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The conventional cross sections of the brain, provided by magnetic resonance imaging (MRI) scanners, comprise a sparse dataset of 2-D gray-level images, that is neither capable of representing the 3-D nature of the brain, nor differentiating its various component parts in a convenient way. The target of the developed work is to fuse more information from the original MRI cross sections, which leads to building a 3-D computerized color-coded model of the normal human brain. The proposed model is beneficial in many areas like medical training, radiation treatment, 3-D model matching, or volume mensuration of brain component parts. This paper presents a revision of the different methods for building 3-D brain models, along with their advantages and disadvantages. A proposed method for building a 3-D brain model is then introduced. The method consists of three stages: interpolation of the original MRI slices, segmentation of the different brain tissues, and 3-D volumetric reconstruction. The resultant model can be geometrically transformed and arbitrarily dissected. The results are shown throughout the paper. Finally, the conclusions drawn from this work, as well as possible future extensions of the work, are listed.

The conventional cross sections of the brain, provided by magnetic resonance imaging (MRI) scanners, comprise a sparse dataset of 2-D gray-level images, that is neither capable of representing the 3-D nature of the brain, nor differentiating its various component parts in a convenient way. The target of the developed work is to fuse more information from the original MRI cross sections, which leads to building a 3-D computerized color-coded model of the normal human brain. The proposed model is beneficial in many areas like medical training, radiation treatment, 3-D model matching, or volume mensuration of brain component parts. This paper presents a revision of the different methods for building 3-D brain models, along with their advantages and disadvantages. A proposed method for building a 3-D brain model is then introduced. The method consists of three stages: interpolation of the original MRI slices, segmentation of the different brain tissues, and 3-D volumetric reconstruction. The resultant model can be geometrically transformed and arbitrarily dissected. The results are shown throughout the paper. Finally, the conclusions drawn from this work, as well as possible future extensions of the work, are listed.

Traumatic brain injury (TBI) is frequently caused by blasts that trigger a series of neuronal biochemical changes. Diagnosis of mild TBI caused by blast is challenging, since the damage to brain tissue progresses slowly over time. It is largely unknown how structural damage at tissue level from blast loading impact affects functional activity at variable time scales after the TBI event. This report describes the experimental approach and preliminary results of our study of cultured hippocampal brain slices impacted by explosively generated blast waves with single or multiple impacts in water. The initial results showed that a single blast had no effect on the immunoreactivity level of GluR1, an integral membrane protein belonging to the glutamate-gated ion channel family, whereas a triple blast insult caused a significant reduction in the GluR1synaptic marker compared to submerged control slices. This might be an indication of a dose-dependent effect and warrants further investigation with hippocampal slice samples to better understand blast-induced brain damage.

Traumatic brain injury (TBI) is frequently caused by blasts that trigger a series of neuronal biochemical changes. Diagnosis of mild TBI caused by blast is challenging, since the damage to brain tissue progresses slowly over time. It is largely unknown how structural damage at tissue level from blast loading impact affects functional activity at variable time scales after the TBI event. This report describes the experimental approach and preliminary results of our study of cultured hippocampal brain slices impacted by explosively generated blast waves with single or multiple impacts in water. The initial results showed that a single blast had no effect on the immunoreactivity level of GluR1, an integral membrane protein belonging to the glutamate-gated ion channel family, whereas a triple blast insult caused a significant reduction in the GluR1synaptic marker compared to submerged control slices. This might be an indication of a dose-dependent effect and warrants further investigation with hippocampal slice samples to better understand blast-induced brain damage.

This article is from Journal of Visualized Experiments : JoVE . Abstract The GABAA channels are present in all neurons and are located both at synapses and outside of synapses where they generate phasic and tonic currents, respectively 4,5,6,7 The GABAA channel is a pentameric GABA-gated chloride channel. The channel subunits are grouped into 8 families (α1-6, β1-3, γ1-3, δ, ε, θ, π and ρ). Two alphas, two betas and one 3rd subunit form the functional channel 8. By combining studies of sub-type specific GABA-activated single-channel molecules with studies including all populations of GABAA channels in the neuron it becomes possible to understand the basic mechanism of neuronal inhibition and how it is modulated by pharmacological agents.We use the patch-clamp technique 9,10 to study the functional properties of the GABAA channels in alive neurons in hippocampal brain slices and record the single-channel and whole-cell currents. We further examine how the channels are affected by different GABA concentrations, other drugs and intra and extracellular factors. For detailed theoretical and practical description of the patch-clamp method please see The Single-Channel Recordings edited by B Sakman and E Neher 10.

