neurodudes

In the provocative-hypothesis-of-the-week department:

Kevin Lafferty, a parasitologist, has put forth the idea that a fairly ubiquitous parasite (infecting O(10%) of Americans, and up to 2/3 of people in places like Brazil) is responsible for some of the diversity of human culures (1). The parasite uses common housecats to increase its transmission to the next host in the life cycle, and has a subtle effect on human personality, with some studies claiming that it even causes neuroticism, and even schizophrenia. (One clinical report (2) claims that “subjects with latent toxoplasmosis had higher intelligence [and] lower guilt proneness.” Hmm!)

Anyway, Lafferty noted that toxoplasmosis varies in prevalence from world region to world region, and then tries to draw correlates between these prevalences and local cultures:

“Drivers of the geographical variation in the prevalence of this parasite include the effects of climate on the persistence of infectious stages in soil, the cultural practices of food preparation and cats as pets. Some variation in culture, therefore, may ultimately be related to how climate affects the distribution of T. gondii, though the results only explain a fraction of the variation in two of the four cultural dimensions, suggesting that if T. gondii does influence human culture, it is only one among many factors.”

I wonder how one could test this hypothesis? Look for recent immigrants from one culture to another, who have lower Toxoplasmosis incidence? (Preferably finding populations that go in opposite directions, as a control.) Track culture change vs. migration vs. climate change?

Unlikely, perhaps. But nice that people are still thinking big

– Ed

(1) Lafferty, K
Can the common brain parasite, Toxoplasma gondii, influence human culture?
Proceedings of the Royal Society B: Biological Sciences
doi:10.1098/rspb.2006.3641

Picked up by the popular press here

(2) Flegr J, Havlicek J.
Changes in the personality profile of young women with latent toxoplasmosis.
Folia Parasitol (Praha). 1999;46(1):22-8.

A Resilient, Low-Frequency, Small-World Human Brain Functional Network with Highly Connected Association Cortical Hubs (Achard et al., 2006)

A study on network properties of the whole brain (functional connectivity data from fMRI)… interesting to see this type of work published in J. Neurosci. Building on previous fMRI/whole brain connectivity studies, the authors use a set of wavelet basis functions to estimate the correlations between different anatomical regions.

Also includes some analyses on resiliency of the system (via a metric like “largest connected cluster”) to random and targeted attack (ie. node deletion). It would be neat if they also did some analysis of common stroke damage. I would think that a stroke probably doesn’t qualify as a “targeted attack”, in the traditional sense, but, due to the predefined structure of the major circulatory structures (eg. circle of Willis), there are likely regions that are near the most commonly blocked arteries, etc. Perhaps someone with some medical qualifications could weigh in here?

There is also a nice discussion of why the human brain does not appear to be a scale-free network: That nodes do not seem to follow the “rich-get-richer” rule of preferential attachment. Evolutionarily recent structures like prefrontal seem to be among the hubs of the system and older structures like limbic regions do not dominate. Here’s a picture of the connectivity map from the paper:

Full abstract after the jump.
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So, Edge has a new question for 2006 for its All-Stars of Academia to answer: What is your dangerous idea? (Suggested to Edge by Steven Pinker, who perhaps got the idea from a colloquium series at his old haunting grounds.)

Offhand, one might expect a broad range of perceived dangerous ideas, varying by research interests and such. What’s surprising is that many of the luminaries think that the “most dangerous idea” is this particular, same idea: As neuroscience progresses, popular realization that the “astonishing hypothesis” — that mind is brain — will create a potentially cataclysmic upheaval of society as we know and have profound (negative) moral implications as people claim less responsibility for their actions.

Of course, this just isn’t true. But, would you believe that
Paul Bloom,
VS Ramachandran,
John Horgan,
Andy Clark,
Marc Hauser,
Clay Shirky,
Eric Kandel,
John Allen Paulos,
and, in a more genetic context, Jerry Coyne and Craig Venter
are all very worried about this issue? (And I didn’t even read 50% of the Edge dangerous ideas… there might be even more… ) Is this really the most dangerous idea out there to all of these talented thinkers?

