Real vs Placebo Coffee. There's a real effect. Though interestingly those who secretly were given decaf didn't notice it in their self-reports.

Labels: Coffee, Neuroscience

ScienceDaily, Genetic Variations Linked To Brain Size. The write-up seems a bit garbled to me, so probably best to read the paper, A common MECP2 haplotype associates with reduced cortical surface area in humans in two independent populations, when it is live on the PNAS site.

Labels: Genetics, Neuroscience

A new neuroscience take on moral psychology, Right or Wrong? The brain's fast response to morally objectionable statements:

How does the brain respond to statements that clash with a person's value system? We recorded EEG potentials while respondents from contrasting political-ethical backgrounds completed an attitude survey on drugs, medical ethics, social conduct and other issues. Our results show that value-based disagreement is unlocked by language extremely rapidly, within 200-250 milliseconds after the first word at which a statement begins to clash with the reader's value system (e.g., "I think euthanasia is an acceptable/unacceptable...."). Furthermore, strong disagreement rapidly influences the ongoing analysis of meaning, indicating that even very early processes in language comprehension are sensitive to a person's value system. Our results testify to rapid reciprocal links between neural systems for language and for valuation.

You can read a preprint at the link, or, ScienceDaily's summary. The authors reference Jonathan Haidt's findings, which suggest that moral values have less to do with reason than emotionally colored intuition. Anyone familiar with the importance of emotion in decision making and judgement, or the heuristics & biases literature, won't be surprised by these results. The main obvious implication is that yes, psychology does manifest biophysically in the brain.

My interest is not in general average propensities, but individual differences. Bryan Caplan has shown for example that intelligence is correlated with economic rationality. To some extent one might view this as another fruit of high g, but another unrelated component might be the way in which emotions express themselves when faced with assertions counter to one's intuition or moral outlook. One problem that I face with many extremely intelligent individuals is a reflexive aversion to entertaining possibilities or thought experiments which are abhorrent to their moral or political orientation. One the one hand these emotional responses probably have an important role in sorting and ranking the order in which one performs cognitive tasks. Many thought experiments are after all useless. But when feeling has reason too tightly on the leash there is unfortunately a tendency for it to constrain the search space of intellectual possibilities.

It would be interested to see if there is an aspect of rationality which is related to the ability of individuals to suppress or shunt aside the power of emotional response, a dynamic which I presume could be ferreted out by various imaging techniques. As an analogy, those with higher g may have more powerful tools, but to some extent there is something to be said for willingness to use the tools one has on hand as well.

Labels: Biological Psychology, Neuroscience

Asymmetric fMRI adaptation reveals no evidence for mirror neurons in humans:

Neurons in macaque ventral premotor cortex and inferior parietal lobe discharge during both the observation and the execution of motor acts. It has been claimed that these so-called mirror neurons form the basis of action understanding by matching the visual input with the corresponding motor program (direct matching). Functional magnetic resonance imaging (fMRI) adaptation can be used to test the direct matching account of action recognition by determining whether putative mirror neurons show adaptation for repeated motor acts independently of whether they are observed or executed. An unambiguous test of the hypothesis requires that the motor acts be meaningless to ensure that any adaptation effect is directly because of movement recognition/motor execution and not contextually determined inferences. We found adaptation for motor acts that were repeatedly observed or repeatedly executed. We also found adaptation for motor acts that were first observed and then executed, as would be expected if a previously seen act primed the subsequent execution of that act. Crucially, we found no signs of adaptation for motor acts that were first executed and then observed. Failure to find cross-modal adaptation for executed and observed motor acts is not compatible with the core assumption of mirror neuron theory, which holds that action recognition and understanding are based on motor simulation.

Many great claims have been made for mirror neurons. V.S. Ramachandran said on Edge MIRROR NEURONS and imitation learning as the driving force behind "the great leap forward" in human evolution.

