The Journal of Neuroscience, March 31, 2004, 24(13)
Next Article 
This Week in the Journal
Cellular/Molecular
Lipid Rafts and the Assembly of Paranodes
Dorothy P. Schafer, Rashmi Bansal, Kristian L. Hedstrom, Steven E. Pfeiffer, and Matthew N. Rasband
(see pages 31763185)
Myelin improves axonal conduction
properties not only by passively insulating
axons but also by participating in the clustering
of voltage-gated ion channels at
nodes of Ranvier. The paranode represents
the front line between axonal cell adhesion
molecules such as Caspr and contactin and
oligodendroglial proteins such as neurofascin-
155 (NF-155). This week, Schafer et
al. report that as paranodes form, a fraction
of NF-155 meets the biochemical criteria for
incorporation into lipid rafts, membrane
microdomains consisting of an amalgam of
protein and lipid components. Raftassociated
NF-155 was not seen in premyelinating
oligodendrocytes in culture, suggesting
that an extrinsic signal is needed to place
NF-155 in lipid rafts. Likewise, mutant animals
with impaired paranodes attributable
to deficient galactolipid synthesis also lacked
raft-associated NF-155. The authors suggest
that paranode formation results from interaction
of NF-155 with its axonal ligand,
which in turn stabilizes NF-155 in a lipid raft
opposing the axonal Caspr/contactin cell
adhesion complex.
Development/Plasticity/Repair
Imaging CA1 Pyramidal Cells In
Vivo
Adi Mizrahi, Justin C. Crowley, Eran Shtoyerman, and Lawrence C. Katz
(see pages 31473151)
Experience and neuronal activity alter the
strength of connections between neurons.
Such synaptic plasticity is associated with
functional, biochemical, and structural
changes. Although changes in dendritic
spine morphology have been correlated
with conditions such as an enriched environment,
whether new spines or changes
in spines are responsible for synaptic plasticity
remains controversial. In this issue,
Mizrahi et al. present an in vivo method
for tracking the structural plasticity of
hippocampal dendritic spines. They took advantage of a transgenic mouse in which
a subset of hippocampal pyramidal neurons
expresses green fluorescent protein
(GFP). After removing the overlying cortex,
they used two-photon laser scanning
microscopy to visualize basal dendritic
trees in stratum oriens of the dorsal hippocampus,
the most superficial and thus
accessible region of the hippocampus.
Perhaps surprisingly, spines were remarkably
stable for several hours, even after induction
of epileptic seizures. This general
approach offers the promise of resolving
the contribution of structural changes to
synaptic plasticity in real time.
Video (3.2 MB): [To view this movie, click the image below. You will need QuickTime player, which can be downloaded from http://www.apple.com/quicktime/download/]
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A series of 49 images at 2.5 µm increments showing GFP-positive basal dendrites and cell bodies in the CA1 region in vivo. The movie begins at the axonal sheets of the cingulum
bundle and ends at the pyramidal cell body layer. |
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Behavioral/Systems/Cognitive
Singing and Talking with FoxP
Ikuko Teramitsu, Lili C. Kudo, Sarah E. London, Daniel H. Geschwind, and Stephanie A. White
Sebastian Haesler, Kazuhiro Wada, A. Nshdejan, Edward Morrisey, Thierry Lints, Eric D. Jarvis, and Constance Scharff
(see pages 31523175)
A seemingly disparate group of vertebrates
(humans, dolphins, whales, bats,
and songbirds) shares the trait of learned
vocalization. Recently, a monogenetic
speech disorder was traced to a mutation
in FoxP2, one of a family of four "forkhead box" transcription factors not previously implicated in brain function. Language function in the index family could not be
attributed to sensory or intellectual deficits
or problems with articulation, suggesting
that the gene was directly related to language.
Two reports in this week's Journal suggest that FoxP2 may contribute to vocal
learning. Haesler et al. compare the spatially
and temporally variable expression of FoxP2 in zebra finch learners and non-learners.
The vocal learners expressed FoxP2 in the
song circuit in a pattern that varied with
song learning and seasonality. Meanwhile,
Teramitsu et al. examined the in situ expression of FoxP2 and FoxP1 and found remarkably similar patterns between humans and zebra finches. Interestingly, FoxP1, but not FoxP2, showed sexual dimorphic expression
in songbirds. One gets the feeling we are going
to hear a lot more about this story.
Neurobiology of Disease
Seizures and Glutamate Transporters
Michael Demarque, Nathalie Villeneuve, Jean-Bernard Manent, Hélène Becq, Alfonso Represa, Yehezkel Ben-Ari, and Laurent Aniksztejn
(see pages 32893294)
Glutamate transporters are expressed
early in development, suggesting that
their function may extend beyond recycling
of free transmitter at mature synapses.
This week, Demarque et al. address
this question using the broad-spectrum
glutamate transporter blocker DL-threo-
-benzyloxyaspartate (TBOA). In neocortical
slices from neonatal rats, the inhibitor
induced network-driven slow
oscillations and intracellular calcium fluctuations.
The activity was blocked by an
NMDA receptor antagonist and was
mimicked by bath application of NMDA.
However, tetrodotoxin and AMPA receptor
antagonists also blocked the oscillations,
indicating that NMDA receptors
were necessary but not sufficient. In vivo,
injections of TBOA produced NMDA
receptor-dependent seizures in postnatal
day 5 pups. Because TBOA is not transported,
and therefore does not increase
glutamate release by reverse transport, the
authors conclude that seizure activity
arose solely from block of glutamate uptake.
The authors suggest that disruption
of glutamate transporters could contribute
to epileptic syndromes in infants.