Subject: [SciPol 558] ScienceWeek April 27, 2007

From: "Dan Agin" <[email-masked]>
Date: Fri, 27 Apr 2007 12:30:24 -0500

SCIENCEWEEK

April 27, 2007

Vol. 11 - Number 16

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A hypothesis or theory is clear, decisive, and positive, but it
is believed by no one but the man who created it. Experimental
findings, on the other hand, are messy, inexact things, which are
believed by everyone except the man who did that work.

-- Harlow Shapley (1885-1972)

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Contents (full text below):

1. Neuroscience: How to Fill a Synapse

2. Physics: The End of an Entanglement

3. Astrophysics: The Answer is Blowing in the Wind

4. Neuroscience: The Brain's Garbage Men

5. History of Science: Crick's Notion of Genetic Information

6. Neuroscience: Mitochondrial Delivery and Synaptic Potentiation

7. Science & Politics: Stephen Jay Gould as a Political Theorist

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1.

Science 27 April 2007: Vol. 316. no. 5824, pp. 551 - 553 DOI:
10.1126/science.1142705

Neuroscience: How to Fill a Synapse

Phillip J. Robinson

The basis of almost all communication between neurons relies on
vesicles containing chemical neurotransmitters. At the junction,
or synapse, between two neurons, synaptic vesicles laden with
neurotransmitter release their contents (exocytosis) from
terminals of one neuron. The chemicals act on the opposing
neuron, propagating a specific signal. Replenishing the
presynaptic neuron with synaptic vesicles is critical to the
signaling that underlies processes such as learning, and failure
to control this cycle of vesicle formation and deployment can
lead to conditions such as epilepsy. On page 570 of this issue,
Ferguson and colleagues (1) show that the mechanism producing new
synaptic vesicles is not as simple as once envisioned, but
involves a family of proteins that manages the supply of vesicles
both during and after a neuron is stimulated. Their discoveries
reveal how a synapse maintains its full complement of synaptic
vesicles to support all functions of the nervous system.

A protein called dynamin 1 has generally been considered the
great ensurer of neurotransmitter-filled synaptic vesicles in a
presynaptic nerve terminal. These vesicles are poised to fuse
with the plasma membrane when the neuron is stimulated. Dynamin 1
acts after fusion and neurotransmitter release in a process
called endocytosis. After the plasma membrane invaginates,
dynamin 1 forms a helix around the neck of the new budding
vesicle, acting as a spring. As dynamin 1 expands and twists, it
pinches the membrane into a synaptic vesicle that can
subsequently be filled with newly synthesized neurotransmitter
(see the figure). But Ferguson et al. show that, unexpectedly,
synaptic vesicles can form in the absence of dynamin 1. By
genetically engineering mice that lack dynamin 1 (knockout mice),
they performed experiments that few thought would be fruitful.
The mice appear normal at birth, with near-normal numbers of
neurons and synaptic vesicles. However, the mice barely survive
the first week after birth, and none survive two.

The data of Ferguson et al. are full of surprises. The first is
that nerve terminals in the synapses of dynamin 1 knockout mice
contain these vesicles at all. This reveals that another
endocytosis mechanism can generate these vesicles. The next
surprise is the heterogeneous size of the synaptic vesicles that
are formed in the absence of dynamin 1. Synaptic vesicles are
considered the smallest cellular vesicle, produced within a
narrow size range of 40 to 43 nm. Indeed, the data of Ferguson et
al. indicate that dynamin 1 is likely responsible for this by
generating the highest possible membrane curvature through its
helical assembly and twist (2). The larger synaptic vesicles in
the dynamin 1 knockout mice were an average of 47 nm and up to
two times larger than normal. This was matched by an increase in
quantal size, an index of the quantity of transmitter in a
vesicle, and they could still support synaptic transmission.

The most surprising observation in these animals is that synaptic
vesicle endocytosis was almost totally absent during intense
stimulation of neurons, yet resumed at a normal rate after the
stimulus was terminated. Normally, endocytosis continues during
and after neuron stimulation. This suggests that the dynamin 1-
independent mechanism is suppressed by the influx of calcium ions
that occurs when a neuron is stimulated.

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2.