Labels: Neuroscience

A Genetically Mediated Bias in Decision Making Driven by Failure of Amygdala Control:

Genetic variation at the serotonin transporter-linked polymorphic region (5-HTTLPR) is associated with altered amygdala reactivity and lack of prefrontal regulatory control. Similar regions mediate decision-making biases driven by contextual cues and ambiguity, for example the "framing effect." We hypothesized that individuals hemozygous for the short (s) allele at the 5-HTTLPR would be more susceptible to framing. Participants, selected as homozygous for either the long (la) or s allele, performed a decision-making task where they made choices between receiving an amount of money for certain and taking a gamble. A strong bias was evident toward choosing the certain option when the option was phrased in terms of gains and toward gambling when the decision was phrased in terms of losses (the frame effect). Critically, this bias was significantly greater in the ss group compared with the lala group. In simultaneously acquired functional magnetic resonance imaging data, the ss group showed greater amygdala during choices made in accord, compared with those made counter to the frame, an effect not seen in the lala group. These differences were also mirrored by differences in anterior cingulate-amygdala coupling between the genotype groups during decision making. Specifically, lala participants showed increased coupling during choices made counter to, relative to those made in accord with, the frame, with no such effect evident in ss participants. These data suggest that genetically mediated differences in prefrontal–amygdala interactions underpin interindividual differences in economic decision making.

Check out the Wikipedia entry on 5-HTTLPR; lots of behavioral phenotypes associated with this variant. ScienceDaily:

The researchers also measured the degree of interaction, or connectivity, between the amygdala and the prefrontal cortex, the brain region most implicated in human intelligence, personality and decision making. When resisting the frame effect, the participants with two copies of the long variant had stronger connectivity between the prefrontal cortex and amygdala, while those with a pair of short variants did not.

"This difference in connectivity is really interesting," says Dr Roiser. "It suggests that the volunteers carrying the long variant might regulate automatic emotional responses, which are driven by the amygdala, more efficiently, lessening their vulnerability to the framing effect.

"This one gene cannot tell the whole story, however, as it only explains about ten per cent of the variability in susceptibility to the framing effect. What determines the other ninety per cent of variability is unclear. It is probably a mixture of people's life experience and other genetic influences.

"An interesting question would be whether the gene might affect real-life decision-making. For example, traders in banks need to make quick and accurate estimations of risk and consistent decisions, no matter how the information is presented to them. So you might hypothesise that traders with the long genetic variant would make more consistent decisions, though this needs to be tested in future research."

So this genetic variation only explains 10% of the variation within the population when it comes to frame effect in behavioral economics. Fair enough. But, I do wonder if in the current political environment fewer would oppose genetically black-balling individuals with the short variants of 5-HTTLPR from becoming traders! (I'm not proposing this seriously myself, but I think there might be some amygdala-driven acceptance of this sort of genetic profiling right now even if the returns are small)

Labels: Behavioral Economics, Economics, Neuroscience

Follow up to the post below, Jake Young at Pure Pedantry has a thorough review.

Labels: IQ, Neuroscience

Transcriptional neoteny in the human brain:

In development, timing is of the utmost importance, and the timing of developmental processes often changes as organisms evolve. In human evolution, developmental retardation, or neoteny, has been proposed as a possible mechanism that contributed to the rise of many human-specific features, including an increase in brain size and the emergence of human-specific cognitive traits. We analyzed mRNA expression in the prefrontal cortex of humans, chimpanzees, and rhesus macaques to determine whether human-specific neotenic changes are present at the gene expression level. We show that the brain transcriptome is dramatically remodeled during postnatal development and that developmental changes in the human brain are indeed delayed relative to other primates. This delay is not uniform across the human transcriptome but affects a specific subset of genes that play a potential role in neural development.

Here are the 4 classes of gene expression trajectories they're focusing on:

They found that there was a relative enrichment of genes which exhibited human neoteny, with delayed expression:

Finally:

We analyzed the genes affected by the neotenic shift in the human prefrontal cortex with respect to their histological location, function, regulation, and expression timing. First, with respect to their histological location, we used published gene expression data from human gray and white matter...and found that, in both brain regions, human neotenic genes are significantly overrepresented among genes expressed specifically in gray matter...but not among genes expressed in white matter....

Labels: Cognitive Science, Neuroscience

Readers of this weblog from back in 2002 know that we used to point to Paul Thompson's research. So see this, Genetics of Brain Fiber Architecture and Intellectual Performance:

The study is the first to analyze genetic and environmental factors that affect brain fiber architecture and its genetic linkage with cognitive function. We assessed white matter integrity voxelwise using diffusion tensor imaging at high magnetic field (4 Tesla), in 92 identical and fraternal twins. White matter integrity, quantified using fractional anisotropy (FA), was used to fit structural equation models (SEM) at each point in the brain, generating three-dimensional maps of heritability. We visualized the anatomical profile of correlations between white matter integrity and full-scale, verbal, and performance intelligence quotients (FIQ, VIQ, and PIQ). White matter integrity (FA) was under strong genetic control and was highly heritable in bilateral frontal....bilateral parietal...and left occipital...lobes, and was correlated with FIQ and PIQ in the cingulum, optic radiations, superior fronto-occipital fasciculus, internal capsule, callosal isthmus, and the corona radiata...for PIQ, corrected for multiple comparisons). In a cross-trait mapping approach, common genetic factors mediated the correlation between IQ and white matter integrity, suggesting a common physiological mechanism for both, and common genetic determination. These genetic brain maps reveal heritable aspects of white matter integrity and should expedite the discovery of single-nucleotide polymorphisms affecting fiber connectivity and cognition.

