A representative confocal image of spinal cord tissue fluorescently immunolabeled for SC121 (red) in conjunction with GFAP (green) – markers that allowed researchers to quantify stem cell differentiation and migration. (Image provided by study author Dr. Aileen J. Anderson)
Research has shown that transplanting human neural stem cells into damaged spinal cords restores locomotor function in a mouse model of spinal cord injury1. Researchers who worked on that study have published another paper examining how these neural stem cells behave in injured tissue as they aid in healing. Learning how stem cells behave in injured tissue will hopefully help researchers develop better treatments for spinal cord injuries.
In the study, researchers used Stereo Investigator to stereologically quantify the survival, migration, proliferation, and differentiation of human neural stem cells transplanted into injured and uninjured mice. Stem cells were analyzed in mouse brain tissue specimens 1, 7, 14, 28, and 98 days after transplantation. The research found that there were fewer stem cells in the injured animals compared to the uninjured animals at all time points, stem cells in injured mice localized near the center of the injury, a delay of stem cell proliferation in injured tissue led to an overall deficit of actively dividing cells, proliferation in injured mice occurred closer to the injection sites (the locations where the stem cells were injected into the mice), and the injured microenvironment increased differentiation to more mature oligodendrocytes.
Continue reading “How Transplanted Stem Cells Behave in Injured Spinal Cord Tissue” »
Almeida-Suhett et al saw delayed loss of GABAergic interneurons in the BLA within the first week after mild CCI. (Representative photomicrographs of GAD-67 immunohistochemically stained GABAergic interneurons in the BLA of sham (left), 1-day CCI (middle), and 7-day CCI (right) animals. Total magnification is 630x; scale bar, 50 µm.)
Soldiers, athletes, and other individuals who suffer a traumatic brain injury often develop anxiety disorders, but scientists aren’t sure why. Some speculate that fear about future health or the stress of the trauma itself contributes to elevated anxiety, while others suspect changes happening inside the brain as a result of the injury are to blame.
Researchers at Maria Braga’s lab at the Uniformed Services University of the Health Sciences in Bethesda, Maryland, recently found direct evidence that physical changes happen in the brain after TBI that coincide with increased anxiety levels.
She and her team studied a rat model of mild TBI, focusing on the basolateral amygdala (BLA) – a brain region often damaged by TBI, which has also been associated with increased fear and anxiety in instances of hyperactivity.
To find out what happens in the BLA that might be causing anxiety after a mild TBI, the researchers analyzed changes in synaptic activity in this region. Using Stereo Investigator with the optical fractionator probe to perform a stereological quantification of Nissl-stained and GAD-67 immunostained brain cells, they found that many of the inhibitory neurons – the cells that quiet activity – were lost seven days after injury. Whole cell recordings from principal neurons confirmed that the inhibitory cells’ synaptic transmissions were impaired during this period, resulting in increased excitability and “open field tests” showed elevated anxiety levels in post-injury rats at the exact same time point. Continue reading “Delayed loss of neurons occurs in mice with mild TBI and anxiety” »
An image of neurofibrillary tangles and neuropil threads
People with Alzheimer’s disease suffer from severe memory loss and often have problems focusing, reasoning, and communicating. About half of all Alzheimer’s patients also experience delusions and hallucinations, this is called Alzheimer’s disease with psychosis, and scientists at the University of Pittsburgh are learning more about this severe version of the disease.
In a recent study, researchers at Dr. Robert Sweet’s lab zeroed in on a protein called tau, which forms tangles in the brains of Alzheimer’s patients, and along with amyloid plaques is one of the major hallmarks of the disease. But despite being involved in these pathological conditions, tau and amyloid may instigate other processes as well – namely, synaptic toxicity, which the authors say is “the strongest correlate of cognitive decline in Alzheimer’s disease.”
Recent research suggests that amyloids (misfolded proteins) drive the deterioration of synapses, but phospho-tau (tau, which has undergone phosphorylation), enables the process. So in their study the Pittsburgh research team analyzed the presence of tau in the prefrontal cortex, a region of the brain involved in higher processes, of 45 Alzheimer’s disease patients with and without psychosis.
Continue reading “Higher levels of pTau found in Alzheimer’s disease patients with psychosis” »
Neurogenesis occurs in the dentate gyrus, pictured here, from birth through adulthood.
A baby laughs at an elephant at the zoo. A toddler runs across a beach. Small children make memories all the time, but how many will they recall as the years pass? Maybe none at all. The phenomenon is called “infantile amnesia,” and scientists may have pinpointed a reason for why it occurs – neurogenesis.
Researchers at the Hospital for Sick Children in Toronto say that when new brain cells integrate into existing circuitry, they remodel the structure of networks already in place, wiping out the information previously stored there. This process is prevalent in infancy and early childhood because this is the time when new brain cells are being generated faster and more frequently than at any other time in a human being’s life. Humans and other mammals spawn new neurons throughout their lifespans, although the rate of neurogenesis decreases significantly with age.
In their paper, published in Science, the researchers explain how recent studies have focused on how new brain cells can lead to new memories, but the Toronto team speculated that neurogenesis could also wipe away memories. To test their hypothesis, they conducted a series of studies on populations of newborn and adult mice. Neuron development in mice occurs in much the same way as in humans, with rapid cell genesis in infancy that tapers off with age.
Continue reading “New Neurons Erase Memories” »
After an initial spinal cord injury, a cascading series of secondary events continues to do damage to the nervous system. One particularly damaging event is the death of oligodendrocytes—neuroglial cells that help protect and support the central nervous system. Scientists are learning more about the mechanisms involved in this process in the hope that their research may lead to the development of new therapeutic treatments for stopping some of the secondary damage before it occurs.
