Activity Of Nerve Cells Research Articles

Dietetic ingredients of small animals suffering from obesity and their biological role

Obesity is a medical condition in which excess body fat has accumulated to the extent that it may have a negative effect on health. The daily ration of an adult cat must contain 40–45% of proteins, 20–25% of fats, 25–30% of carbohydrates. Low- fat diets are recommended to cats with overweight. Necessary amino acids are in the diet of cats with excess weight. Taurine is a sulfonic acid, which synthesizes in the body of animals and humans from the amino acid of cysteine. It plays an essential role in the digestion and assimilation of fats and lipids. The need for cats in taurine is due to their limited ability to synthesize taurine from amino acids that contain sulfur, as well as the fact that it holds bile acids. The latter is very important because cats do not produce bile acid salts associated with glycine, even in the case of taurine deficiency. Taurine has many fundamental biological roles, such as conjugation of bile acids, antioxidation, osmoregulation, membrane stabilization, and modulation of calcium signaling. It is essential for cardiovascular function, and development and function of skeletal muscle, the retina, and the central nervous system. The deficiency of taurine leads to degeneration of the retina and blindness, deafness, cardiomyopathy, disorders in the functioning of the immune and reproductive systems, suppression of neonatal growth, and the occurrence of birth defects. The recommended amount for a cat per day is 100–200 mg. L-Tryptophan is an α-amino acid that is used in the biosynthesis of proteins. Together with vitamin B6, magnesium and niacin, tryptophan is responsible for the serotonin production in the brain (a mediator that regulates the activity of nerve cells and transmits signals between them). Also, tryptophan is involved in the production of hemoglobin and affects the reproductive function of animals. The recommended amount for a cat per day is 0.3 g/1000 kcal of energy value (EV). DL-methionine is a synthetic analog of natural methionine. Methionine is an essential amino acid for animals. As the substrate for other amino acids such as cysteine and taurine, and the important antioxidant glutathione, methionine plays a critical role in the metabolism and health of many species, including humans. Methionine is a source of sulfur that forms the keratin protein. Keratin is simply necessary for the health of the hair, skin, and claws of the animal. The recommended amount for a cat per day (methionine + cystine) is 1.5 g/1000 kcal EV. Nowadays the problem of overweight in small domestic animals, in particular in cats and dogs, is becoming more widespread. In order to prevent the spread of obesity, therapeutic rations should be balanced by all indicators, such as proteins, fats, carbohydrates, amino acids, minerals, and vitamins.

Modelling Transition From Normal To Epileptic Eeg Signals: A Neuron-Astrocyte Mass Action Approach

Epileptic seizures occur intermittently as a result of complex dynamical interactions among many regions of the brain. The sudden and apparently unpredictable nature of refractory seizures is one of the most disabling aspects of the disease. Therefore, there is need for interdisciplinary research efforts directed at better understanding of the mechanisms involved in the emergence of epileptic seizures. Our research objective in this field is the use of applied methods from deterministic and nondeterministic dynamical systems modeling to study epilepsy. Dynamical systems refer to systems whose state variables evolve in time. By the assumption of deterministic system,the physiological system (the brain) can be treated as low dimensional without any random components. Nondeterministic assumption on the other hand allows randomness in some input components. We developed at the macroscopic level physiologically based mathematical models of parts of the brain believed to be eliciting the abnormal signals observed during Generalized Absence Epilepsy (GAE) and Temporal Lobe Epilepsy (TLE). In developing our models, we considered the activities of nerve cells, the surrounding astrocyte cells and the dynamics of extracellular neurotransmitters and conducted parameter sensitivity studies on our models. The models were then validated using Electroencephalogram (EEG) data of epileptic patients. The important conclusion from our findings is that the transition from normal to epileptic brain activity is critically dependent on small variations in few system parameters and/or the balance between a small number of system parameters, be it neural or astrocytes activity dependent

