Hyperbaric oxygen therapy (HBOT) elevates the partial pressure of life-sustaining oxygen (pO2), thereby saving lives. However, HBOT can also cause toxic effects like lung and retinal damage (peripheral oxygen toxicity) and violent myoclonic seizures (central nervous system (CNS) toxicity). The mechanisms behind these effects are not fully understood, hindering the development of effective therapies and preventive strategies. Herein, we critically reviewed the literature to understand CNS oxygen toxicity associated with HBOT to elucidate their mechanism, treatment, and prevention. We provide evidence that (1) increased pO2 increases reactive oxygen species (ROS) concentration in tissues, which irreversibly alters cell receptors, causing peripheral oxygen toxicity and contributing to CNS oxygen toxicity. Furthermore, (2) increased ROS concentration in the brain lowers the activity of glutamic decarboxylase (GD), which lowers concentrations of inhibitory neurotransmitter γ-aminobutyric acid (GABA), thereby contributing to the onset of HBOT-derived seizures. We provide long-overlooked evidence that (3) elevated ambient pressure directly inhibits GABAA, glycine and other receptors, leading to the rapid onset of seizures. Additionally, (4) acidosis facilitates the onset of seizures by an unknown mechanism. Only a combination of these mechanisms explains most phenomena seen in peripheral and CNS oxygen toxicity. Based on these proposed intertwined mechanisms, we suggest administering antioxidants (lowering ROS concentrations), pyridoxine (restoring GD activity), low doses of sedatives/anesthetics (reversing inhibitory effects of pressure on GABAA and glycine receptors), and treatment of acidemia before routine HBOT to prevent peripheral and CNS oxygen toxicity. Theoretically, similar preventive strategies can be applied before deep-sea diving to prevent life-threatening convulsions.

• Klíčová slova
• Central nervous system oxygen toxicity, Diving, High-pressure nervous syndrome, High-pressure neurological syndrome, Hyperbaric medicine, Hyperbaric oxygen convulsions, Hyperbaric oxygen seizures, Hyperbaric oxygen therapy, Hypothesis, Oxygen toxicity, Paul Bert effect, Pressure reversal of anesthesia,
• MeSH
• antioxidancia metabolismus   farmakologie   MeSH
• centrální nervový systém účinky léků   metabolismus   MeSH
• hyperbarická oxygenace * metody   MeSH
• kyslík * metabolismus   MeSH
• lidé MeSH
• reaktivní formy kyslíku metabolismus   MeSH
• záchvaty prevence a kontrola   metabolismus   chemicky indukované   MeSH
• zvířata MeSH
• Check Tag
• lidé MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• přehledy MeSH
• Názvy látek
• antioxidancia MeSH
• kyslík * MeSH
• reaktivní formy kyslíku MeSH

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

Regulation of neuroimmune interactions varies across avian species. Little is presently known about the interplay between periphery and central nervous system (CNS) in parrots, birds sensitive to neuroinflammation. Here we investigated the systemic and CNS responses to dextran sulphate sodium (DSS)- and lipopolysaccharide (LPS)-induced subclinical acute peripheral inflammation in budgerigar (Melopsittacus undulatus). Three experimental treatment groups differing in DSS and LPS stimulation were compared to controls. Individuals treated with DSS showed significant histological intestinal damage. Through quantitative proteomics we described changes in plasma (PL) and cerebrospinal fluid (CSF) composition. In total, we identified 180 proteins in PL and 978 proteins in CSF, with moderate co-structure between the proteomes. Between treatments we detected differences in immune, coagulation and metabolic pathways. Proteomic variation was associated with the levels of pro-inflammatory cytokine mRNA expression in intestine and brain. Our findings shed light on systemic impacts of peripheral low-grade inflammation in birds.