Here's the summary at ScienceDaily.

Labels: IQ, Neuroscience

If you read The Corner you know that John has been in Tucson for the Toward a Science of Consciousness conference the past week. He's now assembled his reflections.

Labels: Neuroscience

Alex Palazzo has a little post on the "brainbow mouse", created using some of the transgenic methods mentioned by amenestic in a post a while back. Each individual neuron in a given mouse brain expresses a random combination of fluorescent proteins, allowing analysis with the naked eye. Pretty amazing stuff.

Labels: Genetic Engineering, Neuroscience

A comparison of resting-state brain activity in humans and chimpanzees:

In humans, the wakeful resting condition is characterized by a default mode of brain function involving high levels of activity within a functionally connected network of brain regions...We find that, like humans, chimpanzees show high levels of activity within default mode areas, including medial prefrontal and medial parietal cortex. Chimpanzees differ from our human sample in showing higher levels of activity in ventromedial prefrontal cortex and lower levels of activity in left-sided cortical areas involved in language and conceptual processing in humans. Our results raise the possibility that the resting state of chimpanzees involves emotionally laden episodic memory retrieval and some level of mental self-projection, albeit in the absence of language and conceptual processing.

Any cognitive neuroscience people want to chip in?

Addendum: Readers might be interested in this post by Chris Chatham on primate evolution & handedness & neuroscience.

Labels: Neuroscience

Be Good Now, Or Else:

Neuroscientists have taken a step closer to a physiological explanation of why some people work and play well with others. Two areas in the brain appear to have key roles in how people conform with social norms. These parts of the brain mature slowly, which may help explain why adolescents are less easily cowed by the threat of punishment than are adults.

Chris likes to joke that cognitive neuroscience basically tells us that "stuff happens in the brain." There's some truth in that, but I still think that methods like fMRI are going to be an important piece of the bigger jigsaw puzzle that is human nature. For example, variation in fMRI combined with behavior genetic expectation that said variation should have a biological (genetic) underpinning seems a lot more compelling than either datum alone.

Also, ever notice how some people who were assholes when they were kids turn out normal? The conventional assumption is that people grow up and learn, but perhaps they couldn't learn for neurological reasons until they grew up!

Labels: Neuroscience

Chris reviews a study on the cognitive neuroscience of liberalism & conservatism (The LA Times has an article on the study). He's skeptical of the relevance and coherency of the findings. I would add that the heritability of political orientation is about 0.5, so I don't doubt that there's some innate predispositions which predispose individuals toward particular world views. Rather, I think this is analogous to genome surveys which can detect natural selection, but can't necessarily offer a plausible rationale for why selection occurred on a particular locus. Finally, I would add that my own hunch is that libertarians would probably be with the liberals here; because fundamentally there are some core axioms (individual self-actualization) and ends (a materialistic utilitarianism) which the Left and libertarians share despite the latter's traditional location on the Right.

Labels: Neuroscience

There's a new paper which uses fMRI to localize an area of the brain which seems to be involved in preventing impulsive actions. I can't but help think that something like this, which might vary from person to person, could be one of the upstream factors which shapes individual time preference. This is on my mind because I just finished Farewell to Alms by Greg Clark, and change in mean time preference is at the root of a shift in behavior which he believes primed the English (among others) for their breakout from the Malthusian trap. But it is one thing to posit a behavior whose distribution is governed by selective forces of a quantitative genetic nature, the case for any such arguments gains a boost if one could tunnel down to the level of biophysical specificity so as to assess variation across individuals and populations.

In other news, watch this space. Our own Herrick has a "10 questions" with Clark pending, so keep an eye out (that means you Ambrosini Critique).

Labels: Neuroscience

I'm assuming that readers who know some neuroscience can make more sense of this paper, Monotonic Coding of Numerosity in Macaque Lateral Intraparietal Area (Neurons for Numerosity: As Quantities Increase, So Does the Neuronal Response, a summary for the general public). But this part of the abstract is what caught my eye:

The responses of these neurons resemble the outputs of "accumulator neurons" postulated in computational models of number processing. Numerical accumulator neurons may provide inputs to neurons encoding specific cardinal values, such as "4," that have been described in previous work. Our findings may explain the frequent association of visuospatial and numerical deficits following damage to parietal cortex in humans.