NEURODESTRUCTION OF HYPOTHALAMIC NUCLEI IN BRAIN INJURY. EFFECT OF CARBACETAM

Relevance. A key role in the pathogenesis of brain injury (BI) is played by destructive changes in the neural tissue of the brain, which consist in damage to neurons and glial cells. To date, various drugs are being intensively developed and studied, which are considered in the perspective of correction and restoration of the functional state of the brain. These substances include the neuroprotector carbacetam, an modulator of the GABA-benzodiazepine receptor complex, a derivative of the alkaloid β-carboline. Objectie. To investigate the effect of carbacetam on neurodestruction processes in the paraventricular and supraoptic nuclei of the hypothalamus in experimental BI. Material and methods. The study was carried out on 20 white non-native male rats weighing 200±10 g. To simulate the BI, rats were subjected to one stroke along the cranial vault with a free-fall load according to the V.N. Yelskyy and S.V. Ziablitsev method (2008). The energy of impact was 0.52 J, the lethality for the first 5 days after injury was 84%. In the control group (n=10) 1 ml of saline was injected intraperitoneally once daily for 10 days after injury. Animals of the experimental group (n=10) received intraperitoneally injections of carbacetam at a dose of 5 mg/kg in 1 ml of saline according to the same scheme. After the experiment was over, the animals were decapitated with the removal of the brain, from which histological preparations were made with a microtome after appropriate histological treatment. Some sections were stained with hematoxylin and eosin, others were immunohistochemically reacted with antibodies against neuronmarkers proteins NSE, S-100 and GFAP. Results. Carbacetam influenced the decrease of degenerative processes in the nervous tissue of the paraventricular and supraoptic nuclei of the hypothalamus. Neurons of animals with BI that received carbacetam, were characterized by the restoration of normal morphological features in contrast to rats not receiving the drug. Immunohistochemical study of brain neuromarkers confirmed the restoration of the functions of neurons and astrocytes in the investigated parts of the rat's hypothalamus after the administration of carbacetam. There was a decrease in the expression level of glial markers GFAP and S-100, which illustrated the decrease in degenerative changes in the nervous tissue. While the expression level of the neuron marker NSE grew, this demonstrated the high metabolic activity of nerve cells. Changes in the expression of markers of neurons and glia indicated a restoration of normal neuronal activity under the action of carbacetam. Conclusion. Further investigation of the effects of carbacetam seems promising in terms of the restoration of neuronal function at BI.

Panax Notoginseng Saponins: A Review of Its Mechanisms of Antidepressant or Anxiolytic Effects and Network Analysis on Phytochemistry and Pharmacology.

Panax notoginseng (Burk) F. H. Chen, as traditional Chinese medicine, has a long history of high clinical value, such as anti-inflammatory, anti-oxidation, inhibition of platelet aggregation, regulation of blood glucose and blood pressure, inhibition of neuronal apoptosis, and neuronal protection, and its main ingredients are Panax notoginseng saponins (PNS). Currently, Panax notoginseng (Burk) F. H. Chen may improve mental function, have anti-insomnia and anti-depression effects, alleviate anxiety, and decrease neural network excitation. However, the underlying effects and the mechanisms of Panax notoginseng (Burk) F. H. Chen and its containing chemical constituents (PNS) on these depression-related or anxiety-related diseases has not been completely established. This review summarized the antidepressant or anxiolytic effects and mechanisms of PNS and analyzed network targets of antidepressant or anxiolytic actions with network pharmacology tools to provide directions and references for further pharmacological studies and new ideas for clinical treatment of nervous system diseases and drug studies and development. The review showed PNS and its components may exert these effects through regulating neurotransmitter mechanism (5-HT, DA, NE), modulation of the gamma-amino butyric acid (GABA) neurotransmission, glutamatergic system, hypo-thalamus-pituitary-adrenal (HPA) axis, brain-derived neurotrophic factor (BDNF), and its intracellular signaling pathways in the central nervous system; and produce neuronal protection by anti-inflammatory, anti-oxidation, or inhibition of neuronal apoptosis, or platelet aggregation and its intracellular signaling pathways. Network target analysis indicated PNS and its components also may have anti-inflammatory and anti-apoptotic effects, which leads to the preservation of brain nerves, and regulate the activity and secretion of nerve cells, exerting anti-depression and anxiolytic effects, which may provide new directions for further in-depth researches of related mechanisms.

