The conventional way steroid hormones work through receptors inside cells is widely acknowledged. There are unanswered questions about what happens to the hormone in the end and why there isn't always a strong connection between how much tissue takes up and its biological effects through receptor binding. Steroid hormones can also have non-traditional effects that happen quickly but don't involve entering the cell. Several possible mechanisms for these non-traditional actions include (a) changes in membrane fluidity, (b) steroid hormones acting on receptors on the outer surface of cells, (c) steroid hormones regulating GABAA receptors on cell membranes, and (d) activation of steroid receptors by factors like EGF, IGF-1, and dopamine. Data also suggests that steroid hormones may be inserted into DNA through receptors, acting as transcription factors. These proposed new mechanisms of action should not be seen as challenging the conventional mechanism. Instead, they contribute to a more comprehensive understanding of how hormones work, allowing for rapid, short-term, and prolonged effects to meet the body's physiological needs.

• Klíčová slova
• Cellular mechanism of steroid receptors, Estrogen receptor, Female sexual behavior, Progesterone receptor, Steroid action,
• MeSH
• centrální nervový systém metabolismus   fyziologie   účinky léků   MeSH
• lidé MeSH
• pohlavní steroidní hormony * metabolismus   MeSH
• steroidní receptory metabolismus   MeSH
• zvířata MeSH
• Check Tag
• lidé MeSH
• ženské pohlaví MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• přehledy MeSH
• Názvy látek
• pohlavní steroidní hormony * MeSH
• steroidní receptory MeSH

Adult mammalian central nervous system axons have intrinsically poor regenerative capacity, so axonal injury has permanent consequences. One approach to enhancing regeneration is to increase the axonal supply of growth molecules and organelles. We achieved this by expressing the adaptor molecule Protrudin which is normally found at low levels in non-regenerative neurons. Elevated Protrudin expression enabled robust central nervous system regeneration both in vitro in primary cortical neurons and in vivo in the injured adult optic nerve. Protrudin overexpression facilitated the accumulation of endoplasmic reticulum, integrins and Rab11 endosomes in the distal axon, whilst removing Protrudin's endoplasmic reticulum localization, kinesin-binding or phosphoinositide-binding properties abrogated the regenerative effects. These results demonstrate that Protrudin promotes regeneration by functioning as a scaffold to link axonal organelles, motors and membranes, establishing important roles for these cellular components in mediating regeneration in the adult central nervous system.

• MeSH
• axony metabolismus   fyziologie   MeSH
• centrální nervový systém fyziologie   MeSH
• endoplazmatické retikulum genetika   metabolismus   MeSH
• endozomy metabolismus   MeSH
• fosforylace MeSH
• integriny metabolismus   MeSH
• krysa rodu Rattus MeSH
• kultivované buňky MeSH
• lidé MeSH
• mutace MeSH
• myši inbrední C57BL MeSH
• myši MeSH
• neurony metabolismus   fyziologie   MeSH
• neuroprotektivní látky aplikace a dávkování   MeSH
• poranění nervus opticus farmakoterapie   metabolismus   patologie   MeSH
• potkani Sprague-Dawley MeSH
• proteinové domény MeSH
• regenerace nervu * účinky léků   MeSH
• retina účinky léků   fyziologie   MeSH
• vezikulární transportní proteiny aplikace a dávkování   chemie   genetika   metabolismus   MeSH
• zvířata MeSH
• Check Tag
• krysa rodu Rattus MeSH
• lidé MeSH
• myši MeSH
• ženské pohlaví MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• Research Support, N.I.H., Intramural MeSH
• Názvy látek
• integriny MeSH
• neuroprotektivní látky MeSH
• vezikulární transportní proteiny MeSH
• ZFYVE27 protein, human MeSH Prohlížeč

NG2 cells, which comprise a cycling population of glial cells, appear in the early phases of development and are present in the adult central nervous system. When a specific subpopulation of NG2 cells give rise to myelinating oligodendrocytes, they are also termed as oligodendrocyte precursor cells. Considering their capacity to proliferate and differentiate into other cellular types, their fate has been extensively investigated in several genetically modified mice. It is generally accepted that NG2 cells are restricted to the oligodendrocyte lineage, but numerous reports describe their differentiation into astrocytes or even neurons. Here, we summarize studies that can prove and also disprove possible neurogenesis from NG2 cells in the different regions of the brain and spinal cord, with the main emphasis on the developmental stages and pathological conditions.