I'm sure most of you know know in psychometrics there is a correlation between visuospatial & mathematical aptitude. There is one group though which decouples these two traits: Ashkenazi Jews (who are weak on visuospatial tests in relation to their mathematical aptitude).

Labels: Neuroscience

There are four kinds of ions involved in the intricate feedback system described in Part I: calcium (Ca²⁺), potassium (K⁺), sodium (Na⁺), and chloride (Cl^-). They all serve different functions, but for now all you need to know is that first three carry a positive charge while last is negative, and that "at rest" the interior of the neuron caries a negative charge relative to its surrounding environment. With me so far? Onward.

Each type of ion exists in different concentrations within the the neuron when it's "at rest", and this concentration is governed by how permeable the cell membrane is under conditions of inactivity. In this state, K⁺ flows pretty freely in and out of the membrane and is close to equlibrium, but the others are all restricted (and thus out of chemical equilibrium) to varying degrees: Na⁺, Cl^-, and Ca²⁺ are all banging at the gates to get inside. Also, each type of ion channel permits flow at different rates, K⁺ being the slowest of the four. I mention this now because it becomes important later on.

So let's say that while a neuron is just minding its own business, some meddling neuroscientist comes along and injects a bunch of Na⁺ ions into it. Since sodium ions carry a positive charge, this would make the voltage across the cell membrane tend to become less negative—i.e. it would move the neuron closer to electrical equilibrium with its environment (known as "depolarization"). If it had been Cl^- ions instead, the opposite would occur: the voltage would become more negative, moving the system further from equilibrium (known as "hyperpolarization"). Or suppose instead that some K⁺ ions were sucked out; hyperpolarization would tend to occur in this case too. But in each case, the excess ions would gradually be pumped out by the cell's regulatory system (or more ions allowed to flow in, in the K⁺ example), bringing it back to the initial set point.

This is exactly what happens in normal neural activity, except instead of a meddling neuroscientist it's mediated by ion channels. When the synaptic endpoints of the neuron's dendrites (which I'll talk more about in a later post) recieve a particular neurotransmitter, their ion channels for Na⁺ or Cl^- will open depending on which neurotransmitter it is. We'll get into neurotransmitters more later, but for now I'll just introduce two of them: GABA and glutamate.

To simplify it in very crude terms for now, GABA is the signal for "open some Cl^- channels" and glutamate is the signal for "open some Na⁺ channels", which will cause an influx of these respective ions into the cell, lowering or raising the voltage accordingly. Glutamatergic transmissions from other neurons are considered "exicitory modulation" because they tend to encourage the neuron to fire, while GABAergic transmissions are considered "inhibitory modulation" because they tend to discourage it.

Whether or not a neuron "fires" depends on whether the summed ionic charges inside it cause the neuron to depolarize below a certain threshold: in the short run, if there's an equal influx of Cl^- ions and Na⁺ ions then the effects will be a wash—the overall voltage doesn't change and nothing happens. Once the dust clears, the sodium and chloride ions get pumped out and the cell goes back to waiting for the next round of stimulus.

But if the influx of Na⁺ outweighs the influx of Cl^- by a certain threshold (i.e. the excitory stimulus outweighs the inhibitory stimulus), it sets off a chain reaction which I'll now describe. Remember that I said in Part I that some (but not all) of the ion channels in the cell were voltage-senstive (or "voltage-gated"); now two of these become important.

First, there are voltage-gated Na⁺ channels that start to open up when the cell depolarizes, allowing more sodium ions in and depolarizing it further in a wave of positive feedback that starts in the dendritic region and spreads along the cell body toward the axon. (When Cl^- ions are predominant, they act to cut this process off at its starting point by overpowering the positive charge and keeping the downstream sodium gates from opening, halting the chain reaction before it really takes off.) Once the cell depolarizes past a certain point, these gates close again and the Na⁺ stops flowing in.

As the influx of Na⁺ spreads through the cell, it triggers the opening of a special set of K⁺ channels that are normally closed, but open up when the cell depolarizes past a certain threshold, allowing K⁺ ions to flow out of the neuron and causing the cell's voltage to start going negative again. As I mentioned a few paragraphs ago, the action of these K⁺ gates is slower than those for Na⁺, so you end up with a second wave of re-polarization lagging behind the initial wave of depolarization.

