• Klíčová slova
• antineuronální protilátky, CASPR2, LGI1, nepřímá imunohistochemie,
• MeSH
• antigeny povrchové imunologie   MeSH
• autoprotilátky * imunologie   krev   MeSH
• encefalitida s protilátkami proti NMDA receptorům * diagnóza   imunologie   patofyziologie   MeSH
• imunohistochemie metody   MeSH
• imunologické techniky metody   MeSH
• lidé MeSH
• limbická encefalitida * diagnóza   imunologie   patofyziologie   MeSH
• membránové proteiny imunologie   MeSH
• paraneoplastické neurologické syndromy diagnóza   imunologie   MeSH
• proteiny nervové tkáně imunologie   MeSH
• receptory GABA-B imunologie   MeSH
• receptory N-methyl-D-aspartátu imunologie   MeSH
• Check Tag
• lidé MeSH
• Publikační typ
• práce podpořená grantem MeSH

Botulinum neurotoxins (BoNTs) and tetanus toxin (TeTX) are the deadliest biological substances that cause botulism and tetanus, respectively. Their astonishing potency and capacity to enter neurons and interfere with neurotransmitter release at presynaptic terminals have attracted much interest in experimental neurobiology and clinical research. Fused with reporter proteins or labelled with fluorophores, BoNTs and TeTX and their non-toxic fragments also offer remarkable opportunities to visualize cellular processes and functions in neurons and synaptic connections. This study presents the state-of-the-art optical probes derived from BoNTs and TeTX and discusses their applications in molecular and synaptic biology and neurodevelopmental research. It reviews the principles of the design and production of probes, revisits their applications with advantages and limitations and considers prospects for future improvements. The versatile characteristics of discussed probes and reporters make them an integral part of the expanding toolkit for molecular neuroimaging, promoting the discovery process in neurobiology and translational neurosciences.

• MeSH
• botulotoxiny chemie   MeSH
• fluorescenční barviva chemie   MeSH
• lidé MeSH
• molekulární sondy chemie   MeSH
• neurony * metabolismus   MeSH
• neurotoxiny * MeSH
• neurozobrazování * metody   MeSH
• synapse * metabolismus   MeSH
• tetanový toxin * chemie   MeSH
• zvířata MeSH
• Check Tag
• lidé MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• přehledy MeSH

• Klíčová slova
• cognitive binding, anesthesia-related unbinding,
• MeSH
• anestetika celková farmakologie   MeSH
• celková anestezie * MeSH
• kognice účinky léků   MeSH
• lidé MeSH
• mozek fyziologie   účinky léků   MeSH
• nabytí vědomí během operace MeSH
• nervový přenos fyziologie   účinky léků   MeSH
• vědomí * fyziologie   účinky léků   MeSH
• Check Tag
• lidé MeSH
• Publikační typ
• přehledy MeSH

Lipoid character of plasma membrane namely the presence of polyenic fatty acids enables to interact with membrane proteins and in certain extent also to modulate their function. During the development, molecules of membrane fatty acids become more and more complex, and the ratio of polyenic fatty acids/saturated fatty acids in the brain rises, while the concentration of monoenic fatty acids remained relatively stable. This phenomenon is apparent also in the ratio of unsaturated fatty acids OMEGA-3 in plasma of newborns which correlates with the birth weight. Plasma membrane reflects local specializations of nerve cells. Its composition varies in functionally specialized regions called domains. Specialized domains of nerve cells determine the function of dendrites, soma, axon, axon hillock ect. Premature weaning of laboratory rats results in structural changes and in the increase of excitability of neuronal circuits in hypothalamus, septum and hippocampus which indicate the possibility of membrane composition changes. In synapses, transport proteins of synaptic vesicles, act together with the specific proteins of the presynaptic membrane. Membrane proteins determine the release of neurotransmitter at different conditions of synaptic activity, and they can contribute to the recovery of neurotransmitter content after the repeated hyperactivity. In the model of experimental kindling, repeated seizures bring about decreases and distribution changes of synaptic vesicles.