Photobiomodulation in Neuroscience: A Summary of Personal Experience

This review summarizes personal experience with laser photobiomodulation and its potentials for the treatment of peripheral and central nerve system injuries. Laser photobiomodulation was shown to induce nerve cell activation, have a positive effect on metabolism of the nerve cells, and to stimulate nerve sprouting processes. Studies investigating the effects of laser photobiomodulation on injured peripheral nerves in rats reported immediate protective effects which increase the functional activity of the nerve, decrease or prevent scar tissue formation at the injured site, prevent or decrease degeneration in corresponding motor neurons of the spinal cord, and significantly increase axonal growth and myelinization. A direct application of laser on the spinal cord had a positive impact on the corresponding injured peripheral nerve and promoted recovery. A 780-nm laser phototherapy was applied following peripheral nerve reconstruction using a guiding nerve tube. Results showed myelinated axons crossing through the nerve tube and the continuation of axonal sprouting through the tube toward the distal part of the nerve. In a double-blind, placebo-controlled randomized pilot clinical trial in patients with incomplete stable long-term peripheral nerve injury (PNI), 780-nm laser irradiation progressively improved peripheral nerve function and led to substantial functional recovery. Muscle atrophy represents a major challenge in restorative medicine. Laser phototherapy was shown to increase biochemical activity and improve morphological recovery in muscle and, thus, could have a direct therapeutic application, especially during progressive muscle atrophy resulting from PNI. The effectiveness of composite implants of cultured embryonal nerve cells and the role of laser irradiation on regeneration and repair of the completely transected rat spinal cord were examined. Results suggested that laser photobiomodulation treatment accelerates the axonal growth. The significance of the performed experimental and clinical studies is in the provision of new laser technology in field of cell therapy and its therapeutic value for peripheral nerve and spinal cord injuries. Additional well-designed clinical studies are needed to evaluate the effectiveness and role of laser photobiomodulation treatment in a clinical setting.

Antiepileptic and Antioxidant Activity of Some Medicinal Plants: A Review

Medicinal plants are the oldest form of healthcare known to mankind. Antioxidants are considered to be important in fighting against the damages done by the free radicals produced due to oxidative stress. Antiepileptic drugs help to minimize or to irradiate the convulsive shocks and seizures as a result of abnormal and excessive nerve cell activity. Standardized, well established in vitro and in vivo methods are available for experimental evaluation of antioxidant and antiepileptic agents. A step wise procedure from in vitro and in vivo seems reasonable to reduce the large quantity of potential drugs to a few promising agents for further clinical testing. This review has focused on some herbal drugs with both antioxidant and antiepileptic property such as Brassica nigra, Bacopa monniera, Ficus religiosa, Convolvulus pluricalis, Jatamansi and Acorus calamus.

Determination of Acid Phosphatase Activity in Nervous Tissue

High levels of acid phosphatase activity in nerve cells allow methods for its detection to be used in morphofunctional studies of nervous tissue elements. Using neurons in the stellate ganglion in cows as an example, the bodies and processes of nerve cells are shown to have different levels of enzyme activity. Nerve endings have consistently high levels. This method provides for detailed morphological investigation of neurons and assessment of their interactions. This report provides a detailed description of an improved method for identifying acid phosphatase activity in nervous tissue structures.

Chemogenetics revealed: DREADD occupancy and activation via converted clozapine.

The chemogenetic technology DREADD (designer receptors exclusively activated by designer drugs) is widely used for remote manipulation of neuronal activity in freely moving animals. DREADD technology posits the use of "designer receptors," which are exclusively activated by the "designer drug" clozapine N-oxide (CNO). Nevertheless, the in vivo mechanism of action of CNO at DREADDs has never been confirmed. CNO does not enter the brain after systemic drug injections and shows low affinity for DREADDs. Clozapine, to which CNO rapidly converts in vivo, shows high DREADD affinity and potency. Upon systemic CNO injections, converted clozapine readily enters the brain and occupies central nervous system-expressed DREADDs, whereas systemic subthreshold clozapine injections induce preferential DREADD-mediated behaviors.