• MeSH
• buněčné linie MeSH
• centrální nervový systém fyziologie   MeSH
• lidé MeSH
• neurogeneze * MeSH
• neuroglie fyziologie   MeSH
• zvířata MeSH
• Check Tag
• lidé MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• přehledy MeSH

Axon regeneration in the CNS is inhibited by many extrinsic and intrinsic factors. Because these act in parallel, no single intervention has been sufficient to enable full regeneration of damaged axons in the adult mammalian CNS. In the external environment, NogoA and CSPGs are strongly inhibitory to the regeneration of adult axons. CNS neurons lose intrinsic regenerative ability as they mature: embryonic but not mature neurons can grow axons for long distances when transplanted into the adult CNS, and regeneration fails with maturity in in vitro axotomy models. The causes of this loss of regeneration include partitioning of neurons into axonal and dendritic fields with many growth-related molecules directed specifically to dendrites and excluded from axons, changes in axonal signalling due to changes in expression and localization of receptors and their ligands, changes in local translation of proteins in axons, and changes in cytoskeletal dynamics after injury. Also with neuronal maturation come epigenetic changes in neurons, with many of the transcription factor binding sites that drive axon growth-related genes becoming inaccessible. The overall aim for successful regeneration is to ensure that the right molecules are expressed after axotomy and to arrange for them to be transported to the right place in the neuron, including the damaged axon tip.

• Klíčová slova
• Axon regeneration, Axonal transport, Chondroitin sulphate proteoglycans, Chondroitinase, Epigenetics, Integrins, NogoA, PTEN, Rabs, RhoA, Schwann cell, Signalling, Trafficking,
• MeSH
• axonální transport fyziologie   MeSH
• axony fyziologie   MeSH
• centrální nervový systém cytologie   fyziologie   MeSH
• lidé MeSH
• nervový útlum fyziologie   MeSH
• neurogeneze fyziologie   MeSH
• proteosyntéza fyziologie   MeSH
• regenerace nervu fyziologie   MeSH
• zvířata MeSH
• Check Tag
• lidé MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• přehledy MeSH

The maintenance of plasma sodium concentration within a narrow limit is crucial to life. When it differs from normal physiological patterns, several mechanisms are activated in order to restore body fluid homeostasis. Such mechanisms may be vegetative and/or behavioral, and several regions of the central nervous system (CNS) are involved in their triggering. Some of these are responsible for sensory pathways that perceive a disturbance of the body fluid homeostasis and transmit information to other regions. These regions, in turn, initiate adequate adjustments in order to restore homeostasis. The main cardiovascular and autonomic responses to a change in plasma sodium concentration are: i) changes in arterial blood pressure and heart rate; ii) changes in sympathetic activity to the renal system in order to ensure adequate renal sodium excretion/absorption, and iii) the secretion of compounds involved in sodium ion homeostasis (ANP, Ang-II, and ADH, for example). Due to their cardiovascular effects, hypertonic saline solutions have been used to promote resuscitation in hemorrhagic patients, thereby increasing survival rates following trauma. In the present review, we expose and discuss the role of several CNS regions involved in body fluid homeostasis and the effects of acute and chronic hyperosmotic challenges.

• MeSH
• centrální nervový systém účinky léků   fyziologie   MeSH
• hemoragický šok farmakoterapie   patofyziologie   MeSH
• homeostáza účinky léků   fyziologie   MeSH
• hypertonický solný roztok aplikace a dávkování   MeSH
• krevní tlak účinky léků   fyziologie   MeSH
• ledviny účinky léků   fyziologie   MeSH
• lidé MeSH
• nervová síť fyziologie   MeSH
• osmóza účinky léků   fyziologie   MeSH
• srdeční frekvence účinky léků   fyziologie   MeSH
• tělesné tekutiny účinky léků   fyziologie   MeSH
• zvířata MeSH
• Check Tag
• lidé MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• přehledy MeSH
• Názvy látek
• hypertonický solný roztok MeSH