• MeSH
• buněčná membrána fyziologie   MeSH
• lidé MeSH
• lipidové dvojvrstvy MeSH
• membránové proteiny fyziologie   MeSH
• neurony fyziologie   MeSH
• neuroplasticita fyziologie   MeSH
• synapse fyziologie   MeSH
• zvířata MeSH
• Check Tag
• lidé MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• přehledy MeSH

Five parameters of one of the most common neuronal models, the diffusion leaky integrate-and-fire model, also known as the Ornstein-Uhlenbeck neuronal model, were estimated on the basis of intracellular recording. These parameters can be classified into two categories. Three of them (the membrane time constant, the resting potential and the firing threshold) characterize the neuron itself. The remaining two characterize the neuronal input. The intracellular data were collected during spontaneous firing, which in this case is characterized by a Poisson process of interspike intervals. Two methods for the estimation were applied, the regression method and the maximum-likelihood method. Both methods permit to estimate the input parameters and the membrane time constant in a short time window (a single interspike interval). We found that, at least in our example, the regression method gave more consistent results than the maximum-likelihood method. The estimates of the input parameters show the asymptotical normality, which can be further used for statistical testing, under the condition that the data are collected in different experimental situations. The model neuron, as deduced from the determined parameters, works in a subthreshold regimen. This result was confirmed by both applied methods. The subthreshold regimen for this model is characterized by the Poissonian firing. This is in a complete agreement with the observed interspike interval data.

• MeSH
• akční potenciály fyziologie   MeSH
• buněčná membrána fyziologie   MeSH
• financování organizované MeSH
• lidé MeSH
• mozek fyziologie   MeSH
• nervové dráhy fyziologie   MeSH
• nervový přenos fyziologie   MeSH
• neuronové sítě MeSH
• neurony fyziologie   MeSH
• počítačové zpracování signálu MeSH
• Poissonovo rozdělení MeSH
• stochastické procesy MeSH
• synapse fyziologie   MeSH
• zvířata MeSH
• Check Tag
• lidé MeSH
• zvířata MeSH

Shared input to a population of neurons induces noise correlations, which can decrease the information carried by a population activity. Inhibitory feedback in recurrent neural networks can reduce the noise correlations and thus increase the information carried by the population activity. However, the activity of inhibitory neurons is costly. This inhibitory feedback decreases the gain of the population. Thus, depolarization of its neurons requires stronger excitatory synaptic input, which is associated with higher ATP consumption. Given that the goal of neural populations is to transmit as much information as possible at minimal metabolic costs, it is unclear whether the increased information transmission reliability provided by inhibitory feedback compensates for the additional costs. We analyze this problem in a network of leaky integrate-and-fire neurons receiving correlated input. By maximizing mutual information with metabolic cost constraints, we show that there is an optimal strength of recurrent connections in the network, which maximizes the value of mutual information-per-cost. For higher values of input correlation, the mutual information-per-cost is higher for recurrent networks with inhibitory feedback compared to feedforward networks without any inhibitory neurons. Our results, therefore, show that the optimal synaptic strength of a recurrent network can be inferred from metabolically efficient coding arguments and that decorrelation of the input by inhibitory feedback compensates for the associated increased metabolic costs.

• MeSH
• akční potenciály fyziologie   MeSH
• modely neurologické MeSH
• nervová síť * fyziologie   MeSH
• nervový přenos * fyziologie   MeSH
• nervový útlum fyziologie   MeSH
• neuronové sítě MeSH
• počítačová simulace MeSH
• reprodukovatelnost výsledků MeSH
• Publikační typ
• časopisecké články MeSH

Vývoj a existenci specifických aktivit nervové buňky si nelze představit bez adekvátně strukturované nosné membrány. Začlenění funkčních proteinových komponent je kauzálně svázáno se stavbou lipidové dvojvrstvy která umožňuje nejen určitou prostorovou stabilitu (fixaci), ale současně i prostorovou návaznost, součinnost a variabilitu. Pohyb bílkovinných molekul v tekuté mozaice membrány je omezen jejich zakotvením do cytoskeletu. Ten má mechanicky podpůrný význam a hraje důležitou úlohu v přenosu informace do nitra buňky. U nervových buněk řídí interakce cytoskeletu a membrány výdej neurotransmitéru z presynaptických zakončení a recyklaci synaptických váčků. V souvislosti s hledáním markerů psychických poruch se předmětem intenzivního výzkumu stala i membrána červených krvinek, která má vysoce komplexní strukturu, srovnatelnou se strukturou membrán většiny eukaryotických buněk. Byly pozorovány četné biochemické abnormality červených krvinek při různých psychických poruchách, jako jsou změny v aktivitě některých membránově vázaných enzymů a receptoru, různé hladiny oxidativního stresu a změny ve složení lipidů.

Development and existence of specific activities of nerve cells are indispensable from the adequate structure of the supporting membrane. Integration of functional protein components determines the structure of lipid bilayer. It brings not only a certain special stability (fixation) but also a specific relationship, cooperation and variability among the components of the membrane. Movements of protein molecules within the fluid mosaic of the membrane are limited by their anchoring to the cytoskeleton. Cytoskeleton has mechanically supporting function and it plays an important role in the transmission of signals into the cell. In nerve cells interaction of cytoskeleton and membrane controls the release of neurotransmitter from the presynaptic terminals and recycling of synaptic vesicles. In relation to the quest for markers of psychic impairments, erythrocytal membrane became intensively studied. In its complex structure, comparable to the membrane of most of eukaryotic cells, biochemical abnormalities related to various psychic disorders were described: Changes in the activity of some membrane-bound enzymes and receptors, in the composition of lipids, and in different levels of oxidative stress.