DREADD not the designer compound

Neuroscience Designer receptors exclusively activated by designer drugs (DREADDs) constitute a powerful chemogenetic strategy that can modulate nerve cell activity in freely moving animal preparations. Gomez et al. used radioligand receptor occupancy measurements and in vivo positron emission tomography to show that DREADDs expressed in the brain are not activated by the designer compound CNO (clozapine N -oxide). Instead, they are activated by the CNO metabolite clozapine, a drug with multiple endogenous targets. This may have important implications for the interpretation of results obtained with this popular technology. Science , this issue p. [503][1] [1]: /lookup/doi/10.1126/science.aan2475

RhEPO Enhances Cellular Anti-oxidant Capacity to Protect Long-Term Cultured Aging Primary Nerve Cells

Erythropoietin (EPO) may protect the nervous system of animals against aging damage, making it a potential anti-aging drug for the nervous system. However, experimental evidence from natural aging nerve cell models is lacking, and the efficacy of EPO and underlying mechanism of this effect warrant further study. Thus, the present study used long-term cultured primary nerve cells to successfully mimic the natural aging process of nerve cells. Starting on the 11th day of culture, cells were treated with different concentrations of recombinant human erythropoietin (rhEPO). Using double immunofluorescence labeling, we found that rhEPO significantly improved the morphology of long-term cultured primary nerve cells and increased the total number of long-term cultured primary cells. However, rhEPO did not improve the ratio of nerve cells. A 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay was used to measure nerve cell activity and showed that rhEPO significantly improved the activity of long-term cultured primary nerve cells. Moreover, Annexin V-fluorescein isothiocyanate (FITC)/propidium iodide (PI) double immunofluorescence labeling flow cytometry revealed that rhEPO reduced the apoptotic rate of long-term cultured primary nerve cells. Senescence-associated β-galactosidase (SA-β-gal) immunohistochemistry staining showed that rhEPO significantly reduced the aging rate of long-term cultured primary nerve cells. Immunochemistry revealed that rhEPO enhanced intracellular superoxide dismutase (SOD) activity and glutathione (GSH) abundance and reduced the intracellular malondialdehyde (MDA) level. In addition, this effect depended on the dose, was maximized at a dose of 100U/ml and was more pronounced than that of vitamin E. In summary, this study finds that rhEPO protects long-term cultured primary nerve cells from aging in a dose-dependent manner. The mechanism of this effect may be associated with the enhancement of the intracellular anti-oxidant capacity. These findings provide a theoretical basis to further the anti-aging mechanism of EPO in the nervous system, and they provide experimental evidence at the cellular level for the clinical application of EPO to protect the nervous system from aging.

Мікроскопічна будова та морфометричні показники грудної і поперекової частин спинного мозку свійського собаки

