ScienceWeek

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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