I feel strongly that science and morality have always been separate domains and that any worry that, by “debunking” the mind, we automatically become immoral machines is just ridiculous. Through this scientific knowledge, we might gain some humility, maybe better see our close relatedness to nonhuman primates and place in nature, etc., but we’re not going to flip out and become crazed zombies. This just isn’t going to happen.

Does anybody else think that this just isn’t a truly dangerous idea (although certainly an “astonishing” one, in the Crick sense)? Or am I wrong here?

Samples of academic worrying after the jump.
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The nice NYT article on the function of sleep follows on a recent NIH-funded Nature insight series.

Some interesting facts from the NYT article:

• Sleep patterns vary greatly. Some bats sleep 20 hours, giraffes get 2 hours. (hmmm… grad students might be evolving toward giraffes…)
• Sleep has recently been found to occur in invertebrates too. Alternatively stated: Sleep is evolutionarily very old.
• Slow wave sleep is also found in fruit flies. (Divergence from fruit flies for us was 600 million years ago.)
• Some people don’t have any REM sleep. Behaviorally, these people are entirely normal, implying that it’s purpose might not be as obvious as one had thought (ie. required for the preservation of new memories, etc.)
• If you put a bunch of ducks in a row, the ones on the inside will sleep more often with both eyes closed. The ones on the outside will sleep with one eye open and it is (always?) the eye facing outward from the huddle. They are able to “sleep” one half of the brain at a time and, apparently, this sleeping with one eye open was lost in higher mammalian evolution. Fascinating.

The Guardian has posted a very well written and entertaining profile of Robert Trivers, an evolutionary biologist who proposed controversial but influential ideas concerning the emergence of concepts such as altruism and justice as a natural consequence of Darwinian evolution. As with all evolutionary {biology, psychology, computation}, you may readily disagree with the strength of the theories, but it is fun to consider their logical structure. Not to mention Trivers is a guy with an amusing biography and quotes.

Human neural stem cells differentiate and promote locomotor recovery in spinal cord-injured mice — PNAS

This article has some very promising results. I haven’t read the paper in detail, but here’s the executive summary. Human neural stem cells (hNSCs) were injected into mice that received a precision contusion (laminectomy) injury at spinal level T9. Control groups had vehicle and human fibroblast cell injections after receiving the same injury.

The group receiving hNSCs showed a significant functional recovery from the vehicle group. The fibroblast group did not. Then, to prove that the functional recovery was due to the new neurons and glia from the hNSC, the investigators injected the recovered mice with diptheria toxin, which affects human neurons while essentially leaving mouse neurons alone. After the toxin injection, the recovered mice with hNSC regressed back to the same behavioral performance as the vehicle group. That is, the functional recovery reversed after selective de-activation of the hNSC-derived neurons.

Additionally, the hNSCs produced both neurons and oligodendrocytes (myelin producers) in the mice. Through EM, it was verified the hNSC-derived neurons formed synapses with endogenous mouse neurons.

Amazing. Work like this shows how genetically similar mouse and human neurons (well, at least spinal cord neurons) must be. And, with regard to the race to understand and control stem cell development, this provides further evidence of how strongly the local environment can influence differentiation.

Almost Before We Spoke, We Swore - New York Times

Fun article from the NYT about swearing through the ages and its biological basis. Some relevants parts:

Reporting in The Archives of General Psychiatry, Dr. David A. Silbersweig, a director of neuropsychiatry and neuroimaging at the Weill Medical College of Cornell University, and his colleagues described their use of PET scans to measure cerebral blood flow and identify which regions of the brain are galvanized in Tourette’s patients during episodes of tics and coprolalia.

They found strong activation of the basal ganglia, a quartet of neuron clusters deep in the forebrain at roughly the level of the mid-forehead, that are known to help coordinate body movement along with activation of crucial regions of the left rear forebrain that participate in comprehending and generating speech, most notably Broca’s area.

The researchers also saw arousal of neural circuits that interact with the limbic system, the wishbone-shape throne of human emotions, and, significantly, of the “executive” realms of the brain, where decisions to act or desist from acting may be carried out: the neural source, scientists said, of whatever conscience, civility or free will humans can claim.

And some input from Frans about angry chimps:

Indeed, chimpanzees engage in what appears to be a kind of cursing match as a means of venting aggression and avoiding a potentially dangerous physical clash.

