Sentences with phrase «when axons»

Vision loss from glaucoma occurs when axons in the optic nerve become damaged and can no longer carry visual information to the brain.

When the axons reaching across the divide were cut with a knife, the interconnectivity between the cortical neurons inside their own compartment was relatively unaffected, whereas the striatal neurons showed no electrophysiological activity.

Deppmann and his graduate student, Kanchana Gamage, the study's lead author, believe that axons communicate the death message to each other during injury as a leftover activity, «borrowed» from the nervous system's developmental period when axons are overproduced and then improper or unnecessary connections are eliminated by a similar communication between axons.

But DTI imaging had a major glitch: When axons from different tracts intersected and crossed en route to their target, the DTI software got confused and couldn't determine each tract's direction with complete accuracy.

When axons burst open, they often distribute amyloid proteins through the neighboring brain tissue.

When an axon reaches the correct part of the brain, it needs to choose among the many neurons there.

These signals travel much faster when the axon is wrapped in myelin, an insulating layer of fats and proteins.

When an axon stretches, these microtubules can slide past one another.

Not exact matches

Axons, which are like cables woven throughout brain tissue, swell up when traumatic brain injury occurs.

However, when the researchers grew nerve cells that had no p75NTR in their observation chamber, they found that virus transport along the axon is less frequent and much slower.

When the same experiment was carried out on adult mice, a decrease in the thickness of the myelin sheaths was also seen, although the diameter of the axons was not affected.

When you stimulate a neuron, ions like sodium and potassium and chloride flow back and forth, causing what's called an action potential to travel down the neuron, through the axon, to a synapse.

When the researchers administered drugs to inhibit the movement of certain «motor» proteins that transport mitochondria and other cargo within the cell by traveling along microtubules, the mitochondria accumulated in the axon of the neuron and never made it to the synaptic terminal.

In separate experiments, when Rab32 rises in response to stress in the endoplasmic reticulum, or ER, several things happen: The nerve cell fibers (both axons and the message - receiving dendrites) are shorter, mitochondria are bulkier than normal and their numbers spike.

«If these RNAs do not disappear when they should, the axon does not position itself properly — it may go right instead of left — and the wiring will be incorrect and the circuit may be faulty,» Dr. Jaffrey says.

The new study by the Inagaki lab showed that neurons will produce four times more traction force when placed on adhesive substrates coated with laminin than those without laminin, assuring the axons reach their final destination.

Maybe high retinoic acid levels in the extremities would make the motor neuron axons freak out when they get there.

When they tracked the cells» axons from the eye into the brain, they saw that many of them terminated in the lateral geniculate nucleus (LGN), the first relay station in the brain for visual information.

«When an embryo is building its nervous system, there can be inappropriate or excessive axonal sprouts, or axons that are only needed at one time in development and not later,» DiAntonio says.

The findings raise the possibility that blocking the Phr1 protein with a drug could keep damaged axons alive and functional when the body would normally cause the axons to self - destruct.

Experiments conducted in mice and in human ALS cells reveal that when RIPK1 is out of control, it can spark axonal damage by setting off a chemical chain reaction that culminates in stripping the protective myelin off of axons and triggering axonal degeneration — the hallmark of ALS.

Instead, the researchers discovered a different protein, p75, that binds to the axon's myelin when nerve damage occurs in these animals.

The method demonstrates that injured axons can be preserved for at least 10 times longer when their communication with neighbors is blocked.

However, the researchers also found that the death spiral can be slowed when this communication is blocked using a laboratory method that could inspire pharmacological therapies to treat pathological axon degeneration.

When I looked at fish that were six months old, I still saw this problem of undermyelinated axons.»

Most importantly, when their axonal processes stretch out and connect to neighboring cells, they almost always do so at the same location on that neuron — the axon initial segment — and nowhere else.

Sheng and his research fellow Bing Zhou, the first author of the study, initially found that when mature mouse axons are severed, nearby mitochondria are damaged and become unable to provide sufficient ATP to support injured nerve regeneration.