• Klíčová slova
• Cerebrospinal fluid, Dextran sulphate sodium, Endotoxin, Parrot, Plasma, Proteomics,
• MeSH
• centrální nervový systém * metabolismus   imunologie   MeSH
• cytokiny metabolismus   MeSH
• lipopolysacharidy * imunologie   MeSH
• Melopsittacus * imunologie   MeSH
• mozek metabolismus   imunologie   MeSH
• nemoci ptáků imunologie   metabolismus   MeSH
• neuroimunomodulace MeSH
• neurozánětlivé nemoci imunologie   MeSH
• proteom * metabolismus   MeSH
• proteomika metody   MeSH
• ptačí proteiny metabolismus   genetika   MeSH
• síran dextranu * MeSH
• střeva imunologie   MeSH
• zánět * imunologie   metabolismus   MeSH
• zvířata MeSH
• Check Tag
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• Názvy látek
• cytokiny MeSH
• lipopolysacharidy * MeSH
• proteom * MeSH
• ptačí proteiny MeSH
• síran dextranu * MeSH

Transient receptor potential cation channels subfamily V member 4 (TRPV4) are non-selective cation channels expressed in different cell types of the central nervous system. These channels can be activated by diverse physical and chemical stimuli, including heat and mechanical stress. In astrocytes, they are involved in the modulation of neuronal excitability, control of blood flow, and brain edema formation. All these processes are significantly impaired in cerebral ischemia due to insufficient blood supply to the tissue, resulting in energy depletion, ionic disbalance, and excitotoxicity. The polymodal cation channel TRPV4, which mediates Ca2+ influx into the cell because of activation by various stimuli, is one of the potential therapeutic targets in the treatment of cerebral ischemia. However, its expression and function vary significantly between brain cell types, and therefore, the effect of its modulation in healthy tissue and pathology needs to be carefully studied and evaluated. In this review, we provide a summary of available information on TRPV4 channels and their expression in healthy and injured neural cells, with a particular focus on their role in ischemic brain injury.

• Klíčová slova
• Ca2+ signaling, TRPV4, astrocytes, glia, ischemia,
• MeSH
• astrocyty * metabolismus   MeSH
• centrální nervový systém metabolismus   MeSH
• cerebrální infarkt MeSH
• ischemie mozku * metabolismus   MeSH
• kationtové kanály TRPV * metabolismus   MeSH
• lidé MeSH
• mozek metabolismus   MeSH
• Check Tag
• lidé MeSH
• Publikační typ
• časopisecké články MeSH
• přehledy MeSH
• Názvy látek
• kationtové kanály TRPV * MeSH
• TRPV4 protein, human MeSH Prohlížeč

In humans, most free tryptophan is degraded via kynurenine pathways into kynurenines. Kynurenines modulate the immune system, central nervous system, and skeletal muscle bioenergetics. Consequently, kynurenine pathway metabolites (KPMs) have been studied in the context of exercise. However, the effect of vitamin D supplementation on exercise-induced changes in KPMs has not been investigated. Here, we analyzed the effect of a single high-dose vitamin D supplementation on KPMs and tryptophan levels in runners after an ultramarathon. In the study, 35 amateur runners were assigned into two groups: vitamin D supplementation group, administered 150,000 IU vitamin D in vegetable oil 24 h before the run (n = 16); and control (placebo) group (n = 19). Blood was collected for analysis 24 h before, immediately after, and 24 h after the run. Kynurenic, xanthurenic, quinolinic, and picolinic acids levels were significantly increased after the run in the control group, but the effect was blunted by vitamin D supplementation. Conversely, the decrease in serum tryptophan, tyrosine, and phenylalanine levels immediately after the run was more pronounced in the supplemented group than in the control. The 3-hydroxy-l-kynurenine levels were significantly increased in both groups after the run. We conclude that vitamin D supplementation affects ultramarathon-induced changes in tryptophan metabolism.

• Klíčová slova
• kynurenine, skeletal muscle damage, ultramarathon, vitamin D,
• MeSH
• centrální nervový systém metabolismus   MeSH
• kynurenin * metabolismus   MeSH
• lidé MeSH
• potravní doplňky MeSH
• tryptofan * metabolismus   MeSH
• vitamin D MeSH
• Check Tag
• lidé MeSH
• Publikační typ
• časopisecké články MeSH
• randomizované kontrolované studie MeSH
• Názvy látek
• kynurenin * MeSH
• tryptofan * MeSH
• vitamin D MeSH