BACKGROUND: Stroke is devastating cerebrovascular event which is responsible for 6.7 million deaths each year worldwide. Inflammation plays an important role in the pathophysiology of stroke. Targeting inflammation after stroke is highly actual topic for both experimental and clinical research. METHODS: Research articles related to cholinergic anti-inflammatory pathway (CHAIP) and stroke were reviewed. The first part of review describes the basic characteristics of inflammatory response after stroke, main components and function of CHAIP. The second part reviews studies focused on CHAIP as a therapeutic target for ischemic and hemorrhagic stroke. Both pharmacological stimulation of α7 nAChR and vagus nerve stimulation after stroke are reviewed. RESULTS: Cholinergic anti-inflammatory pathway (CHAIP) is a physiological mechanism by which central nervous system regulates immune response and controls inflammation. Vagus nerve, spleen and α7 nicotinic acetylcholine receptor (α7 nAChR) are the main components of CHAIP. CONCLUSION: Targeting cholinergic anti-inflammatory pathway is a promising way of immunomodulation which attenuates inflammation in a complex manner without causing immunosuppression.

• Klíčová slova
• Cerebral ischemia, Vagus nerve stimulation, cholinergic anti-inflammatory pathway, inflammation, intracerebral hemorrhage, stroke, subarachnoid hemorrhage, α7 nicotinic acetylcholine receptor (α7 nAChR),
• MeSH
• alfa7 nikotinové acetylcholinové receptory fyziologie   MeSH
• centrální nervový systém fyziologie   MeSH
• cévní mozková příhoda imunologie   patofyziologie   MeSH
• lidé MeSH
• nervus vagus fyziologie   MeSH
• slezina fyziologie   MeSH
• zánět patofyziologie   MeSH
• Check Tag
• lidé MeSH
• Publikační typ
• časopisecké články MeSH
• přehledy MeSH
• Názvy látek
• alfa7 nikotinové acetylcholinové receptory MeSH

Obesity currently represents one of the most important global health problems. According to the World health organization's prediction the number of obese patients in the adult population will increase to 700 million by 2015. The reasons of constantly increasing prevalence of obesity include a combination of genetic predisposition, the predominance of energy intake over energy expenditure due to easy availability of calorie-rich meals and permanently decreasing energy expenditure from physical activity. Understanding the precise mechanisms of food intake regulation is essential for development of body weight-reducing drugs with long-term effects. The central nervous system plays the main role in the regulation of food intake. This system is influenced by a number of long-acting and short-acting peripheral signals informing about the degree of saturation, the amount of energy reserves and the overall state of energy homeostasis. Hormones produced in the gastrointestinal tract play an important role in the regulation of food intake. The aim of this article is to summarize the significance of selected gut hormones in the regulation of food intake and to discuss their possible use in the treatment of obesity and its associated comorbidities.

• MeSH
• centrální nervový systém fyziologie   MeSH
• gastrointestinální hormony fyziologie   MeSH
• lidé MeSH
• neurosekreční systémy fyziologie   MeSH
• obezita patofyziologie   terapie   MeSH
• regulace chuti k jídlu fyziologie   MeSH
• Check Tag
• lidé MeSH
• Publikační typ
• časopisecké články MeSH
• přehledy MeSH
• Názvy látek
• gastrointestinální hormony MeSH

BACKGROUND/AIMS: Central dopaminergic activity is probably linked to regulation of glucose and lipid metabolism and weight maintenance. The aim of our study was to evaluate the relationship between central dopaminergic activity measured using the apomorphine challenge test and metabolic parameters in healthy men. METHODS: Forty-two healthy men (average age 43.5 ± 7.4 years, body mass index, BMI, 27.4 ± 5.7) were examined anthropometrically and biochemically (glycemia, lipids, glycated hemoglobin). Central dopaminergic activity was assessed as the area under the curve (AUC) of prolactin (PRL) and growth hormone (GH) responses to the apomorphine challenge test after sublingual administration of apomorphine in a dose of 0.033 mg/kg. Insulin resistance was quantified by calculation of glucose disposal and metabolic clearance rate during a euglycemic hyperinsulinemic clamp on two insulin levels (1 and 10 mIU/kg/min). Linear regression was used for statistical analysis. RESULTS: Hormonal responses correlated negatively with age (for AUC/GH r = -0.33; p = 0.031) and BMI (AUC/GH r = -0.41; p = 0.007). After adjustment for age and BMI, a statistically significant negative correlations between AUC/PRL and total cholesterol (r = -0.41; p = 0.007), AUC/GH and HbA1c (r = -0.37; p = 0.016) and AUC/GH and HOMA (homeostasis model assessment; r = -0.345; p = 0.025) were observed. CONCLUSION: Central dopaminergic activity declines with age and BMI. Higher total cholesterol, glycated hemoglobin and insulin resistance parameters are connected with lower central dopamine tone.