The article describes the features of the macroscopic and microscopic structure of the spinal cord of the chest and lumbar parts of a mature dog for the use of morphological, neurohistological, morphometric and statistical methods of research. According to the results of histomorphology, the area and shape of the transverse section of the spinal cord is determined, the latter in the thoracic region has a round shape, in the lumbar – oval. Gray substance of the spinal cord in the form of a butterfly on a transverse section is formed by ventral, dorsal and lateral horns, in which are centers of the sympathetic nervous system. According to our research, in the gray matter of the spinal cord of a domestic dog, the core of the dorsal horn, the Clark core, the lateral and medial intermediate nuclei, the lateral and medial ventral nuclei are clearly differentiated.According to histometry of the spinal cord of the mature dog, conducted by us, the largest cross-sectional area is characteristic of the lumbar spinal cord (23.32 ± 0.44 mm²), is slightly lower in the breast (21.31 ± 0.34 mm2). In this case, the ratio of gray cerebrospinal fluid to white in the lumbar part is 1: 3.32, which is 2 times less in comparison with the such indicator of the thoratic part.The cytopupulation of the nerve cells is represented by large, medium and small neurocytes, which, in its turn, depend on their placement in certain areas of the gray matter of the spinal cord: the most small neurons are found in the lumbar part of the cord (22.58%), the least are in the thoracic (19.88%), medium neurons are the highest in the thoracic part (44.11%), the least are in the lumbar (24.37%), the largest cells are in the lumbar part (44.11%), the least are in the thoracic (36.01%).Our cytomorphometric studies indicate that the nerve cells of the gray matter of the spinal cord of mature dogs have a different volume of pericarions and their nuclei and, accordingly, a different nuclear-cytoplasmic ratio (NCR), which is an indicator of the functional activity of nerve cells. The largest average volume of pericarios of nerve cells is found in the lumbar part (17723.26 ± 816.72 mcm³), the smallest are in the chest (12913.53 ± 915.41 mcm³). The largest nuclear-cytoplasmic ratio was found in the thoracic part of the cord (0.120 ± 0.005), less are in the lumbar (0.110 ± 0.004).

Antiepileptičko dejstvo magnezijuma

Magnesium is a bioessential mineral. Magnesium ion is an important regulator of multiple ion channels' function. Magnesium has many neuroactive effects at cellular, network and whole body level. Magnesium shows stabilizing effects on electrophysiological properties and electrical activity of nerve cells and suppresses pathophysiological neuronal hyperexcitability. Magnesium deficiency has epileptogenic effect and its recompense - antiepileptic potential. Anticonvulsive action of MgSO4 infusions is clinically best known for the control of eclamptic convulsions. Under experimental conditions Mg2+ also exerts inhibitory effect on animal models of nonsynaptic epileptiform activity. Perspectives of future translational research on magnesium in epileptology point to potential benefit from magnesium therapy for better seizure control in refractory epilepsy.

Neural correlates of ticklishness in the rat somatosensory cortex.

Rats emit ultrasonic vocalizations in response to tickling by humans. Tickling is rewarding through dopaminergic mechanisms, but the function and neural correlates of ticklishness are unknown. We confirmed that tickling of rats evoked vocalizations, approach, and unsolicited jumps (Freudensprünge). Recordings in the trunk region of the rat somatosensory cortex showed intense tickling-evoked activity in most neurons, whereas a minority of cells were suppressed by tickling. Tickling responses predicted nontactile neural responses to play behaviors, which suggests a neuronal link between tickling and play. Anxiogenic conditions suppressed tickling-evoked vocalizations and trunk cortex activity. Deep-layer trunk cortex neurons discharged during vocalizations, and deep-layer microstimulation evoked vocalizations. Our findings provide evidence for deep-layer trunk cortex activity as a neural correlate of ticklishness.

Cooperative roles of glucose and asparagine-linked glycosylation in T-type calcium channel expression.

T-type calcium channels are key contributors to neuronal physiology where they shape electrical activity of nerve cells and contribute to the release of neurotransmitters. Enhanced T-type channel expression has been causally linked to a number of pathological conditions including peripheral painful diabetic neuropathy. Recently, it was demonstrated that asparagine-linked glycosylation not only plays an essential role in regulating cell surface expression of Cav3.2 channels, but may also support glucose-dependent potentiation of T-type currents. However, the underlying mechanisms by which N-glycosylation and glucose levels modulate the expression of T-type channels remain elusive. In the present study, we show that site-specific N-glycosylation of Cav3.2 is essential to stabilize expression of the channel at the plasma membrane. In contrast, elevated external glucose concentration appears to potentiate intracellular forward trafficking of the channel to the cell surface, resulting in an increased steady-state expression of the channel protein at the plasma membrane. Collectively, our study indicates that glucose and N-glycosylation act in concert to control the expression of Cav3.2 channels, and that alteration of these mechanisms may contribute to the altered expression of T-type channels in pathological conditions.