A new method of exposing tissues to X rays in a lead Faraday cage has made it possible to examine directly radiation damage is isolated neuronal tissue. Thin slices of hippocampus from brains of euthanized guinea pigs were exposed to 17.4 keV X radiation. Electrophysiological recordings were made before, during and after exposure to doses between 5 and 65 Gy at a dose rate of 1.54 Gy/min. Following exposure to doses of 40 Gy and greater, the synaptic potential was enhanced, reaching a steady level soon after exposure. The ability of the synaptic potential to generate a spike was reduced and damage progressed after termination of the radiation exposure. Recovery was not observed following termination of exposure. These results demonstrated that an isolated neuronal network can show complex changes in electrophysiological properties following moderate doses of ionizing radiation. An investigation of radiation damage directly to neurons in vitro will contribute to the understanding of the underlying mechanisms of radiation-induced nervous system dysfunction. Reprints.

Epilepsy is a disorder of recurrent seizure activity caused by rhythmic firing of neurons. Epileptiform activity can be generated by incubating brain slices in magnesium-free artificial cerebrospinal fluid (ACSF). In the present study, epileptiform discharges induced by the omission of magnesium ions from ACSF has been studied in hippocampal slices obtained from young rats using patch clamp tight-seal whole cell recording technique. Effects of AP5 to block NMDA receptor activation and acidic pH shift of ACSF on the epileptiform current was studied. It was found that magnesium-free ACSF induced epileptiform activity frequency was attenuated with AP5 application more than 50 %. The pH shift of the magnesium-free ACSF from 7.3 to 7.1 depressed the epileptiform activity. Both effects were shown to be reversible. According to the results of this study, epileptiform activity and mild extracellular acidic shifts do not interact to aggravate excitotoxicity conditions in CA1 pyramidal neurons.

Cavitation-induced shock wave, as might occur in the head during exposure to blast waves, was investigated as a possible damage mechanism for soft brain tissues. A novel experimental scheme was developed to visualize and control single bubble cavitation and its collapse, and the influence of this process on a nearby tissue surrogate was investigated. The experiment utilized a Hopkinson pressure bar system which transmits a simulated blast pressure wave (with over and under pressure components) to a fluid-filled test chamber implanted with a seed gas bubble.

http://uf.catalog.fcla.edu/uf.jsp?st=UF024929457&ix=pm&I=0&V=D&pm=1

Quantify cavitation conditions within the cerebrospinal fluid (CSF) and develop 'pressure-deformation-injury' maps for brain slices.

This article is from Frontiers in Cellular Neuroscience , volume 8 . Abstract Although transcranial magnetic stimulation (TMS) is a popular tool for both basic research and clinical applications, its actions on nerve cells are only partially understood. We have previously predicted, using compartmental modeling, that magnetic stimulation of central nervous system neurons depolarized the soma followed by initiation of an action potential in the initial segment of the axon. The simulations also predict that neurons with low current threshold are more susceptible to magnetic stimulation. Here we tested these theoretical predictions by combining in vitro patch-clamp recordings from rat brain slices with magnetic stimulation and compartmental modeling. In agreement with the modeling, our recordings demonstrate the dependence of magnetic stimulation-triggered action potentials on the type and state of the neuron and its orientation within the magnetic field. Our results suggest that the observed effects of TMS are deeply rooted in the biophysical properties of single neurons in the central nervous system and provide a framework both for interpreting existing TMS data and developing new simulation-based tools and therapies.

This article is from Frontiers in Cellular Neuroscience , volume 8 . Abstract Although transcranial magnetic stimulation (TMS) is a popular tool for both basic research and clinical applications, its actions on nerve cells are only partially understood. We have previously predicted, using compartmental modeling, that magnetic stimulation of central nervous system neurons depolarized the soma followed by initiation of an action potential in the initial segment of the axon. The simulations also predict that neurons with low current threshold are more susceptible to magnetic stimulation. Here we tested these theoretical predictions by combining in vitro patch-clamp recordings from rat brain slices with magnetic stimulation and compartmental modeling. In agreement with the modeling, our recordings demonstrate the dependence of magnetic stimulation-triggered action potentials on the type and state of the neuron and its orientation within the magnetic field. Our results suggest that the observed effects of TMS are deeply rooted in the biophysical properties of single neurons in the central nervous system and provide a framework both for interpreting existing TMS data and developing new simulation-based tools and therapies.

