Blindsight depends on the lateral geniculate nucleus

Blindsight is an intriguing phenomenon that really should lead us to question a lot of what we ‘know’ about consciousness. Someone with blindsight will get in an elevator and insist they can’t see the buttons. But after being pushed and cajoled to press their floor’s button, they will consistently succeed every time. A more classic experiment goes something like this: give a blind or blindsighted person an envelope and ask them to fit it through a slot which is either horizontal or vertical. A blind person has trouble and never does above chance. A blindsighted person does perfectly, at exactly the same level as a seeing person. So they cannot consciously ‘see’, but the visual information seems to all be in there somewhere.

Schmid et al test the hypothesis that the LGN has a causal role in blindsight. Blindsight is often (always?) caused by damage to V1, so they must show that the LGN has a role in V1-independent visual processing. Many pathways have been proposed to be crucial to blindsight; most prominent are the superior colliculus and a secondary thalamic nucleus, the pulvinar, which projects to extrastriate cortex.

Schmid et al lesioned two adult macaques in V1. When high-contrast stimuli were presented in the scotoma, the monkeys could accurately saccade to the location; low-contrast stimuli elicited no response, as if the monkey were unable to perceive it. fMRI scans showed that extrastriate responses in V1-lesion hemispheres showed activity that are consistent with human blindsight data, about 20% of normal. By inactivating the (posterior) LGN with injections of the GABAA agonist THIP, scans now showed noactivity and removed the animals’ ability to detect high-contrast stimuli. This indicates that extrastriate activation routes through LGN rather than some other pathway. The figure above shows how well the two monkeys perform when the stimulus is presented in the scotoma or contralaterally; the left two are for the normal condition, the right two are for inactivated LGN.

What have we seen? That visual activation of extrastriate areas requires LGN. It has been shown elsewhere that superior colliculus is actively involved in blindsight; interestingly, V1-bypassing neurons receive input from the superior colliculus. As always, it is not one or the other that is important, but both regions that are required in concert to support V1-independent vision. It would have been nice to see an example of blindsight in this blindsight paper (where was the unconscious detection of the stimuli?), but otherwise it is a nice demonstration of the confluence of various techniques to produce an interesting result.

Schmid M, Mrowka S, Turchi J, Saunders R, Wilke M, Peters A, Ye F, Leopold D (2010). Blindsight depends on the lateral geniculate nucleus. Nature. DOI: 10.1038/nature09179


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Thoughts on the mind, 6/28

Apparently during Einstein’s autopsy, the pathologist stole Einstein’s brain instead of placing it back in the skull. I didn’t realize there was such skulduggery involved (sorry). Anyway, now they find that Einstein had an abnormally large number of astrocytes and oligodendrocytes in his brain. I guess maybe that’s interesting?

Broca’s area is not the seat of syntax.

Testosterone gets the short end of the stick – it’s oestrogen we have to blame.

Creative people are just like schizophrenics, because they both have relatively fewer D2 receptors in thalamus. D2 receptors perform a lot of roles: in the striatum they are strongly associated with addiction and obesity (seemingly from here). Many diseases give potential benefits (neurodiversity), which is probably why things like Tourette’s persist (better timing or self-control or something?).

Birds can give us insight into how neurogenesis happens at differing rates. Here is some more information on neurogenesis in the dentate gyrus. Finally, here are some nice visualizations of calbindin and zinc transporter expression in mouse hippocampus.

Amnesiacs frequently give new insight into how memory works. It is thus exciting to find someone with a new type of amnesia – ’50 first dates amnesia’.

Someone was covering a seminar on the neuroscience of honeybees (and various invertebrates)! I think I’m in heaven.

Reviewing a paper that reports stable cortical maps for non-body functions, with an aim toward neuroprostheses.

From the same blog, here is coverage of a paper examining feedback control. Here’s the important quote:

Thus, the conclusion is that when you have uncertainty in your predictive system, you actually change your cost function while you’re learning a new internal model. I find this really interesting because it’s a good piece of evidence that uncertainty in the predictive system feeds into the selection of a new cost function for a movement, rather than the motor system just sticking with the old cost function and continuing to bash away.

These movable micromotor brain implants are going to be really, really nice when they’re usable.

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Post-docs: A lot of work

What’s scary is that even though I find this letter ridiculous, I also find it completely plausible.

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Distribution of voltage-gated Na+ channels throughout dendrites and axon

There are three primary voltage-gated Na+ channel subunits expressed in adult brains: Nav1.1, Nav1.2, and Nav1.6 (Nav1.5 seems to only be in cardiac/etc cells, and the rest are only expressed during development). Each of these channel types has different activation kinetics and thresholds, possibly allowing each of them to perform distinct functions in a single cell. Since channels are not homogeneously distributed throughout cells, but rather distributed in specific fashions, understanding Na+ channel localization is important to understanding function at the signal neuron level.

Hu et al. investigated the distribution of Nav1.2 and Nav1.6 channels in axon in the context of action potential initiation and propagation. It is has been known for a while that action potentials are not initiated at the soma, but rather proximally on the axon at the axon initial segment (AIS). Using immunostaining in layer 5 pyramidal neurons of rat prefrontal cortex, they find peak immunoreactivity ~20 um from the soma, with voltage-clamp recordings confirming peak Na+ current decreases with distance from the soma. Importantly, immunostaining showed a peak for Nav1.2 between 5 to 15 um from the soma and a peak for Nav1.6 between 30 and 50 um from the soma.

