News tips from the Journal of Neuroscience

November 21, 2006

1. Moving Calcium from Store to Store
Yu Mi Choi, Shin Hye Kim, Sungkwon Chung, Dae Yong Uhm, and Myoung Kyu Park

Most cells, including neurons, have developed multiple safeguards to keep internal calcium low; thus, calcium signals are usually restricted to areas near the source of calcium influx or of release from intracellular stores. In this issue, Choi et al. take a look at the topology of endoplasmic reticulum (ER) calcium stores in isolated dopamine neurons from PN 9-14 rats. The ER essentially consists of a convoluted set of tunnels that throughout the cell. The authors used imaging to detect calcium transients, local application of caffeine to release calcium, and fluorescence recovery after photobleaching to measure calcium diffusion. Because cell bodies contained more ER, and thus a larger calcium pool, than each dendrite, the ER in cell bodies served as a calcium reservoir. As a result, the ER in dendrites repeatedly released calcium in response to local stimulation without running dry, as the dendrite stores were rapidly refreshed from reservoirs in the cell body.


2. Nogo and Axonal Growth Revisited
William B. J. Cafferty and Stephen M. Strittmatter

Several molecules associated with myelin sheaths can keep damaged axons from regenerating. But studies examining one of these myelin-associated inhibitors, Nogo-A protein and its main receptor NgR1, have had surprisingly mixed results when assessed in knock-out mice. To clear up some of the confusion, Cafferty and Strittmatter examined the roles of Nogo-A and NgR1 in mice whose left or right medullary pyramid had been cut. This corticospinal tract lesion does not produce an astrocytic scar and thus is well suited for analyzing myelin-mediated inhibition of axonal growth. Four weeks after injury, transgenic mice lacking either Nogo-A or NgR1 showed a dramatic increase in collateral sprouting of labeled corticospinal axon collaterals crossing from the intact side of the spinal cord to the denervated side. These same animals do not show long-distance regeneration after dorsal hemisection, indicating that the injury-induced axonal growth varies with fiber tract and lesion paradigm.


3. Timing in the Substantia Nigra
Marjan Jahanshahi, Catherine R. G. Jones, Georg Dirnberger, and Christopher D. Frith

Timing is everything. Take away motor timing, and you cannot tap your finger to a tune on the radio; take away perceptual timing, and you cannot guess at how long you have been waiting for the elevator. This week, Jahanshahi et al. examined the roles of the cerebellum and basal ganglia in several timing tasks. Using positron emission tomography scanning, the authors measured brain activity while subjects performed three tasks: "short" (500 ms) and "long" (2 s) time reproduction tasks in which the subjects pressed a button after the perceived interval and a control task in which they responded immediately after a tone. Both time reproduction tasks produced activation in the cerebellum and basal ganglia structures. When the time reproduction tasks were compared with the control tasks, there was timing-specific activation in the left substantia nigra and left lateral premotor cortex, suggesting a role for basal ganglia and associated cortical projections in temporal processing.


4. Dynactin 1 Dysregulation in a Mouse Model of SBMA
Masahisa Katsuno, Hiroaki Adachi, Makoto Minamiyama, Masahiro Waza, Keisuke Tokui, Haruhiko Banno, Keisuke Suzuki, Yu Onoda, Fumiaki Tanaka, Manabu Doyu, and Gen Sobue

Expansion of a trinucleotide CAG repeat within the first exon of the androgen receptor gene causes spinal and bulbar muscular atrophy (SBMA). This inherited neurodegenerative disease targets motor neurons in adult males, whereas female carriers are usually unaffected. Katsuno et al. report that the mechanism may involve impaired retrograde axonal transport. In a transgenic mouse model of SBMA, the authors found that neurofilaments and synaptic vesicles accumulated in the terminals of motor neurons, consistent with a defect in retrograde axonal transport. Expression of dynactin 1, an axonal-motor-associated protein, was reduced in SBMA neurons and in the ventral horns of SBMA patients, possibly as a result of a disruption in transcription by mutant protein. Consistent with this idea, overexpression of dynactin 1 in cells expressing mutant SBMA reduced toxicity, and oral treatment of SBMA mice with a histone deacetylase inhibitor to promote gene transcription restored dynactin 1 levels in spinal motor neurons.
-end-


Society for Neuroscience

Related Protein Articles from Brightsurf:

The protein dress of a neuron
New method marks proteins and reveals the receptors in which neurons are dressed

Memory protein
When UC Santa Barbara materials scientist Omar Saleh and graduate student Ian Morgan sought to understand the mechanical behaviors of disordered proteins in the lab, they expected that after being stretched, one particular model protein would snap back instantaneously, like a rubber band.

Diets high in protein, particularly plant protein, linked to lower risk of death
Diets high in protein, particularly plant protein, are associated with a lower risk of death from any cause, finds an analysis of the latest evidence published by The BMJ today.

A new understanding of protein movement
A team of UD engineers has uncovered the role of surface diffusion in protein transport, which could aid biopharmaceutical processing.

A new biotinylation enzyme for analyzing protein-protein interactions
Proteins play roles by interacting with various other proteins. Therefore, interaction analysis is an indispensable technique for studying the function of proteins.

Substituting the next-best protein
Children born with Duchenne muscular dystrophy have a mutation in the X-chromosome gene that would normally code for dystrophin, a protein that provides structural integrity to skeletal muscles.

A direct protein-to-protein binding couples cell survival to cell proliferation
The regulators of apoptosis watch over cell replication and the decision to enter the cell cycle.

A protein that controls inflammation
A study by the research team of Prof. Geert van Loo (VIB-UGent Center for Inflammation Research) has unraveled a critical molecular mechanism behind autoimmune and inflammatory diseases such as rheumatoid arthritis, Crohn's disease, and psoriasis.

Resurrecting ancient protein partners reveals origin of protein regulation
After reconstructing the ancient forms of two cellular proteins, scientists discovered the earliest known instance of a complex form of protein regulation.

Sensing protein wellbeing
The folding state of the proteins in live cells often reflect the cell's general health.

Read More: Protein News and Protein 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.