This article is from Experimental Neurobiology , volume 22 . Abstract Parkinson's disease (PD) is the second most common neurodegenerative motor disease caused by degeneration of dopaminergic neurons in the substantia nigra. Because brain inflammation has been considered a risk factor for PD, we analyzed whether PTEN induced putative kinase 1 (PINK1), an autosomal recessive familial PD gene, regulates brain inflammation during injury states. Using acutely prepared cortical slices to mimic injury, we analyzed expression of the pro-inflammatory cytokines tumor necrosis factor-α, interleukin (IL)-1β, and IL-6 at the mRNA and protein levels. Both mRNA and protein expression of these cytokines was higher at 6-24 h after slicing in PINK1 knockout (KO) slices compared to that in wild-type (WT) slices. In serial experiments to understand the signaling pathways that increase inflammatory responses in KO slices, we found that IκB degradation was enhanced but Akt phosphorylation decreased in KO slices compared to those in WT slices. In further experiments, an inhibitor of PI3K (LY294002) upstream of Akt increased expression of pro-inflammatory cytokines. Taken together, these results suggest that PINK1 deficiency enhance brain inflammation through reduced Akt activation and enhanced IκB degradation in response to brain injury.

Council for Tobacco Research Records; abstract; st suggests that neuromedin c excites a distinct subpopulation of neurones in the scn by decreasing a potassium conductance and increasing a non-specific cation conductance; mul

This article is from Scientific Reports , volume 4 . Abstract The lifespan of an acute brain slice is approximately 6–12 hours, limiting potential experimentation time. We have designed a new recovery incubation system capable of extending their lifespan to more than 36 hours. This system controls the temperature of the incubated artificial cerebral spinal fluid (aCSF) while continuously passing the fluid through a UVC filtration system and simultaneously monitoring temperature and pH. The combination of controlled temperature and UVC filtering maintains bacteria levels in the lag phase and leads to the dramatic extension of the brain slice lifespan. Brain slice viability was validated through electrophysiological recordings as well as live/dead cell assays. This system benefits researchers by monitoring incubation conditions and standardizing this artificial environment. It further provides viable tissue for two experimental days, reducing the time spent preparing brain slices and the number of animals required for research.

This article is from Optics Express , volume 20 . Abstract An optical coherence tomography (OCT) system employing a microelectromechanical system (MEMS) mirror was used to measure the refractive index (RI) of anatomically different regions in acute brain tissue slices, in which viability was maintained. RI was measured in white-matter and grey-matter regions, including the cerebral cortex, putamen, hippocampus, thalamus and corpus callosum. The RI in the corpus callosum was found to be ~4% higher than the RIs in other regions. Changes in RI with tissue deformation were also measured in the cerebral cortex and corpus callosum under uniform compression (20-80% strain). For 80% strain, measured RIs increased nonlinearly by up to 70% and 90% in the cerebral cortex and corpus callosum respectively. Knowledge of RI in heterogeneous tissues can be used to correct distorted optical images caused by RI variations between different regions. Also deformation-dependent changes in RI can be applied to OCT elastography or to mechanical tests based on optical imaging such as indentation tests.

This article is from Neural Regeneration Research , volume 8 . Abstract Oligodendrocyte lineage gene-1 expressed in oligodendrocytes may trigger the repair of neuronal myelin impairment, and play a crucial role in myelin repair. Hypoxia-inducible factor 1α, a transcription factor, is of great significance in premature infants with hypoxic-ischemic brain damage. There is little evidence of direct regulatory effects of hypoxia-inducible factor 1α on oligodendrocyte lineage gene-1. In this study, brain slices of Sprague-Dawley rats were cultured and subjected to oxygen-glucose deprivation. Then, slices were transfected with hypoxia-inducible factor 1α or oligodendrocyte lineage gene-1. The expression levels of hypoxia-inducible factor 1α and oligodendrocyte lineage gene-1 were significantly up-regulated in rat brains prior to transfection, as detected by immunohistochemical staining. Eight hours after transfection of slices with hypoxia-inducible factor 1α, oligodendrocyte lineage gene-1 expression was upregulated, and reached a peak 24 hours after transfection. Oligodendrocyte lineage gene-1 transfection induced no significant differences in hypoxia-inducible factor 1α levels in rat brain tissues with oxygen-glucose deprivation. These experimental findings indicate that hypoxia-inducible factor 1α can regulate oligodendrocyte lineage gene-1 expression in hypoxic brain tissue, thus repairing the neural impairment.

This article is from Nature Communications , volume 5 . Abstract Organization of signalling molecules in biological membranes is crucial for cellular communication. Many receptors, ion channels and cell adhesion molecules are associated with proteins important for their trafficking, surface localization or function. These complexes are embedded in a lipid environment of varying composition. Binding affinities and stoichiometry of such complexes were so far experimentally accessible only in isolated systems or monolayers of cell culture. Visualization of molecular dynamics within signalling complexes and their correlation to specialized membrane compartments demand high temporal and spatial resolution and has been difficult to demonstrate in complex tissue like brain slices. Here we demonstrate the feasibility of single-particle tracking (SPT) in organotypic brain slices to measure molecular dynamics of lipids and transmembrane proteins in correlation to synaptic membrane compartments. This method will provide important information about the dynamics and organization of surface molecules in the complex environment of neuronal networks within brain slices.