The myelin sheath is an essential, multilayered membrane structure that insulates axons, enabling the rapid transmission of nerve impulses. The tetraspan myelin proteolipid protein (PLP) is the most abundant protein of compact myelin in the central nervous system (CNS). The integral membrane protein PLP adheres myelin membranes together and enhances the compaction of myelin, having a fundamental role in myelin stability and axonal support. PLP is linked to severe CNS neuropathies, including inherited Pelizaeus-Merzbacher disease and spastic paraplegia type 2, as well as multiple sclerosis. Nevertheless, the structure, lipid interaction properties, and membrane organization mechanisms of PLP have remained unidentified. We expressed, purified, and structurally characterized human PLP and its shorter isoform DM20. Synchrotron radiation circular dichroism spectroscopy and small-angle X-ray and neutron scattering revealed a dimeric, α-helical conformation for both PLP and DM20 in detergent complexes, and pinpoint structural variations between the isoforms and their influence on protein function. In phosphatidylcholine membranes, reconstituted PLP and DM20 spontaneously induced formation of multilamellar myelin-like membrane assemblies. Cholesterol and sphingomyelin enhanced the membrane organization but were not crucial for membrane stacking. Electron cryomicroscopy, atomic force microscopy, and X-ray diffraction experiments for membrane-embedded PLP/DM20 illustrated effective membrane stacking and ordered organization of membrane assemblies with a repeat distance in line with CNS myelin. Our results shed light on the 3D structure of myelin PLP and DM20, their structure-function differences, as well as fundamental protein-lipid interplay in CNS compact myelin.

• Klíčová slova
• Atomic force microscopy, DM20, Integral membrane protein, Myelin, Proteolipid protein, Small-angle scattering,
• MeSH
• axony metabolismus   MeSH
• centrální nervový systém metabolismus   MeSH
• lidé MeSH
• lipidové dvojvrstvy * metabolismus   MeSH
• myelinová pochva metabolismus   MeSH
• myelinový proteolipidový protein * metabolismus   MeSH
• protein - isoformy metabolismus   MeSH
• Check Tag
• lidé MeSH
• Publikační typ
• časopisecké články MeSH
• Názvy látek
• lipidové dvojvrstvy * MeSH
• myelinový proteolipidový protein * MeSH
• protein - isoformy MeSH

Current understanding of the mechanisms underlying central nervous system (CNS) injury is limited, and traditional therapeutic methods lack a molecular approach either to prevent acute phase or secondary damage, or to support restorative mechanisms in the nervous tissue. microRNAs (miRNAs) are endogenous, non-coding RNA molecules that have recently been discovered as fundamental and post-transcriptional regulators of gene expression. The capacity of microRNAs to regulate the cell state and function through post-transcriptionally silencing hundreds of genes are being acknowledged as an important factor in the pathophysiology of both acute and chronic CNS injuries. In this study, we have summarized the knowledge concerning the pathophysiology of several neurological disorders, and the role of most canonical miRNAs in their development. We have focused on the miR-20, the miR-17~92 family to which miR-20 belongs, and their function in the normal development and disease of the CNS.

• Klíčová slova
• central nervous system, miR-20a, microRNA,
• MeSH
• centrální nervový systém metabolismus   MeSH
• lidé MeSH
• mikro RNA * genetika   metabolismus   MeSH
• nemoci nervového systému * metabolismus   MeSH
• poranění nervového systému * metabolismus   MeSH
• Check Tag
• lidé MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• přehledy MeSH
• Názvy látek
• mikro RNA * MeSH

Worker honey bees are subject to biochemical and physiological changes throughout the year. This study aimed to provide the reasons behind these fluctuations. The markers analysed included lipid, carbohydrate, and protein levels in the haemolymph; the activity of digestive enzymes in the midgut; the levels of adipokinetic hormone (AKH) in the bee central nervous system; the levels of vitellogenins in the bee venom and haemolymph; and the levels of melittin in the venom. The levels of all the main nutrients in the haemolymph peaked mostly within the period of maximal bee activity, whereas the activity of digestive enzymes mostly showed a two-peak course. Furthermore, the levels of AKHs fluctuated throughout the year, with modest but significant variations. These data suggest that the role of AKHs in bee energy metabolism is somewhat limited, and that bees rely more on available food and less on body deposits. Interestingly, the non-metabolic characteristics also fluctuated over the year. The vitellogenin peak reached its maximum in the haemolymph in winter, which is probably associated with the immunoprotection of long-lived winter bees. The analysis of bee venom showed the maximal levels of vitellogenin in autumn; however, it is not entirely clear why this is the case. Finally, melittin levels showed strong fluctuations, suggesting that seasonal control was unlikely.

