Tag Archives: Neuroscience

Shakera Begum at MRC BNDU – Oxford

 

“My impending aspirations have been transformed since this placement and I look forward to what the future holds for me thanks to in2scienceUK”

My placement was with the University of Oxford in the Brain Network Dynamics Unit, alongside Petra Fischer and Eduardo Martin Moraud. I don’t think ‘passion’ is a strong enough word to describe their love for the infamous Basal Ganglia and its role in Parkinson’s disease.

Yes, I too first thought Basal Ganglia was an Italian dish and I couldn’t have been further away from the truth!

During my placement, I participated in several experiments and observed methods for recording or stimulating brain activity during different behavioural tasks. An EEG procedure was one of these, where Petra designed a programme to record brain activity during rhythmic movement to investigate how this activity changes with cognitive load.

In case you were wondering, this cap cannot be purchased anywhere on the high street – I know, what a shame!

The cap was connected to an amplifier in order to record the signals. The same amplifier can also be used to record activity of the basal ganglia from Parkinson’s disease patients to understand their involvement in movement related or cognitive tasks. We were shown different types of oscillations and readings to expect and how to filter a signal, which really just makes the data look clean and pretty.

We also had some fun controlling Edu’s movements with TMS, a tool that is not only used for research but also for example to treat depression. TMS relies on electromagnetic induction to stimulate a focal region of the brain. The procedure involves placing a magnetic field generator or coil near the head of the person receiving the treatment.

Researchers use TMS to measure the connection between the brain and a muscle to evaluate damage from stroke, multiple sclerosis, movement disorders, motor neuron disease and other disorders affecting the spinal cord.

 

As if all these new research skills were not already enough, we conducted a practical regarding muscle movement led by the King of the Spinal Cord himself. Edu showed us how to analyse muscle activity when movement change in speed or when they follow a template or shape in comparison to when freely performed. We observed greater muscle activity when movements were fast and more tightly constrained.

The past two weeks have not only been eye-opening for a new career path and a wonderful experience to learn new skills, but I genuinely feel it has been such a privilege to work with some of the world’s top scientists! I don’t think I have enough words to express my gratitude for the knowledge shared and the hospitality shown by the entire team. My impending aspirations have been transformed through this placement and I look forward to what the future holds for me thanks to in2scienceUK.

The Wonders of FTCD

by Britney Afram

My supervisor (Heather Payne) works within UCL’s Institute of Cognitive Neuroscience in the Visual Communication Group, who conduct research looking at how the brain processes language in people who are born profoundly deaf. The language they use is very variable such as British Sign Language and spoken language. Looking at language processing in people born deaf gives a unique perspective because they can compare BSL and spoken language and contrast the networks shared to know what brain areas are interested in language whether it is visual or auditory.

So what is Cognitive Neuroscience?

Cognitive Neuroscience is the study of the neural basis of behavior. It aims to explain cognitive processes in terms of brain-based mechanisms- ‘what part of the brain does what’!

What are some of the methods used by the Visual Communication Group?

As they are not able to observe brain processes, VCG use a Near infrared spectroscopy to examine neural basis of signed and spoken language processing. Eye tracking allows to study how infants attend to visual language input early in life. The Visual Communication Group also use functional transcranial Doppler sonography (fTCD) and functional magnetic resonance imaging (fMRI).

Why Functional Transcranial Doppler sonography (fTCD)?

Some deaf children may even have a cochlear implant which is unsuitable for a MRI scan. Functional Transcranial Doppler sonography (fTCD) assesses relative blood flow to the left and right sides of the brain.  A benefit to this method is its portability allowing it to be used in different environments.

The set-up of the equipment requires attention to the various wires and ports. The fTCD uses two laptops: one to observe the results from the Doppler box and another to show the stimulus to the participant. Additionally there needs to be a connection between both laptops by the parallel port replicator which allows signals to be sent much quicker and several wires are connected to the laptops and Doppler box.

What do we do in a testing session with children born deaf?

During the actual procedure the ultrasound probes are attached with a conductive gel on the left and right sides of the head, just in front of the ears approximately perpendicular to the direction of blood flow. This enables it to monitor the rate of blood flow in the middle cerebral artery to each brain hemisphere whilst the participant performs a description of a 12 seconds long silent moving penguin animation. Software called QL allows us to visualize the signal simultaneously letting us know we are in the right place for the artery and showing the speed of blood.

How were the results analyzed?

The results are then put into a toolbox for Matlab (a programming language) which extracts the average Doppler signal from the left and right hemispheres over a period of interest in which the task was performed. The graph produced shows the difference in left and right activations to extract a laterality index. Positive values indicate left lateralization and  negative values indicate right lateralization. In most people language is processed predominantly by the left hemisphere of the brain.

My favorite moment of my placement was getting to try the technique out:

Britney spent a week in UCL’s Institute of Cognitive Neuroscience, in the group of Dr Mairead McSweeney, and under the supervision of Heather Payne.

Bees seem to be forgetting how to make the honey

There has been constant debate over the past decade revolving around the cause or many causes for the decline in the number of bumblebees situated in the British countryside.  Many scientists believe this decrease is caused by ubiquitous contrails which contain water vapour, carbon dioxide, oxides of sulphur and nitrogen along with metal particles such as aluminium. These nanoparticles are released from the jet’s exhaust at such a high altitude with lower vapour pressure that the water vapour condenses and may freeze (deposition) forming tiny ice crystals. This mixture of crystals and particles forms a sort of cloud. Scientists therefore assume that the nanoparticles of  aluminium found in these artificial clouds or contrails is inhaled directly via the olfactory nerves by animals in this case or insects as the particles begin to disperse and descend due to gravity and eventually absorbed by the plants.