Once the depolarizing wave reaches the axon, the real action begins. Most axons in mammals are coated with a sheath of myelin (basically a special extra-thick layer of phospholipids), which acts as an insulator preventing any ion transfer across the cell membrane and makes the axon the most highly conductive region of the neuron. If it isn't obvious why, you can think of an unmeylinated axon as a leaky pipe: when a pipe is full of holes, it takes a lot of force to push water all the way through it because the water keeps diffusing outward. Myelin effectively "plugs the holes", which means it requires less force to push "water" (charge) through the "pipe" (axon) at a faster rate. So myelin speeds up transmission along the length of the axon by easing propagation of electrical charge.[1]

However, there are still only so many ions, so in order to keep the charge from dimnishing as it travels the length of the axon, fresh influxes of Na⁺ are necessary. For this purpose, there are periodic breaks in the myelin sheath about a micron wide, known as nodes of Ranvier.[2] These nodes are each loaded with a whole bunch of hair-trigger Na⁺ channels that will open up under conditions of depolarization, and their combined effect is to make the current move along the axon in a series of fast hops, basically acting as voltage repeaters.

The K⁺ channels continue to play catch-up, bringing the charge back to normal negative polarity in the wake of the wave of positive charge. Eventually the ion pumps in the cell will clean everything up and bring all the ion levels back to baseline, but right now the cell is busy just trying to normalize its voltage. This entire process is called an "action potential", or simply a "spike" because of the spike that appears on a voltmeter monitoring the neuron during an action potential. One important feature of an action potential is that "a spike is a spike is a spike"—the amplitude of the wave is always the same for every single action potential. This is the only part of the neuron that can be considered "digital": either it fires or it doesn't, with no grey area. (What can change is the number and frequency of spikes, but that's for later posts.)

Once the wave of positive charge reaches the endpoints of the axons ("axon terminals"), sodium's job is done and voltage-gated calcium channels are waiting to pick up the ball. When the voltage at the axon terminal goes positive, there's a flood of Ca²⁺ into the axon terminal, which triggers . . . well, we'll get into that later after we cover synapses in the next post.

Addendum: There are, of course, many more ways of modulating neural activity than I've presented here, but when writing an introduction to the workings of any complex system you have to balance the need for thoroughness against the need to avoid overwhelming the reader with too much at once. For instance, there's almost no such thing as a neurotransmitter or ion that just does one thing in the brain, but the goal for now is to get the gist across so everyone has a working mental model of neural processes and then build up the complexities from there.

Notes:

[1] Those of you with an interest in Ashkenazi intelligence & diseases will rightly perk up here. Some of recessive diseases they're prone to like Niemann-Pick screw up the myelin sheath in ways that likely result in faster signal propagation in a heterozygote.

[2] How these guys got a piece of neuroanatamy named after them, I'll never know.

Labels: Neuroscience

One of the awkward things about GNXP is that we've got an audience that's very mixed in terms of knowledge, so it's hard to know just how much background information you should assume when writing posts. In the archives we've got "basic concepts" posts on population genetics and psychometrics that hopefully help lay-readers follow the more technical posts on these subjects, but so far we don't have too much "neuroscience 101" stuff. With that in mind, this is going to be the first in a series of posts that try to give the uninitated reader an adequate background to follow the more advanced posts by Amnestic.

Most people are familiar with terms like "neuron", "synapse", and "neurotransmitter" and have a vague notion that the brain operates with electrical impulses and chemical messenger molecules like serotonin and dopamine, but don't have a clear idea of how these things all fit together—much the same way that I know that there are things called an "alternator" and "transmission" under the hood of a car but don't really know how these things work together to make the car go. But the basic idea of how neurons work is pretty easy to understand.

Neurons are fundamentally devices for transmitting and storing small amounts of information in an analog format. Most of you have probably seen diagrams of what neurons look like: a fat cell body called the "soma" with a lot of branches radiating from it called "dendrites", and a big fat tube extending from it called the "axon" which also has a bunch of braches sprouting from it. The dendrites are the input sites, the axon is the output, and synapses are the sites where the endpoints of dendrites and axons meet. A synapse is where the actual communication between two neurons occurs, but before we get to that it'd be better to understand what decides whether they even communicate at all.

