Johns Hopkins researchers at American Society of Cell Biology Annual Meeting

December 18, 2012

San Francisco, CA, Dec. 15-19, 2012 Moscone Center, 747 Howard Street

ORGANIZING THE EYE'S NEURONS

Poster: 2342/B1205

Special Interest Subgroup: Tissue Development and Morphogenesis II

Tuesday, Dec. 18, 2012; Exhibit Halls A-C, 12:30 - 2 p.m.

Authors: A. R. Tomás and M. R. Deans

Tomás and Deans have identified a protein needed for neuron organization in the developing retina. The team says that the study helps reveal how the healthy retina -- the part of the eye that detects light -- is built, and will lead to a greater understanding of what goes wrong in eye disease.

In order for the eye to see, light-detecting cells must transmit information to neurons in the retina that relay the signal to the brain. One type of eye neuron, amacrine cells, pools information from the other eye neurons and directs output neurons, called retinal ganglion cells, to transmit the visual information to the brain. Normally the amacrine and retinal ganglion cells are found in distinct layers of the retina. However, when the researchers engineered mice to lack the protein Fat3 in their retinal ganglion cells, the researchers found that the amacrine cells moved into the space usually reserved for the retinal ganglion cells. The researchers also observed that the amacrine cells in these modified mice contained extra projections used to detect information from neighboring retina cells. These extra projections extended into parts of the retina where they usually aren't found.

"Studies in fruit flies show that Fat3 is important for tissue growth, but surprisingly, in the mouse retina, Fat3 has nothing to do with growth and everything to do with neuron organization and development," says Michael Deans, Ph.D., assistant professor of neuroscience and otolaryngology. Deans says they haven't determined whether loss of Fat3 in the eye's neurons affects vision yet, but the group plans to continue studies on Fat3's other roles in the eye.




MOTOR NEURON DISEASE CAUSED BY CELLULAR "TRAFFIC JAM"

Poster: 1786/B231

Special Interest Subgroup: Dynein

Tuesday, Dec. 18, 2012; Exhibit Halls A-C, 12:30 - 2 p.m.

Authors: J. Machamer, S. Collins, Y. Yang, S. Collins and T. Lloyd

Johns Hopkins researchers found that, in fruit flies, a form of motor neuron disease causes a traffic jam of cellular materials in the neurons' outer appendages. The scientists learned that the motor neurons -- cells that control muscle movement -- were unable to transport cargo such as signaling molecules and proteins in need of recycling from the tips of their appendages back to the main hub of the cell.

To study how motor neuron disease affects the body's neurons, researchers duplicated a genetic change found in patients with an inherited motor neuron disease. The protein affected by the genetic change, p150glued, is a piece of a transporter that delivers materials from the outer reaches of the cell to its central core. Like the people with some types of motor neuron disease, the fruit flies developed progressive paralysis and died early; they also couldn't fly. The scientists observed that in normal neurons, the cargo moved from one end of the appendages all the way back to the main hub of the cell, but in the defective neurons, the cargo at the very ends of the appendages was stuck there. The cargo along the main appendages moved normally.

"By determining what goes wrong on the cellular level in motor neuron disease, we can begin to develop therapeutics that mitigate these effects to treat the disease," says Thomas Lloyd, M.D., Ph.D., assistant professor of neurology and neuroscience at the Johns Hopkins University School of Medicine.




BASIS OF SOME INHERITED HEART DISEASE MAY BE HYPERCONTRACTED MUSCLE

Poster: 1802/B248

Special Interest Subgroup: Actin and Actin-Associated Proteins III

Tuesday, Dec. 18, 2012; Exhibit Halls A-C, 2 - 3:30 p.m.

Authors: M.C. Viswanathan, S. Haigh, J.C. Sparrow, W. Lehman and A. Cammarato

By studying flies genetically engineered to have muscle defects, scientists have taken a step toward explaining the mechanism and pathology of certain heart diseases in people. After making changes to the building blocks of the fruit fly version of a protein called troponin T, the researchers performed open-heart surgery and used microscopy to observe how the heart functioned differently than that of healthy fruit flies. Healthy fly hearts consist of a single tube that relaxes and expands to pump hemolymph -- "fly blood." However, the fly hearts with the defective troponin T did not relax and expand as well as healthy fly hearts, and also stayed contracted longer during the pumping phase. "This suggests that people with similar defects in this heart muscle protein may have hypercontracted hearts that aren't able to relax, properly fill and pump as much blood through the body," says Anthony Cammarato, Ph.D., assistant professor of cardiology at the Johns Hopkins University School of Medicine.

Fruit flies with defective troponin T were also unable to fly. When the researchers examined the muscles responsible for powering their wings, they realized that the muscles were torn to shreds from chronic hypercontraction. In addition to continuing work with troponin T, Cammarato says he plans to use fruit fly genetics to look for additional drug targets that could be used to develop treatments for inherited heart disease, like muscle proteins that promote relaxation
-end-


Johns Hopkins Medicine

Related Neurons Articles from Brightsurf:

Paying attention to the neurons behind our alertness
The neurons of layer 6 - the deepest layer of the cortex - were examined by researchers from the Okinawa Institute of Science and Technology Graduate University to uncover how they react to sensory stimulation in different behavioral states.

Trying to listen to the signal from neurons
Toyohashi University of Technology has developed a coaxial cable-inspired needle-electrode.

A mechanical way to stimulate neurons
Magnetic nanodiscs can be activated by an external magnetic field, providing a research tool for studying neural responses.

Extraordinary regeneration of neurons in zebrafish
Biologists from the University of Bayreuth have discovered a uniquely rapid form of regeneration in injured neurons and their function in the central nervous system of zebrafish.

Dopamine neurons mull over your options
Researchers at the University of Tsukuba have found that dopamine neurons in the brain can represent the decision-making process when making economic choices.

Neurons thrive even when malnourished
When animal, insect or human embryos grow in a malnourished environment, their developing nervous systems get first pick of any available nutrients so that new neurons can be made.

The first 3D map of the heart's neurons
An interdisciplinary research team establishes a new technological pipeline to build a 3D map of the neurons in the heart, revealing foundational insight into their role in heart attacks and other cardiac conditions.

Mapping the neurons of the rat heart in 3D
A team of researchers has developed a virtual 3D heart, digitally showcasing the heart's unique network of neurons for the first time.

How to put neurons into cages
Football-shaped microscale cages have been created using special laser technologies.

A molecule that directs neurons
A research team coordinated by the University of Trento studied a mass of brain cells, the habenula, linked to disorders like autism, schizophrenia and depression.

Read More: Neurons News and Neurons Current Events
Brightsurf.com is a participant in the Amazon Services LLC Associates Program, an affiliate advertising program designed to provide a means for sites to earn advertising fees by advertising and linking to Amazon.com.