This may be a very valid theory, however recently, there has been dispute as to whether the industrial discharge containing aluminium is also implicating the aetiology of sporadic Alzheimer’s Disease (AD) and affecting the mental functioning of bumblebees. The bumblebees fail to differentiate between normal nectar and nectar that contains aluminium.

Scientists at Keele  and Sussex University found that there was a large amount of aluminium in the pupae collected, between 13 and 200 ppm whilst a minimum of chronic exposure of 3ppm would be harmful to the human brain. At high levels in the brain, aluminium acts as a neurotoxin and thus  causing a myriad of problems due to it inhibiting or altering the chemical impulses between neurones (delivering messages to the brain and back).  Excess aluminium promotes formation and accumulation of insoluble A beta and hyperphosphorylated tau. Insoluble amyloid beta protein (A beta) leading to defective phosphorylation-dephosphorylation reactions and reduced glucose utilization, all contributing to the appearance of  neurological disorders such as AD.

Since this is the destructive effect on humans with such a little dosage, there must be some sort of correlation with animals and insects such as a bumblebee that had x70 as much aluminium in its system.

Scientists believe that this detrimental quantity of aluminium would cause cognitive decline, the theory being simultaneous to how it affects the human brain causing Alzheimer’s Disease.  The figures farming the bewildering and intriguing spectre suggest  that aluminium-induced cognitive dysfunction may be catalysing the decline in the bumblebee population. Injections of aluminium in animals produce behavioural, neuropathological and neurochemical changes that partially model AD.

Sara Belazregue spent two weeks in Professor Maria Fitzgerald’s group in UCL’s Department of Neuroscience, Physiology & Pharmacology, supervised by Dr Madeleine Verriotis.

Paul’s placement in Neuroscience, Physiology & Pharmacology

During my time in Professor Alasdair Gibb’s lab, I followed him and his students in their study of brain tissue, specifically NMDA receptors found on the membranes of dopamine cells. The research carried out in his lab corresponds to Parkinson’s disease, as the effects of the disease are caused by the loss of dopamine cells.

In the experiments a dopamine cell is first located. They are usually identified as having a ‘tear drop’ shape. Once the cell is located, it is then broken into and the first recording of the normal cell activity is taken using a computer programme called WinEDR.

paul 1

After the normal cell activity is recognised, the first dose of NMDA is added to the sample for 120 seconds. This changes the activity of the cell, which is represented by a peak (blocker) in the graph. Once the 120 second exposure to NMDA is over, a control solution is added to stabilise the cell to return the cell to its normal functional rate. This is done for about 5 minutes and then the NMDA is added again for 120 seconds and the results are taken down.

paul 2

I’ve noticed that the work carried out in the lab, despite being very detailed, isn’t far from what I studied at AS Level, for example, the NMDA receptors found in the membranes of the dopamine cells remind me of transport proteins in the phospholipid bilayer of cells.  I really liked how I was able to use my knowledge of my school syllabus to understand elements of the work studied in the lab here. This scheme is definitely for anyone passionate in doing a science degree and it has cleared my mind and enabled me to see what I want to study at university.

By Paul Izevbuwa

Ruvimbo’s Rainbow Mitochondria

Ruvimbo spent two weeks in UCL’s Research Department of Neuroscience, Physiology & Pharmacology, in the group of Prof Josef Kittler and under the supervision of Christian Covill-Cooke.

We wanted to see the effect of antimycin-A on the production of  mitochondria derived vesicles (MDVs), a way to get rid of faulty mitochondia that contain ROS which is toxic to the cell, to compare to data provided by a published a paper about it. MDVs are vesicles have budded off the mitochondria that go to the lysosome to be destroyed.

In the experiment we had a control Cos cells (fibroblast-like cell line derived from monkey kidney tissue) in liquid with all needed nutrients, and Cos cells that were in antimycin-A and the nutrition liquid for 2 hours.  The cells were on top of microscope cover-slips.

After the time the cells were washed to remove the liquid and, in the other case, the antimycin-A. Then paraformaldehyde was added for 10 minutes to the cells to fix the cells to the cover slip. Then the cells were washed again then, a block was added for 40 minutes to stop the other proteins from interfering with the antibodies.

Then water was added to an ice cube tray. We used tweezers to remove the cover slips from the dish they were in, and dunked them individually in each ice cube tray slot to wash off the excess block.

Then on parafilm we separated it into 6 sections: 3 sections were of the control where there would be the primary antibodies of rabbit Tom 20 (a mitochondrial protein) and mouse miro 1; rabbit miro 1 and finally mouse Tom 20 and rabbit miro 1. The same procedure is done for the antimycin-A. Then two drops of each primary antibody was attached to the parafilm and then the cover slips were put on top of each, dropped cell side down so they would float and we left them there for an hour. Then they were washed again with the water in the ice cube tray. After the secondary antibodies were added in the same way as the primary antibodies and dropped cell side down (so they would attach to the primary antibodies) they have a fluorescent protein attached, so they can show us what we are looking for (Tom20). They were left for 40 minutes, then washed with the water in the ice cube tray.

Then we put the cover slips on glass slides: one for control, the other for antimycin-a, and were stuck (cells facing upwards) with a mounting solution and it was left to dry under a box, so that the fluorescence would not be affected by the light. Then clear nail vanish was added to the edge of each cover slip to ensure the cover slip does not move around on the glass slide when they are viewed under the microscope.

Ruvimbo's rainbow mitochondria
This image is a picture of mitochondria cells in a neuron that were attached with green fluorescent protein under a confocal microscope. I changed the settings so that the mitochondria would be shown with rainbow colours.

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