Neurons, like all animal cells, have a membrane "skin" composed of two layers of phospholipids (fatty acids attached to a phosphate group). This is what keeps the cell's insides inside and everything else outside, and it works in a rather ingenious way: the phospholipids are polar molecules which at one end are attracted to fats and at the other end attracted to water. The reason why oil and water don't mix is the same reason your cells stay cohesive: the lipid molecules cling together and form a collective barrier that most molecules won't pass through. In the case of a cell membrane, instead of just forming round globules they form a uniform wall.

Of course this membrane isn't totally impermeable, since a cell needs to allow certain chemicals to enter and exit, just as complex living organisms do. There are a variety of different doors embedded within the wall—specialized channels that permit this or that kind of atom or molecule to bypass the membrane based on their electrical charges and/or shape, like bouncers at a nightclub. This selective permeability is central to cell function in general, and in neurons the most important purpose it serves is to control the difference in electric charge between the inside and outside of the cell via different concentrations of ions.

If you recall your chemistry classes, ions are atoms that have had one or more electrons either removed or added to their outermost electron shell, giving them either a positive or negative charge. Ions are the basis of bioelectricity—the bridge between biochemistry and electricity. When people talk about electrical impulses in your nervous system, they're talking about changes in the proportions of various ions.

In accordance with the second law of thermodynamics, ions (like everything else) tend to spread out evenly unless impeded. That's where the cell membrane comes in: by selectively channeling ions in and out of the cell while maintaining a barrier, it can control the difference in concentrations of ions inside and outside the cell. Because of the electric charge of ions, this creates a difference in charge, AKA "potential [electrical] difference"—in a word, voltage. (Voltage is defined as the difference in electrical charge between two points with a resistive barrier between them.) So cells in general and neurons in particular are always operating out of equilibrium with their environments, chemically and electrically.

The neuron has a negative feedback system that works to maintain a voltage "set point", just as your thermostat works to keep your house's atmosphere at a temperature set point. Just what that set point is will vary from neuron to neuron for reasons I'll explain in later posts; for now all you need to know is what role that system plays in neural activity—arguably, this feedback system is the foundation of all neural function.

Many of the ion channels embedded within the cell membrane are voltage-senstive and will alter their shape if the voltage gets "too high" or "too low", thereby closing or opening those channels to the free flow of particular kinds of ions (there are different channels for potassium ions, calcium ions, etc). You can probably see how this works now: when the voltage drops or rises beyond a certain point, some of the gates will open and permit ions to go the way they want to—toward equilibrium, which could be into or out of the cell depending on the charge of the ions and the voltage across the membrane. This will tend to bring the neuron back to its voltage set point.

Ohm's law governs the relationship between current, voltage and resistance in a conductive medium: voltage equals current multiplied by resistance. In the cell, the impermeability of the membrane corresponds to resistance and ion flow corresponds to current. Holding voltage constant (the set point), changing the resistance (permeability) necessarily means a corresponding change in the current (ion flow). I highlight this because this simple relationship is a helpful way to summarise the whole process I've just described, and is easier to remember than the details about the biochemical specifics.

So now that we've got the basic mechanism down, next up I'll discuss the exogenous causes of changes in voltage, which is where dendrites and axons come in.

Labels: Neuroscience

The Leutgebs and the Mosers have brought us another interesting datapoint regarding how the hippocampus segregates or lumps the representation of spatial environmens. They recorded from the CA3 and dentate gyrus subregions of the hippocampus while they moved rats between a series of 'morphed' environments, moving gradually from a circular to a square arena. The idea is that CA3 tends to lump representations while DG tends to split them apart. No time to chat right now, but here's an excerpt from the commentary by Andre Fenton:

The authors confirm that CA3 place cells respond to small deviations in the spatial environment by lumping. In other words, the same neuronal discharge patterns were observed in CA3 regardless of whether the rat was in a morphed or unmorphed circular or square box. Larger deviations from either environment caused rate remapping in CA3. The dentate gyrus was quite different. Single dentate granule cells had more firing fields than did individual CA3 cells. Granule cells responded to small morph deviations in the rat's environment by changing both firing rates and firing fields unpredictably. Thus, the dentate gyrus proves a consummate information splitter and the CA3 more of a lumper (see the figure). Small changes in spatial input information caused large changes in dentate gyrus output to CA3 but virtually no changes in CA3 output to CA1.

I had a dream last night that I was at a seminar where Stefan Leutgeb was explaining these findings and Edvard Moser was in the audience and began correcting Leutgeb and they got into an argument but started speaking in French. Miraculously in my dream I could understand French and was able to impress the student next to me by explaining the argument. I don't remember what they were arguing about though. Too-da-loo.

Labels: Hippocampus, Neuroscience