Science 27 April 2007: Vol. 316. no. 5824, pp. 555 - 557 DOI:
10.1126/science.1142654

Physics: The End of an Entanglement

J. H. Eberly and Ting Yu

In quantum physics, decoherence is a catch-all term that usually
implies degradation of the purity of a quantum state. Over the
past few decades it has been used as a guide to understand the
loss of the two-body coherence called entanglement, which is an
intrinsically quantum effect. In this context, it is relevant to
fundamental questions such as: Why is the world mostly classical
when we believe quantum theory provides all of the governing
principles (1, 2)? The answer lies in the critical role of
"largeness"; simply put, larger bodies lose coherence more
quickly. This is the essential ingredient in producing nearly
instantaneous decay of entanglement between two large bodies or
between a large body and a small one. The role of largeness is
seen when decoherence occurs increasingly faster with the size of
the environment. [See, for example, (3) for an instance of the
effect.] Preservation of coherence is important in maintaining
steady behavior of quantum systems whose coordinated action is
critical, for example, among the working units of quantum
computers when they become available.

A small body (spin, photon, atom, exciton, quantum dot, Cooper
pair, etc.), on the other hand, can continue to behave as a
quantum mechanical unit, even if not macroscopically entangled. A
topic that remains open in almost all decoherence discussions,
however, is the preservation or destruction of two-body quantum
coherence when both bodies are small. For example, it has been
predicted only recently that the one-body and two-body responses
to a noisy environment can follow surprisingly different pathways
to complete decoherence (4, 5). Experimental entry into this new
domain is needed, and impressive results are now reported on page
579 of this issue by Almeida et al. (6). They have devised an
elegantly clean way to check and to confirm the existence of so-
called "entanglement sudden death" (ESD) (7), a two-body
disentanglement that is novel among known relaxation effects
because it has no lifetime in any usual sense--that is,
entanglement terminates completely after a finite interval,
without a smoothly diminishing long-time tail.

The lack of a smooth and lengthy degradation has to be regarded
as unexpected and potentially troubling. Error correction
technology applied to entangled quantum information networks (8,
9) allows even the smallest amount of degraded entanglement to be
restored to full usefulness. However, error correction comes up
short in the face of exactly zero entanglement, i.e., sudden
death. As a practical matter, familiar local (one-body) lifetimes
have been commonly used to estimate all accompanying nonlocal
(multibody entanglement) lifetimes. Until recently there has been
no reason to think, and certainly no evidence, that these
lifetimes would be substantially different. The experiment of
Almeida et al. puts the first evidence on the table.

Since the discovery of ESD (4, 5), a large number of instances of
this surprising effect have been identified in the theoretical
literature [see (10-17) and references in (6)]. All of these
share the property that while local (one-body) coherence decays
smoothly to zero, requiring an infinite time to do so, nonlocal
(two-body) entanglement vanishes after a finite time (see the
figure for a schematic representation).

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3.

Nature 446, 986-987 (26 April 2007) | doi:10.1038/446986a;
Published online 25 April 2007

Astrophysics: The Answer is Blowing in the Wind

Yousaf M. Butt

A source of astoundingly energetic gamma-rays associated with a
star cluster might provide a clue to a century-old question:
where do the cosmic rays that constantly bombard Earth come from?

Massive stars have extreme lifestyles. They are born in clusters
of up to several thousand members, blow fierce charged-particle
winds during their short lives, and die - more or less together -
in powerful supernova explosions. Now comes word from the High
Energy Stereoscopic System (HESS) collaboration, to be published
in Astronomy and Astrophysics1, that gamma-rays of very high
energy have been spotted coming from the powerful young stellar
association Westerlund 2 located in the southern sky1 (Fig 1).
This emission is of a higher energy than ever seen before from a
group of stars, and pushes the limits of our understanding of the
processes behind it.

Stars typically emit light around the visible part of the
spectrum, where photons have an energy of a few electronvolts
(eV). The gamma-rays that HESS detected have energies in the
range of tera-electronvolts (TeV), or 1012 eV. Previously, TeV
gamma-rays have been seen emanating from only a handful of exotic
celestial objects. These include energetic pulsars (rapidly
spinning and highly magnetized neutron stars just 30 or so
kilometres across); the huge interstellar shock waves associated
with the remnants of powerful supernovae; binary systems of a
neutron star or a black hole coupled with a regular star; jets
from distant 'active galaxies'; and the supermassive black hole
thought to lurk at the centre of our Galaxy. So the HESS
collaboration's discovery1, dubbed HESS J1023-575, amounts to
finding a completely new species of celestial gamma-ray source.
In fact, another TeV source discovered recently2 might also be a
member of the same species. Designated TeV J2032+4130, this
source is probably related to a subgroup of powerful stars in the
Cygnus OB2 stellar association3, but this identification is not
quite as firm as in the case of Westerlund 2.

