as it has become apparent that it is present in the mammalian brain (Clark and Häusser, 2006; Marder, 2006). It has been suggested that it adds a previously unappreciated analog component to spike-mediated synaptic transmission (Alle and Geiger, 2006, 2008).

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The growing realization that electrical coupling is present in the mammalian brain has sparked renewed interest in determining its functional significance and contrasting it with chemical transmission. One question of interest is whether the two types of transmission can be selectively regulated, e.g.

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Compensatory mechanisms are often used to achieve stability by reducing variance, which can be accomplished via negative feedback during homeostatic regulation. In principle, compensation can also be implemented through feedforward mechanisms where a regulator acts to offset the anticipated output variation; however, few such neural mechanisms have been demonstrated. We provide evidence that an Aplysia neuropeptide, identified using an enhanced representational difference analysis procedure, implements feedforward compensation within the feeding network.

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Network outputs elicited by a specific stimulus may differ radically depending on the momentary network state. One class of networks states-experience-dependent states-is known to operate in numerous networks, yet the fundamental question concerning the relative role that inputs and states play in determining the network outputs remains to be investigated in a behaviorally relevant manner. Because previous work indicated that in the isolated nervous system the motor outputs of the Aplysia feeding network are affected by experience-dependent states, we sought to establish the behavioral relevance of these outputs.

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Two distinct mechanisms mediate potentiating effects of depolarization on synaptic transmission. Recently there has been renewed interest in a type of plasticity in which a neuron's somatic membrane potential influences synaptic transmission. We study mechanisms that mediate this type of control at a synapse between a mechanoafferent, B21, and B8, a motor neuron that receives chemical synaptic input.

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In the Aplysia mechanoafferent B21, afferent transmission is in part regulated via the control of active spike propagation. When B21 is peripherally activated at its resting membrane potential, spikes fail to propagate to an output process, and afferent transmission does not occur. In this report, we show that the propagation failure is in part a result of the fact that the somatic region of B21 is relatively inexcitable.

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