Unlike peripheral nerves, which re-sprout axons when they are damaged, mature spinal neurons do not regrow axons in the part of the body where the injury has occurred — such as when the spinal cord is cut or crushed — which results in paralysis below the injury.

When the researchers looked at the spinal cords under a microscope they found that the drug induced sprouting of axons that use the neurochemical serotonin to communicate.

This slower type of axon death may happen when someone suffers mild but repeated brain injuries, exactly the kind that football players experience as they crash into each other in game after game.

When pathologists perform autopsies on people with diffuse axonal injury, they see severed axons with swollen tips, just like what Smith sees in his experiments.

A computer simulation of the scientists predicts that this effect is particularly pronounced when the information flow from other dendrites to the axon is suppressed by inhibitory input signals at the cell body.

When the researchers exposed goldfish axons to rat Nogo - A, the nerves stopped growing.

Previous work by Freeman's lab identified another enzyme, a gene called SARM, which was the first shown to activate a process that causes axons to disintegrate when damaged.

They found that when Axed function was blocked, injured axons not only maintained their integrity but remained capable of transmitting signals within the brain's complex circuitry for weeks.

An unpredictable disease that disrupts the flow of information within the brain and between the brain and the body, MS is triggered when the immune system attacks the myelin sheath, the protective covering around the axons of nerve fibers.

When it is experimentally prevented (either by severing the projecting axons, by treating them with the drug vinblastine, which blocks axonal transport, or by administering 6 - hydroxydopamine, which destroys the nerve endings), the innervating sympathetic neurons in the ganglion die off.

«When an embryo is building its nervous system, there can be inappropriate or excessive axonal sprouts, or axons that are only needed at one time in development and not later,» DiAntonio said.

When the genomes «wake up,» new virus particles are made and these can travel along the axon back out to the peripheral tissue, which creates the cold sores that can spread infection to new hosts.

Koyuncu discovered this when she infected isolated axons with a small number of virus particles, which would normally travel to the cell bodies and be silenced, while simultaneously exposing the cell bodies to a large number of inactivated virus particles that have been dosed with ultraviolet radiation (UV).

When neurons are dissociated, which has been the standard approach for studying latency until now, the cell bodies with their axons are jumbled together, making it impossible to mimic the natural route of nervous system invasion via isolated axons.

In the peripheral nervous system, myelin forms when «membrane tongues» extend from Schwann cells to spirally wrap around an adjacent axon.

mRNAs and Protein Synthetic Machinery Localize into Regenerating Spinal Cord Axons When They Are Provided a Substrate That Supports Growth.

When the mitochondria potential falls, the mitochondria is moved to the center of the axon and moved back to the cell body for recycling.

Forced expression of this SMN1 variant in cultured non-neuronal cells induces the formation of neurite - like extensions, a change in cell shape reminiscent of that occurring when motor neurons send out axons to their muscle targets.

When a nerve cell is activated, it sends an electrical impulse down its axon to the terminal, which stimulates a vesicle within the terminal to migrate to the terminal's surrounding membrane.

Abstract Brain assembly is hypothesized to begin when pioneer axons extend over non-neuronal cells, forming tracts guiding follower axons.

When retinal ganglion cell (RGC) axons are injured, before completely degenerating, they exhibit a phase during which their internal «skeletal» structure (normally consisting of a highly organized arrangement of fibers) becomes disorganized.

However some technical challenges still need to be taken to make the technology more accessible and usable to its full potential: gaining selective and comprehensive genetic access to the neurons of interest, controlling variation in the expression of the optogenetic tools (when using viruses) and its precise localization (axon vs. presynaptic terminals), tailoring light - delivery system signals to individual cells in a population rather than the population as a whole, developing observation techniques which have the same spatial and temporal resolution as those tools... to cite only a few of them.

Searching the entire genome, a Yale research team has identified a gene that when eliminated can spur regeneration of axons in nerve cells severed by spinal cord injury.