The most likely model for the origin of these highly energetic
gamma-rays is that multiple, supersonic winds of charged
particles blowing from the dozens of massive stars (for our
purposes, stars bigger than 8 solar masses) create violent plasma
motions within Westerlund 2. This turbulence can accelerate
particles to TeV energies (ref. 4 and references therein), and
these particles can then interact with the ambient material and
light to produce the detected gamma-rays. This type of turbulent
particle acceleration process is called the second-order Fermi
mechanism, or Fermi-II acceleration for short. First-order Fermi
(Fermi-I) acceleration is thought to be at work in the better-
formed interstellar shock waves created by isolated supernova
explosions.

Could such an isolated supernova remnant be behind the HESS
J1023-575 detection? This possibility is rendered unlikely by the
presence of a great deal of turbulence caused by the massive
stars of the Westerlund 2 association. The evolution of a
supernova remnant would be greatly perturbed in such an
environment, and it could hardly be considered as 'isolated'.

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4.

Nature 446, 987-989 (26 April 2007) | doi:10.1038/nature05713;
Published online 4 April 2007

Neuroscience: The Brain's Garbage Men

Helmut Kettenmann

Microglial cells, the immune elements of the brain, are activated
in disease or following injury. New findings indicate how these
cells are switched on to remove damaged cells and cellular
debris.

Brain function is generally considered as the activity of the
neuronal network. So brain dysfunction or damage is thought to be
caused by a disturbance to this network through the loss or
malfunction of neurons. But the brain also contains another
population of cells called glia, which in humans outnumber the
neurons. In the disease context, a subtype of glial cells - the
microglia - has attracted attention as sensors of any brain-
damaging event. In response to injury, for example, microglia are
activated, resulting in their interaction with immune cells,
active migration to the site of injury, release of pro-
inflammatory substances, and the engulfment of damaged cells and
cellular parts by a process known as phagocytosis. On page 1091
of this issue, Koizumi et al.1 report that microglia express a
particular kind of cell-membrane receptor - a subtype of the
purinergic family - which mediates their phagocytic activity *.

Generally, members of the purinergic family of receptors are
activated by the nucleotide ATP, which not only serves as an
intracellular energy substrate but is also an extracellular
signalling molecule. Although neurons and astrocytes - another
subtype of glia - normally release ATP, under disease conditions
any damaged cell can release this molecule.

So far, at least 15 purinergic receptors have been identified,
and these are separated into two groups - the P2X ion-channel
receptors and the P2Y metabotropic (non-ion-channel) seven-
transmembrane-domain receptors. Microglia express several
receptors of each group, which control their various functions
under both resting and activated states. The P2Y12 receptor has
been identified as an essential control element for the movement
of microglial projections, as indicated by imaging studies in
live animals2, 3. This receptor is downregulated when microglia
are activated following injury to the brain.

Now, Koizumi and colleagues1 report that the opposite is true for
P2Y6 receptors - that is, following injury, these receptors are
upregulated and their activation triggers phagocytosis (Fig. 1).
The authors found that, on stimulation with the P2Y6-specific
agonist (the UDP nucleotide), microglia grown in cell culture
engulf fluorescently tagged particles. They then studied cell
death caused by the injection of kainic acid into mouse brains,
which produces damage to the hippocampal region. They observed an
increase in the expression of the P2Y6 receptor in the activated
microglia.

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5.

The British Journal for the Philosophy of Science 2007 58(1):13-
24; doi:10.1093/bjps/axl018

History of Science: Crick's Notion of Genetic Information and the
`Central Dogma´ of Molecular Biology

Predrag Sustar

An assessment is offered of the recent debate on information in
the philosophy of biology, and an analysis is provided of the
notion of information as applied in scientific practice in
molecular genetics. In particular, this paper deals with the
dependence of basic generalizations of molecular biology, above
all the `central dogma´, on the so-called `informational talk´
(Maynard Smith [2000aGo]). It is argued that talk of information
in the `central dogma´ can be reduced to causal claims. In that
respect, the primary aim of the paper is to consider a solution
to the major difficulty of the causal interpretation of genetic
information: how to distinguish the privileged causal role
assigned to nucleic acids, DNA in particular, in the processes of
replication and protein production. A close reading is proposed
of Francis H. C. Crick's On Protein Synthesis (1958Go) and
related works, to which we owe the first explicit definition of
information within the scientific practice of molecular biology.