• MeSH
• cytoskelet MeSH
• duševní poruchy patofyziologie   MeSH
• erytrocytární membrána fyziologie   MeSH
• lipidové dvojvrstvy MeSH
• neurony cytologie   ultrastruktura   MeSH
• struktury buněčné membrány MeSH
• synaptické membrány fyziologie   MeSH
• synaptické vezikuly fyziologie   MeSH

In this paper we investigate the rate coding capabilities of neurons whose input signal are alterations of the base state of balanced inhibitory and excitatory synaptic currents. We consider different regimes of excitation-inhibition relationship and an established conductance-based leaky integrator model with adaptive threshold and parameter sets recreating biologically relevant spiking regimes. We find that given mean post-synaptic firing rate, counter-intuitively, increased ratio of inhibition to excitation generally leads to higher signal to noise ratio (SNR). On the other hand, the inhibitory input significantly reduces the dynamic coding range of the neuron. We quantify the joint effect of SNR and dynamic coding range by computing the metabolic efficiency-the maximal amount of information per one ATP molecule expended (in bits/ATP). Moreover, by calculating the metabolic efficiency we are able to predict the shapes of the post-synaptic firing rate histograms that may be tested on experimental data. Likewise, optimal stimulus input distributions are predicted, however, we show that the optimum can essentially be reached with a broad range of input distributions. Finally, we examine which parameters of the used neuronal model are the most important for the metabolically efficient information transfer.

• MeSH
• adenosintrifosfát metabolismus   MeSH
• akční potenciály fyziologie   MeSH
• excitační postsynaptické potenciály fyziologie   MeSH
• membránové potenciály fyziologie   MeSH
• modely neurologické * MeSH
• nervové vedení fyziologie   MeSH
• nervový přenos fyziologie   MeSH
• nervový útlum fyziologie   MeSH
• neurony fyziologie   MeSH
• počítačová simulace MeSH
• poměr signál - šum MeSH
• výpočetní biologie MeSH
• zvířata MeSH
• Check Tag
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH

BACKGROUND: Although irritable bowel syndrome (IBS) is a symptom-based diagnosis, clinicians' management of and communication about the disorder is often hampered by an unclear conceptual understanding of the nature of the problem. We aimed to elucidate an integrated explanatory model (EM) for IBS from the existing literature for pragmatic use in the clinical setting. METHODS: Systematic and exploratory literature searches were performed in PubMed to identify publications on IBS and EMs. KEY RESULTS: The searches did not identify a single, integrated EM for IBS. However, three main hypotheses were elucidated that could provide components with which to develop an IBS EM: (i) altered peripheral regulation of gut function (including sensory and secretory mechanisms); (ii) altered brain-gut signaling (including visceral hypersensitivity); and (iii) psychological distress. Genetic polymorphisms and epigenetic changes may, to some degree, underlie the etiology and pathophysiology of IBS and could increase the susceptibility to developing the disorder. The three model components also fit into one integrated explanation for abdominal symptoms and changes in stool habit. Additionally, IBS may share a common pathophysiological mechanism with other associated functional syndromes. CONCLUSIONS & INFERENCES: It was possible to elucidate an integrated, three-component EM as a basis for clinicians to conceptualize the nature of IBS, with the potential to contribute to better diagnosis and management, and dialog with sufferers.

• MeSH
• dysbióza komplikace   patofyziologie   MeSH
• gastrointestinální trakt inervace   patofyziologie   sekrece   MeSH
• genetická predispozice k nemoci MeSH
• lidé MeSH
• nervový přenos MeSH
• polymorfismus genetický MeSH
• psychický stres komplikace   psychologie   MeSH
• signální transdukce MeSH
• somatosenzorické poruchy komplikace   patofyziologie   MeSH
• střevní mikroflóra MeSH
• syndrom dráždivého tračníku etiologie   patofyziologie   psychologie   MeSH
• vzdělávání pacientů jako téma * MeSH
• Check Tag
• lidé MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• přehledy MeSH

• MeSH
• buněčná membrána fyziologie   MeSH
• membránové proteiny fyziologie   MeSH
• molekulární biologie MeSH
• reakce antigenu s protilátkou MeSH
• receptory neurotransmiterů MeSH
• signální transdukce fyziologie   MeSH
• vazebná místa genetika   MeSH
• Publikační typ
• přehledy MeSH