• Klíčová slova
• Adipokinetic hormone, Metabolism, Seasonal fluctuations, Venom, Vitellogenin,
• MeSH
• biologické markery metabolismus   MeSH
• centrální nervový systém metabolismus   MeSH
• hemolymfa metabolismus   MeSH
• hmyzí hormony metabolismus   MeSH
• kyselina pyrrolidonkarboxylová analogy a deriváty   metabolismus   MeSH
• melitten metabolismus   MeSH
• oligopeptidy metabolismus   MeSH
• roční období * MeSH
• trávicí systém enzymologie   MeSH
• včelí jedy metabolismus   MeSH
• včely fyziologie   MeSH
• vitelogeniny metabolismus   MeSH
• zvířata MeSH
• Check Tag
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• Názvy látek
• adipokinetic hormone MeSH Prohlížeč
• biologické markery MeSH
• hmyzí hormony MeSH
• kyselina pyrrolidonkarboxylová MeSH
• melitten MeSH
• oligopeptidy MeSH
• včelí jedy MeSH
• vitelogeniny MeSH

Methamphetamine (MA), as massively abused psychoactive stimulant, has been associated with many neurological diseases. It has various potent and neurotoxic properties. There are many mechanisms of action that contribute to its neurotoxic and degenerative effects, including excessive neurotransmitter (NEU) release, blockage of NEU uptake transporters, degeneration of NEU receptors, process of oxidative stress etc. MA intoxication is caused by blood-brain barrier disruption resulted from MA-induced oxidation stress. In our laboratory we constantly work on animal research of MA. Our current interest is to investigate processes of MA-induced alteration in neurotransmission, especially during development of laboratory rat. This review will describe current understanding in role of NEUs, which are affected by MA-induced neurotoxicity caused by altering the action of NEUs in the central nervous system (CNS). It also briefly brings information about NEUs development in critical periods of development.

• MeSH
• centrální nervový systém účinky léků   růst a vývoj   metabolismus   MeSH
• chování zvířat účinky léků   MeSH
• krysa rodu Rattus MeSH
• lidé MeSH
• methamfetamin toxicita   MeSH
• nervový přenos účinky léků   MeSH
• neurogeneze účinky léků   MeSH
• neurotoxické syndromy etiologie   metabolismus   patologie   MeSH
• neurotransmiterové látky toxicita   MeSH
• stimulanty centrálního nervového systému toxicita   MeSH
• zvířata MeSH
• Check Tag
• krysa rodu Rattus MeSH
• lidé MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• přehledy MeSH
• Názvy látek
• methamfetamin MeSH
• neurotransmiterové látky MeSH
• stimulanty centrálního nervového systému MeSH

Serotonin (5-hydroxytryptamine, 5-HT) plays two important roles in humans-one central and the other peripheral-depending on the location of the 5-HT pools of on either side of the blood-brain barrier. In the central nervous system it acts as a neurotransmitter, controlling such brain functions as autonomic neural activity, stress response, body temperature, sleep, mood and appetite. This role is very important in intensive care, as in critically ill patients multiple serotoninergic agents like opioids, antiemetics and antidepressants are frequently used. High serotonin levels lead to altered mental status, deliria, rigidity and myoclonus, together recognized as serotonin syndrome. In its role as a peripheral hormone, serotonin is unique in controlling the functions of several organs. In the gastrointestinal tract it is important for regulating motor and secretory functions. Apart from intestinal motility, energy metabolism is regulated by both central and peripheral serotonin signaling. It also has fundamental effects on hemostasis, vascular tone, heart rate, respiratory drive, cell growth and immunity. Serotonin regulates almost all immune cells in response to inflammation, following the activation of platelets.

• Klíčová slova
• critically ill, energy metabolism, immunoregulatory functions, intestinal motility, neurotransmitter, peripheral hormone, serotonin, serotonin syndrome,
• MeSH
• centrální nervový systém metabolismus   patologie   MeSH
• delirium metabolismus   patologie   MeSH
• gastrointestinální motilita fyziologie   MeSH
• gastrointestinální trakt metabolismus   patologie   MeSH
• hematoencefalická bariéra metabolismus   patologie   MeSH
• kritický stav * MeSH
• lidé MeSH
• myoklonus metabolismus   patologie   MeSH
• serotonin biosyntéza   metabolismus   MeSH
• serotoninový syndrom metabolismus   patologie   MeSH
• zánět metabolismus   patologie   MeSH
• Check Tag
• lidé MeSH
• Publikační typ
• časopisecké články MeSH
• přehledy MeSH
• Názvy látek
• serotonin MeSH