Among the issues characterizing recent debates in the philosophy
of biology, the role of information is undoubtedly one of the
most prominent (see, e.g. Kitcher 2000Go).1 Most significantly,
its general importance has been confirmd by Maynard Smith's The
Concept of Information in Biology ([2000a]), and by a rich series
of replies and comments which followed (Godfrey-Smith [2000bGo];
Sarkar 2000Go; Sterelny 2000Go; Winnie 2000Go; Griffiths 2001Go;
Jablonka 2002Go).

We can formulate the basic problem regarding the use of the
notion of information within contemporary biological sciences,
specifically those related to molecular biology, such as
molecular genetics and molecular developmental biology, through
the following question:

(1) What is the meaning of the following locution used in the
biological practice: `a macromolecular sequence of the type S
carries information for a macromolecular sequence of the type
S*´?

For instance `S´ stands for the molecules of nucleic acids, the
DNA and various kinds of RNA, and `S*´ stands for the primary
structure of protein molecules. The question raised above is
basically related to the way in which the notion of information
has been used in the standard account of molecular biology, an
account which goes back to Francis H. C. Crick's famous paper, On
Protein Synthesis (1958Go). As we shall see in more detail in the
following sections, Crick (1958Go, p. 153) explicitly argues that
only the macromolecular sequences of a certain type, which
generally can be called `genetic´, display the property of
carrying information for the synthesis of other macromolecular
sequences, i.e. the primary structure of protein molecules.2

In attempting to answer question (1), the philosophical debate on
information has brought into focus other semantic notions widely
used in different sectors of recent molecular biology. In that
respect, Maynard Smith ([2000aGo], pp. 177-81) points out a
certain `informational talk´ in molecular biology, i.e. the fact
that technical terms in this scientific field appeal to theories
of communication. In particular, the semantic notions here in
question may be determined on these grounds: when molecular
biology assigns a semantic property to a genetic entity, it means
that (i) a gene G represents, instructs or enables programming of
the corresponding phenotypic trait G* (Godfrey-Smith [2000aGo],
p. 36, [2000c], p. S322); (ii) the gene G is taken to be a sign
for the synthesis of the corresponding phenotypic trait G*. In
other words, the semantic notions are introduced in molecular
biology to capture the property of the gene G being about G*
(Sarkar 2000Go, pp. 210-1).3

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6.

Biol. Bull.  212: 169-175. (April 2007)

Neuroscience: Mitochondrial Delivery and Synaptic Potentiation

James Jiayuan Tong

Mitochondria, as portable generators that power synaptic
function, regulate the ATP supply and calcium homeostasis in the
neuron. As molecular interactions within the synapses before and
after the potentiation are beginning to be elucidated, the
deciding moment during the tetanic stimulation that gives rise to
the strengthening of the synapse remains a mystery. Here, I
recorded electrically from an intact Drosophila nervous system,
while simultaneously using time-lapse confocal microscopy to
visualize mitochondria labeled with green fluorescent protein. I
show that tetanic stimulation triggers a fast delivery of
mitochondria to the synapse, which facilitates synaptic
potentiation. Rotenone, an inhibitor of mitochondrial electron
transport chain complex I, suppresses mitochondrial transport and
abolishes the potentiation of the synapse. Expression of
neurofibromin, which improves mitochondrial ATP synthesis in the
neuron, enhances the movements of mitochondria to the synapse and
promotes post-tetanic potentiation. These findings provide
unprecedented evidence that the mitochondrial delivery to the
synapse is critical for cellular learning.

Mitochondria play a central role in a variety of cellular
processes, including ATP production by oxidative phosphorylation,
robust regulation of calcium homeostasis, generation of reactive
oxygen species, and initiation of apoptosis (Morris and
Hollenbeck, 1993; Wallace, 1999). The neuronal mitochondria vary
constantly in their morphology and movement in response to
changes in the local energy state (Nicholls and Budd, 2000; Li et
al., 2004; Lisman and Spruston, 2005). Because the soma of the
neuron is distant from its terminals, mitochondrial trafficking
will substantially shape neuronal function (Chen and Chan, 2006).