When they examined the voltage dependence of activation showed a half-activation of -29.7 mV at the soma and -43.9 mV at the axon, with no difference in slope. Half-inactivation showed a similar shift. This means that somatic Na+ channels are harder to activate, though less inactivated at steady state. Using this data for a computational model of the axon, they attempted to determine what the role of each channel was. Threshold changes are primarily due to Nav1.6 density, with less effect seen from Nav1.2 density. However, Nav1.2 density seems to control action potential backpropagation failure rate – removal or reduction of Nav1.2 leads to a hyperpolarized failure threshold. That is, distal Nav1.6 is primarily involved in generating action potentials, and Nav1.2 is responsible for spreading it into the somatodendritic compartments. I’d be curious to know what computational role the lower distal threshold of AP initiation plays.

More recently, Lorincz and Nusser investigated the identity of Nav channels in the soma. Conventional immunofluorescence techniques are not sensitive enough to detect Nav subunits in dendrites. For a technical reason I do not fully understand, a low pH approach managed to increase the strength of reactions. Even though it is quite noisy, they managed to get a decent snapshot of channel density. In CA1 pyramidal cells, they confirmed that Nav1.6 appears to show a gradient increase distally from the soma. They could not detect Nav1.2 immunoreactivity in soma or dendrites – though they could in AIS – and could only find Nav1.1 in axonlike processes and AISs of GABAergic interneurons. This appears different from Hu et al’s somatic data in layer 5, where they did find Nav1.2. Nav1.6, however, was found in somata and dendritic compartments. Comparing Nav1.6 at the same distance from the soma, oblique dendrites contain less Nav1.6 than the main apical dendrites. The data looks noisy so I’d be careful about overinterpreting that for now, however.

Hu W, Tian C, Li T, Yang M, Hou H, Shu Y. (2009). Distinct contributions of Nav1.6 and Nav1.2 in action potential backpropagation. Nature Neuroscience 12 (8): 996-1002. DOI: 10.1038/nn.2359

Lorincz A, Nusser Z. (2010). Molecular identity of dendritic voltage-gated sodium channels. Science 328: 906-909. DOI: 10.1126/science.1187958

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Things on the mind, 5/30

Can you eat bacteria to boost ‘brain power’ (personally, I keep my brain power level on HIGH at all times)? But be wary of books about your brain on food.

Life without a cerebellum isn’t all bad. The pons isn’t all it’s cracked up to be either.

Syntax processing may not be in Broca’s area. Instead, evidence is accumulating that it’s in the anterior temporal lobe. So what’s the connectivity between the two areas like?

Chimps prefer to copy from those who are more prestigious

When the onlookers were given tokens of their own, they were far more likely to stick them in the box favoured by the older, high-ranking female, whether it was striped or spotty. As groups, they opted for her choice on around 70% and 90% of the time. As individuals, they also showed the same favouritism.

Examining data on autism and myelination, this blog post proposes a connection with creativity and psychosis.

Bipolar disorder sufferers commonly shows circadian rhythm disfunction. What’s the evidence that bipolar disorder is actually a circadian rhythm problem?

Cool study on event causality and how it relates to perceived time compression.

Again on creativity: dopamine receptor (D2) levels in the thalamus correlate negatively with ‘creativity scores’. I hadn’t fully realized there were dopamine receptors in thalamus. Where do the projections arise from? It looks complicated.

Attentional bias is related to gaydar?

Record spikes on your iPhone. Too cool.

Is depression linked to (lack of) neurogenesis? They use a CREB-deficient mouse in a kind of reverse-depression test.

Hub neurons have been identified in hippocampus, and they’re primarily GABAergic. They also have extensive axonal arborisations and low response latency. An old (~1 year) paper, but important for our understanding of the graph structure of the brain. If neurons are described by a small world network, you need hub neurons.

New lessons from sensory representations in auditory cortex. Subthreshold maps were more ordered than suprathreshold maps. I think this is in opposition to visual cortex where subthreshold responses are more broadly tuned, and spiking activity drastically narrows the activity. Or am I wrong?

What happens when you mutate genes required for proper bilateralization? Unsurprisingly, messing with the axons that connect across the midline causes motor difficulties.

Does TMS live up to the hype?

I just watched La Jetee which is a pretty amazing movie. Find it on youtube or get it legally (or torrent). It’s worth half an hour of your time.

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Things on the mind, 5/20

Social onychophorans! Don’t say you’re not excited. These worm-like creatures exhibit complex social behaviors with a strict hierarchy.

Do it like you dopamine it. Distinctions between phasic and tonic dopamine, and how that affects behavioral responses.

Noisy genes and the limits of strict determinism. Why are monozygotic twins not phenotypically identical? How noise in the system disrupts expression.

How charisma affects the brain. In an experiment pairing Pentecostals or secular subjects with a non-christian/christian/christian with “healing powers”, the Pentecostals had decreased activation in the executive network – specifically, dlPFC, mPFC, inferior temporal cortex, tempoparietal junction, and lOFC. This is similar to reports from hypnosis studies.

In honor of Ada Lovelace day, a post on Emily Noether, mathematical badass

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