Novel carboxyl functional spherical electromagnetic polypyrrole nanocomposite polymer particles with good magnetic and conducting properties

AbstractMagnetic conducting nanoparticles with reactive functional groups are attractive materials for applications in electromagnetic interference shielding, magneto‐optical storage, biomedical sensing, gas and humidity sensors, flexible electronics etc. The objective of this work was to prepare carboxyl functionalized polypyrrole (PPy) nanocomposite particles having good magnetic properties. Electromagnetic PPy nanostructures, abbreviated as PPy/γ‐Fe2O3, were first prepared by a chemical one‐step method. In this reaction process FeCl3 is used as an oxidant for the polymerization of pyrrole and as a source of Fe3+ for the formation of γ‐Fe2O3. The formation of γ‐Fe2O3 is also aided by the initial presence of Fe2+, and p‐toluenesulfonic acid (p‐TSA) acted as a dopant. The effects of different stabilizers on the stability and morphology of PPy/γ‐Fe2O3 particles were evaluated. The presence of citric acid/sodium dodecyl sulfate during chemical oxidative polymerization produced a relatively stable PPy/γ‐Fe2O3 colloidal emulsion. PPy/γ‐Fe2O3/poly(methylmethacrylate‐methacrylic acid) (PPy/γ‐Fe2O3/P(MMA‐MAA)) nanocomposite polymer particles were then prepared by the seeded copolymerization of MMA and MAA in the presence of magnetic PPy/γ‐Fe2O3 nanocomposite seed particles. The structure and morphology of the prepared nanocomposites were confirmed by different instrumental techniques such as Fourier transform IR spectroscopy, UV−visible spectroscopy, electron micrographs, XRD and X‐ray photoelectron spectroscopy. The electrical and magnetic properties were also investigated. The carboxyl functional electromagnetic PPy nanocomposite polymer particles should be useful for the immobilization of drugs or biomolecules to design electrically stimulated drug delivery systems for modulating the activities of nerve, cardiac, skeletal muscle and bone cells. © 2016 Society of Chemical Industry

Cell-Type Specific Phase Precession in Layer II of the Medial Entorhinal Cortex.

It is a great challenge for neuroscience to reveal the cellular basis of cognitive functions. One such function is the ability to learn and recollect temporal sequences of events. The representation of sequences in the brain is thought to require temporally structured activity of nerve cells. How different types of neurons generate temporally structured activity is currently unknown. In the present study, we use a computational classification procedure to separate different cell types and find that a subpopulation of cells, so-called stellate neurons, exhibits clear temporal coding. Contrary to the stellate cells, pyramidal cells show weaker temporal coding. This discovery sheds light on the cellular basis of temporal coding in the brain.

COMPARISON OF THE EFFECTS OF PRE-TRAINING ADMINISTRATION OF ZINC OXIDE AND ZINC OXIDE NANOPARTICLES ON LONG-TERM MEMORY OF ADULT MALE MICE

BACKGROUND AND OBJECTIVE: Zinc oxide nanoparticles are one of the most widely used nanoparticles in fields of industry, medicine, pharmaceutical sciences, cosmetics, and nutrition. Multiple studies have demonstrated the negative effects of zinc oxide nanoparticles on the nervous system, while others have revealed their enhancing effects on the activity of nerve cells, involved in memory processes. The aim of this study was to compare the effects of zinc oxide nanoparticles and zinc oxide on long-term memory of mice. METHODS: In this experimental study, 49 NMRI adult male mice, with the mean weight of 25±5 g, were randomly divided into seven groups, each consisting of seven mice: control group, three treatment groups receiving zinc oxide nanoparticles (1, 2.5, and 5 mg/kg of zinc oxide nanoparticles, respectively), and three treatment groups receiving zinc oxide (1, 2.5, and 5 mg/kg of zinc oxide, respectively). Intraperitoneal injections were performed before training (electric shock). Passive avoidance memory of mice was evaluated, using the Step-Down device. The latency time to descend the platform was regarded as an indicator of memory on days 1, 3, and 7 following training. FINDINGS: Pre-training administration of zinc oxide nanoparticles and zinc oxide at a dose of 2.5 mg/kg yielded no effects on the motor activity of mice. However, a significant decline was reported in the latency time to descend the platform on days 1, 3, and 7 following training (58±17, 45±13, and 39±14 in the zinc oxide group and 93±18, 62±12, and 14±3 in the nano zinc oxide group, respectively) (p<0.01); however, the dosage of 5 mg/kg had less significant short-term effects (130±38, 49±14, and 68±10 in the zinc oxide group and 132±46, 41±13, and 58±24 in the nano zinc oxide group, respectively). Also, the dosage of 1 mg/kg was almost ineffective. CONCLUSION: The results showed that weakened long-term memory, caused by zinc oxide administration, is not influenced by the size of particles.