The synchronization between mitochondrial conductivity and
calcium dynamics in the presynaptic terminal suggests an active
role of mitochondria in synaptic plasticity (Jonas et al., 1999).
The studies on Milton protein, dynamin-related protein (drp1),
and mitochondrial GTPase dMiro suggest that unimpaired transport
and distribution of mitochondria are required for normal synaptic
transmission (Stowers et al., 2002; Verstreken et al., 2005; Guo
et al., 2005). In the case of drp1, the dependence of reserve-
pool vesicular recruitment and mobilization on mitochondria
indicates a specific role for mitochondria in regulating synaptic
strength (Verstreken et al., 2005). Finally, porin-a building
block of the mitochondrial permeability transition pore-functions
in both fear conditioning and spatial learning in mice (Weeber et
al., 2002) and in the selective up-regulation of mitochondria-
encoded genes resulted from learning and memory (Pinter et al.,
2005). These findings suggest that changes in mitochondrial
function could modulate behavioral plasticity.

Mitochondrial trafficking depends primarily on kinesins for
anterograde transport and dyneins for retrograde transport
(Goldstein and Yang, 2000). The rapid movements of mitochondria
are microtubule-based and the slower movements are actin-based.
It is reasonable to envision that mitochondria take an "express
train" microtubule to the targeted synapse and employ "local
taxi" actin for flexibility in reaching a precise location among
the synaptic terminals (Hollenbeck, 1996).

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7.

Politics and the Life Sciences

DOI: 10.2990/1471-5457(2006)25[2:SJGAAP]2.0.CO;2

Article: pp. 2-14

Science & Politics: Stephen Jay Gould as a Political Theorist

David Prindle

Before his death in 2002, paleontologist Stephen Jay Gould
elaborated a large and inclusive theory of life's change. In this
essay I concentrate on the aspects of Gould's vast theory that
have the most direct political relevance. I briefly discuss his
views on the philosophy of science. I examine the way he combined
political values and methodology in a seamless, critical analysis
of intelligence-testing and sociobiology. I concentrate most
extensively on the impact his "punctuated equilibria" concept has
made on contemporary political analysis, and I demonstrate that
in their appropriation of this concept political scientists have
violated the rules that Gould himself articulated for its use. In
closing, I consider the possibility that a comprehensive theory
of life, a theory that must include political values, might
approach traditional questions of political thought more
satisfyingly than has conventional philosophy.

When he died at the young age of sixty in 2002, evolutionary
biologist Stephen Jay Gould was arguably the best known natural
scientist in the United States and probably the second-best known
in the world, after Stephen Hawking. Gould's three hundred
consecutive monthly essays in Natural History magazine from 1974
to 2000, many of which had been collected into books, had been
widely read and worked their way into American public thought in
a variety of settings. His 1989 book Wonderful Life had become a
best-seller. His "personal rule" of composition, that "the
concepts of science, in all their richness and ambiguity, can be
presented without any compromise, without any simplification
counting as distortion, in language accessible to all intelligent
people,"1 successfully implemented, had caused his writings to be
popular among non-scientists, even those who fundamentally
opposed his worldview, such as Christian creationists.

In this article, however, I will argue that Gould was much more
than a theorist of evolutionary biology. It is my thesis that,
over the course of three decades of remarkable productivity, he
elaborated a meta-philosophy of life's change. Because human
beings are part of life, and because Gould had intense political
commitments, this meta-philosophy included within its purview
much that was directly relevant to political theorizing. His
individual ideas must be interpreted as facets of one large
integrated factual and moral system that encompasses a natural-
scientific, social-scientific, and normative worldview - in other
words, as facets of an ideology. At the end of the paper, I will
discuss his relationship to more conventional political
philosophy.

As a public intellectual who never flinched from participating in
scientific polemics, Gould spent more than the usual amount of
time in the academic spotlight. Many of the ideas he promoted
over his career at Harvard became familiar well outside the
confines of evolutionary biology, and many became subjects of
contention within those confines. As one of the most prolific,
and written-about, scientific figures of the last three decades
of the twentieth century, he may be dismissed as already
overexposed. Whether anything new is left to be said about him at
this date is a fair question.

I offer three major justifications for discussing Gould as a
political theorist. First, while he and his ideas have been
praised and criticized endlessly in the scientific literature and
the popular press, those discussing him have rarely or never been
political scientists. I am motivated to discuss him because I see
that his biological positions were seamlessly connected to his
political positions. An explicitly political analysis of his
thought, while not necessarily unearthing new evidence, might
derive value from its freshness of view.

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