Frans de Waal, a professor of primate behavior at Emory University in Atlanta, said that when chimpanzees were angry “they will grunt or spit or make an abrupt, upsweeping gesture that, if a human were to do it, you’d recognize it as aggressive.”

Such behaviors are threat gestures, Professor de Waal said, and they are all a good sign.

Bacterial speech bubbles : Nature

Bacteria secrete signals to other bacteria of the same species through vesicle packets.

Mashburn and Whiteley describe the unexpected convergence of two seemingly unrelated areas of microbiological research: how bacteria talk to their friends, and how they attack their enemies. The authors studied the bacterial pathogen Pseudomonas aeruginosa, which releases a hydrophobic molecule called the ‘pseudomonas quinolone signal’ (PQS) to send messages to other bacteria of the same species. The surprise is that, rather than being secreted as single molecules, PQS is released in bubble-like ‘vesicles’ that also contain antibacterial agents and probably toxins aimed at host tissue cells as well.

I wonder if this is evolutionarily connected to synaptic vesicles or if this is a case of something like convergent evolution…

Microcephalin, a Gene Regulating Brain Size, Continues to Evolve Adaptively in Humans — Evans et al. 309 (5741): 1717 — Science

Although the finding itself isn’t terribly shocking, the analysis is interesting and raises some even more interesting ethical questions. Methodology: The researchers tracked the occurence of a particular haplotype, which “increased in frequency too rapidly to be compatible with neutral drift [and] this indicates that it has spread under strong positive selection.” Strikingly this gene is not very old (37,000 years) and it has been changing rapidly… the real message: make no mistake, we’re still evolving!

Another interesting issue involves this figure from the paper:

Fig. 3. Global frequencies of Microcephalin haplogroup D chromosomes (defined as having the derived C allele at the G37995C diagnostic SNP) in a panel of 1184 individuals. For each population, the country of origin, number of individuals sampled, and frequency of haplogroup D chromosomes are given (in parentheses) as follows: 1, Southeastern and Southwestern Bantu (South Africa, 8, 31.3%); 2, San (Namibia, 7, 7.1%); 3, Mbuti Pygmy (Democratic Republic of Congo, 15, 3.3%); 4, Masai (Tanzania, 27, 29.6%); 5, Sandawe (Tanzania, 32, 39.1%); 6, Burunge (Tanzania, 28, 30.4%); 7, Turu (Tanzania, 23, 15.2%); 8, Northeastern Bantu (Kenya, 12, 25%); 9, Biaka Pygmy (Central African Republic, 32, 26.6%); 10, Zime (Cameroon, 23, 8.7%); 11, Bakola Pygmy (Cameroon, 24, 10.4%); 12, Bamoun (Cameroon, 28, 17.9%); 13, Yoruba (Nigeria, 25, 24%); 14, Mandenka (Senegal, 24, 16.7%); 15, Mozabite [Algeria (Mzab region), 29, 53.5%]; 16, Druze [Israel (Carmel region), 44, 60.2%]; 17, Palestinian [Israel (Central), 40, 63.8%]; 18, Bedouin [Israel (Negev region), 44, 54.6%]; 19, Hazara (Pakistan, 20, 85%); 20, Balochi (Pakistan, 23, 78.3%); 21, Pathan (Pakistan, 23, 76.1%); 22, Burusho (Pakistan, 25, 66%); 23, Makrani (Pakistan, 24, 62.5%); 24, Brahui (Pakistan, 25, 78%); 25, Kalash (Pakistan, 24, 62.5%); 26, Sindhi (Pakistan, 25, 78%); 27, Hezhen (China, 9, 77.8%); 28, Mongola (China, 10, 100%); 29, Daur (China, 10, 85%); 30, Orogen (China, 10, 100%); 31, Miaozu (China, 9, 77.8%); 32, Yizu (China, 10, 85%); 33, Tujia (China, 10, 75%); 34, Han (China, 41, 82.9%); 35, Xibo (China, 9, 83.3%); 36, Uygur (China, 10, 90%); 37, Dai (China, 9, 55.6%); 38, Lahu (China, 10, 85%); 39, She (China, 9, 88.9%); 40, Naxi (China, 10, 95%); 41, Tu (China, 10, 75%); 42, Cambodian (Cambodia, 11, 72.7%); 43, Japanese (Japan, 27, 77.8%); 44, Yakut [Russia (Siberia region), 25, 98%]; 45, Papuan (New Guinea, 17, 91.2%); 46, NAN Melanesian (Bougainville, 18, 72.2%); 47, French Basque (France, 24, 83.3%); 48, French (France, 28, 78.6%); 49, Sardinian (Italy, 26, 90.4%); 50, North Italian [Italy (Bergamo region), 13, 76.9%]; 51, Tuscan (Italy, 8, 87.5%); 52, Orcadian (Orkney Islands, 16, 81.3%); 53, Russian (Russia, 24, 79.2%); 54, Adygei [Russia (Caucasus region), 15, 63.3%]; 55, Karitiana (Brazil, 21, 100%); 56, Surui (Brazil, 20, 100%); 57, Colombian (Colombia, 11, 100%); 58, Pima (Mexico, 25, 92%); 59, Maya (Mexico, 25, 92%).