• MeSH
• agonisté dopaminu farmakologie   MeSH
• apomorfin farmakologie   MeSH
• centrální nervový systém účinky léků   metabolismus   fyziologie   MeSH
• dopamin metabolismus   farmakologie   MeSH
• dopaminergní neurony účinky léků   metabolismus   fyziologie   MeSH
• dospělí MeSH
• energetický metabolismus * účinky léků   MeSH
• index tělesné hmotnosti MeSH
• inzulin krev   metabolismus   MeSH
• inzulinová rezistence fyziologie   MeSH
• krevní glukóza metabolismus   MeSH
• lidé středního věku MeSH
• lidé MeSH
• zdraví MeSH
• Check Tag
• dospělí MeSH
• lidé středního věku MeSH
• lidé MeSH
• mužské pohlaví MeSH
• Publikační typ
• časopisecké články MeSH
• klinické zkoušky MeSH
• práce podpořená grantem MeSH
• Názvy látek
• agonisté dopaminu MeSH
• apomorfin MeSH
• dopamin MeSH
• inzulin MeSH
• krevní glukóza MeSH

Current research on the etiopathogenesis of diseases of peripheral organs is primarily focused on the study of processes affecting those organs directly altered by diseases. As a result, therapeutic interventions are focused on the cells of those organs affected by pathological processes. However, pathological processes are not restricted to any "circumscribed" group of cells. Cells of tissue affected by pathological process interact with cells in the surrounding tissues. Moreover, pathologic processes also induce changes in the activity of the neuroendocrine and immune systems, which also affect the progression of pathological processes. The neurobiological view of diseases is based on the assumption that the nervous system processes signals related to pathological processes in peripheral organs and then consequently modulates it via the autonomic, neuroendocrine, and neuroimmune regulations. The aim of this paper is to explain the basis of the neurobiological view of diseases of the peripheral organs, and then discuss possible therapeutic consequences.

• MeSH
• centrální nervový systém fyziologie   patofyziologie   MeSH
• lidé MeSH
• nemoc etiologie   MeSH
• neurobiologie MeSH
• neuroimunomodulace MeSH
• neurosekreční systémy fyziologie   patofyziologie   MeSH
• zvířata MeSH
• Check Tag
• lidé MeSH
• zvířata MeSH
• Publikační typ
• anglický abstrakt MeSH
• časopisecké články MeSH
• přehledy MeSH

The fetus reacts to nociceptive stimulations through different motor, autonomic, vegetative, hormonal, and metabolic changes relatively early in the gestation period. With respect to the fact that the modulatory system does not yet exist, the first reactions are purely reflexive and without connection to the type of stimulus. While the fetal nervous system is able to react through protective reflexes to potentially harmful stimuli, there is no accurate evidence concerning pain sensations in this early period. Cortical processes occur only after thalamocortical connections and pathways have been completed at the 26th gestational week. Harmful (painful) stimuli, especially in fetuses have an adverse effect on the development of humans regardless of the processes in brain. Moreover, pain activates a number of subcortical mechanisms and a wide spectrum of stress responses influence the maturation of thalamocortical pathways and other cortical activation which are very important in pain processing.

• MeSH
• bolest patofyziologie   MeSH
• centrální nervový systém embryologie   fyziologie   MeSH
• gestační stáří MeSH
• krysa rodu Rattus MeSH
• lidé MeSH
• nervové dráhy embryologie   fyziologie   MeSH
• percepce fyziologie   MeSH
• plod fyziologie   MeSH
• práh bolesti fyziologie   MeSH
• těhotenství MeSH
• vývoj plodu MeSH
• zvířata MeSH
• Check Tag
• krysa rodu Rattus MeSH
• lidé MeSH
• těhotenství MeSH
• ženské pohlaví MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• přehledy MeSH