Researchers at the Miami Project to Cure Paralysis previously found that astrocytes play a role in oligodendrocyte death after spinal cord injury, but they weren’t quite sure how. Their new study identifies a culprit – an enzyme called NADPH oxidase. According to their paper, published in PLOS One, astrocytes activate NADPH oxidase within oligodendrocytes after an injury, triggering a toxic effect in the tiny neural cells.
In their study, the researchers set out to see what would happen if they could prevent post-trauma NADPH oxidase activation. Their results proved promising, with both in vitro and in vivo experiments resulting in lower oligodendrocyte death.
Continue reading “Scientists Use Stereo Investigator in Spinal Cord Injury Study” »
a. Topographic mapping of photoreceptor cells. a Scleral eyecup with the retina uppermost, where peripheral slits have been made to allow flattening. The retina is then carefully removed from the sclera, freed of the underlying choroidal tapetum lucidum and wholemounted onto a non-subbed slide. Scale bar = 1 cm. b. Screen shot taken from Stereo Investigator showing the green inclusion line and the red exclusion line overlaid on the rod photoreceptor array, viewed here on the axial plane. Colors are visible online only. Scale bar = 10 μm. c. Optic nerve head as seen under a light microscope. Note the fascicles or bundles of ganglion cell axons converging on the optic nerve head. Scale bar = 200 μm.
The deepest parts of the ocean are dark. For marine animals living one thousand feet below sea level and lower, the absence of light makes it challenging to find food, attract a mate, and identify predators.
Some animals make their own light through a process called bioluminescence. Others have adapted in ways that help them detect light in an environment beyond the reach of the sun’s rays.
In the first stereological study of the eyes of deep sea sharks, scientists in Queensland, Australia quantified photoreceptor cell populations and mapped their topography in the retina of five different species of deep sea sharks.
The sharks, including the Borneo catshark, the longsnout dogfish, the prickly dogfish, the beige catshark, and McMillan’s catshark, were caught in the nets of deep-sea fishermen off the coast of New Zealand. Each type of shark featured large, round pupils and a tapetum lucidum, a reflective structure at the back of the eye – two common adaptations deep-sea animals use to enhance sensitivity in environments where bioluminescence is the only available light source, according to the paper.
Continue reading “Scientists Map Photoreceptor Cells of Deep-Sea Sharks” »
Human cerebellum section with silver staining. Image from the Iowa Virtual Slidebox
The human brain undergoes extraordinary development in utero, with major growth continuing throughout childhood, especially during the first year. Scientists know a lot about how the neurons and circuits of the human brain develop in infancy, but a lack of specific knowledge about key elements has left doctors mystified by certain childhood disorders like SIDS and autism.
Neuroscientists at Ludwig-Maximillians-University of Munich have made new revelations about the development of cerebellar granule neurons. The smallest and most numerous type of neuron in the human brain, these cells transmit motor and sensory information to Purkinje cells, large neurons that are said to play a role in coordinating motor movement and are the sole source of output for the cerebellar cortex.
Continue reading “Humans Generate Most Cerebellar Granule Cells Postnatally” »
The granule cell layer of the dentate gyrus. Image provided by Mark Maynard.
Binge drinking damages brain regions responsible for memory, decision-making, and behavioral control. After a binge, the brain begins to heal itself but not much is known about this self-repair process. In a study published in PLoS ONE, researchers used rats to find that binge drinking damages the hippocampus, and exercise reverses this damage.
The study found that excessive ethanol killed granule neurons in the dentate gyrus (DG), a part of the hippocampus, and significantly decreased the volume of the DG. Rats that exercised after binging had more DG granule neurons and a larger DG than rats that did not exercise after a binge. In fact, rats that exercised after binging had a similar number of DG neurons and a similar DG volume to that of controls, indicating that exercise almost fully reversed damaged to the DG caused by binge drinking.
Continue reading “Exercise Heals the Brain After Binge Drinking” »
Scientists studied cresyl-violet stained sections of the left brain hemispheres of isolated and group-housed rodents. Image courtesy of the Venero Lab at The National University of Distance Education in Madrid, Spain.
Social isolation is stressful. Scientists have known it for decades. They also know that isolation causes changes to occur in the brains of rodents and primates. But most studies examine the effects of isolation during childhood; and the ones that do focus on adulthood tend to use male subjects. For the first time, researchers in Spain show that long-term social isolation causes part of the brain to shrink in the adult female degu, a highly social rat-like animal native to South America.
Continue reading “Scientists use Stereo Investigator to Discover that Part of the Hippocampus Shrinks in Socially Isolated Rodents” »
A montage of three images of single striatal neurons transfected with a disease-associated version of huntingtin, the protein that causes Huntington’s disease; By: Dr. Steven Finkbeiner, Gladstone Institute of Neurological Disease, The Taube-Koret Center for Huntington’s Disease Research, and the University of California San Francisco; licensed under the Creative Commons Attribution 3.0 Unported license.
Patients with Huntington’s disease deteriorate physically, cognitively, and emotionally. There is no cure for the inherited illness, but scientists may have found a way to slow down the onset of symptoms. Researchers in Quebec increased the expression of a molecule known as pre-enkephalin (pENK) in a mouse model of Huntington’s disease (HD) and saw promising results.
Since reduced expression of pENK is a hallmark of the disease, and neurons containing this molecule are some of the first cells to die in the brains of HD patients, the researchers hypothesized that an HD brain over-expressing pENK might have beneficial results. Their study offers the first evidence that increased pENK expression leads to a delay in muscle dysfunction, improved motor activity, memory, and lower anxiety in early-onset HD. Continue reading “Researchers from Quebec Delay Symptoms of Huntington’s Disease in Mouse Model” »