Cell proliferation and apoptosis in optic nerve and brain integration centers of adult trout Oncorhynchus mykiss after optic nerve injury.

Fishes have remarkable ability to effectively rebuild the structure of nerve cells and nerve fibers after central nervous system injury. However, the underlying mechanism is poorly understood. In order to address this issue, we investigated the proliferation and apoptosis of cells in contralateral and ipsilateral optic nerves, after stab wound injury to the eye of an adult trout Oncorhynchus mykiss. Heterogenous population of proliferating cells was investigated at 1 week after injury. TUNEL labeling gave a qualitative and quantitative assessment of apoptosis in the cells of optic nerve of trout 2 days after injury. After optic nerve injury, apoptotic response was investigated, and mass patterns of cell migration were found. The maximal concentration of apoptotic bodies was detected in the areas of mass clumps of cells. It is probably indicative of massive cell death in the area of high phagocytic activity of macrophages/microglia. At 1 week after optic nerve injury, we observed nerve cell proliferation in the trout brain integration centers: the cerebellum and the optic tectum. In the optic tectum, proliferating cell nuclear antigen (PCNA)-immunopositive radial glia-like cells were identified. Proliferative activity of nerve cells was detected in the dorsal proliferative (matrix) area of the cerebellum and in parenchymal cells of the molecular and granular layers whereas local clusters of undifferentiated cells which formed neurogenic niches were observed in both the optic tectum and cerebellum after optic nerve injury. In vitro analysis of brain cells of trout showed that suspension cells compared with monolayer cells retain higher proliferative activity, as evidenced by PCNA immunolabeling. Phase contrast observation showed mitosis in individual cells and the formation of neurospheres which gradually increased during 1–4 days of culture. The present findings suggest that trout can be used as a novel model for studying neuronal regeneration.

A signal processing based analysis and prediction of seizure onset in patients with epilepsy.

One of the main areas of behavioural neuroscience is forecasting the human behaviour. Epilepsy is a central nervous system disorder in which nerve cell activity in the brain becomes disrupted, causing seizures or periods of unusual behaviour, sensations and sometimes loss of consciousness. An estimated 5% of the world population has epileptic seizure but there is not any method to cure it. More than 30% of people with epilepsy cannot control seizure. Epileptic seizure prediction, refers to forecasting the occurrence of epileptic seizures, is one of the most important but challenging problems in biomedical sciences, across the world. In this research we propose a new methodology which is based on studying the EEG signals using two measures, the Hurst exponent and fractal dimension. In order to validate the proposed method, it is applied to epileptic EEG signals of patients by computing the Hurst exponent and fractal dimension, and then the results are validated versus the reference data. The results of these analyses show that we are able to forecast the onset of a seizure on average of 25.76 seconds before the time of occurrence.

Proliferative and Synthetic Activity of Nerve Cells after Combined or Individual Exposure to Hypoxia and Hypercapnia.

We compared synthetic and proliferative activity of brain cells in rats exposed hypoxia, hypercapnia, or both prior to experimental focal stroke. The mean number of nucleolus organizer regions in penumbra neurons did not change after normobaric hypoxia, but increased after permissive hypercapnia or hypercapnic hypoxia. These data attest to activation of proliferative and synthetic functions in nerve cells, which plays an important role in the neuroprotective mechanisms under conditions of combined exposure to hypoxia and hypercapnia.