Haplogroup D describes a set of mutations in the gene encephalin that, according to the study, have been selected for. The figure/caption above shows that this haplotype occurs at a much lower rate in sub-Saharan populations and highest in East Asian, European, and Latin American populations. Let me be clear: The paper is intended to demonstrate the selective pressure for this haplogroup. Although the authors suggest it, this does not necessarily give us the causal connection that encephalin was selected for because the gene results in a bigger brain.

It is known that encephalin definitely plays a role in determing brain size, but, as this well done NYT article (highly recommended for those unable to access the original Science article) points out, there could be another function of the gene product (perhaps even some non-neural role) that explains the selection.

I do feel strongly that this kind of science is interesting and needs to be done, both for improving our understanding of the world and for public health benefits, but it will be only more controversial as we find more genes and evolutionary scenarios like this. One very nice side-effect I think is that these new levels of individual genotyping precision will really challenge what we think of as race. Once we discover everyone is a genetic mutt, can anyone really be said to belong to one race? .

This was news to me, but maybe not to everyone. Everyone’s all impressed with the regularity of cerebellar wiring. Well, how much neater it is when you hear that that architecture may not be just in the cerebellum; in various species, there are a handful of structures similar to cerebellums. And they may have similar functions.

These are separate structures found in species which also have cerebellums (all vertebrates have cerebellums, by the way). At this point, it is debatable how “similar” they really are, but they tend to have:

• analogs to granule cells
• analogs to Purkinje cells
  • with spiny apical dendrites and also either basilar dendrites or smooth proximal regions of the apical dendrites
• sensory input to the Purkinje-like cells organized in a topographic map. The afferents synapse onto the basilar dendrites or the proximal parts of the apical dendrites.
• parallel fibers going from the granule cells to the Purkinje cells, each one contacting many Purkinje cells in many parts of the topographic map.
• embryological origins in the alar or sensory plate

Some of them have also been shown in in vivo experiments to have electrophysiological responses which learn in ways similar to the way the cerebellum does in classical conditioning (think rabbit eye puff experiment).

A notable difference between these structures and the cerebellum is that they don’t have climbing fibers.

Curtis Bell (below) theorizes that all of these structures’ function is to filter expected patterns out of incoming sensory signals.

Quoting/paraphrasing from the paper below, the structures are:

• medial octavolateral nucleus (MON) (in most basal aquatic vertebrates and in some myxinoids)
• dorsal octavolateral nucleus (DON) (in most of the same basal aquatic vertebrates as the MON, except for the bony fish (neopterygii), where it is entirely absent)
• marginal layer of the optic tectum (in all ray finned fish (actinopterygii)
• electro-sensory lobe (ELL) (in a few groups of advanced bony fish (teleosteii))
• the rostrolateral nucleus (RLN) of the thalamus (in a few groups of bony fish)
• dorsal cochlear nucleus (DCN) (in almost all mammals)

For more about this, check out this paper:

Curtis C. Bell. Evolution of Cerebellum-Like Structures. Brain, Behavior and Evolution 2002;59:312-326 (DOI: 10.1159/000063567)

See also:

Anna Devor. Is the cerebellum like cerebellar-like structures?. Brain Research Reviews, Volume 34, Issue 3, December 2000, Pages 149-156.