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Divergence of fMRI and Neural Signals in V1
Alfredo Pereira Jr
Tuesday, 09 September 2008 04:23 UTC
Dear All:
I would like to make an invitation for discussion of this result (below). As the main author of the paper is a BPCC member, maybe he could help us with the discussion.
My question is: could the result be explained by means of the action of astrocytes? Assuming that astrocytes receive the conscious signal and feedback to neurons’ LFPs and vascular system, in the absence of the signal they could feedback negatively on them, while neuronal afferent processing is not affected.
Best
Alfredo
Nat Neurosci. 2008 Aug 24. [Epub ahead of print]
Divergence of fMRI and neural signals in V1 during perceptual suppression in the
awake monkey.
Maier A, Wilke M, Aura C, Zhu C, Ye FQ, Leopold DA.
Unit on Cognitive Neurophysiology and Imaging, Laboratory of Neuropsychology,
National Institute of Mental Health, 49 Convent Dr., B2J-45, MSC 4400, Bethesda,
Maryland 20892, USA.
The role of primary visual cortex (V1) in determining the contents of perception
is controversial. Human functional magnetic resonance imaging (fMRI) studies of
perceptual suppression have revealed a robust drop in V1 activity when a stimulus
is subjectively invisible. In contrast, monkey single-unit recordings have failed
to demonstrate such perception-locked changes in V1. To investigate the basis of
this discrepancy, we measured both the blood oxygen level-dependent (BOLD)
response and several electrophysiological signals in two behaving monkeys. We
found that all signals were in good agreement during conventional stimulus
presentation, showing strong visual modulation to presentation and removal of a
stimulus. During perceptual suppression, however, only the BOLD response and the
low-frequency local field potential (LFP) power showed decreases, whereas the
spiking and high-frequency LFP power were unaffected. These results demonstrate
that the coupling between the BOLD and electrophysiological signals in V1 is
context dependent, with a marked dissociation occurring during perceptual
suppression.
Updated 09 September 2008 04:23 UTC
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Replies
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These are fascinating results for what they suggest – the brain only increases blood flow to the parts of the brain that correspond to what we’re actively paying attention to – but it may be too early to leap to that conclusion.
For a causal relationship between perception and BOLD/LFP to manifest would require feedback from the deeper areas of the brain in which perception is manifest, to the specific areas of V1 (and presumably any sensory cortex that is not the current focus of perception) – feedback IOW to astrocytes that govern blood flow etc.
If such a mechanism did exist however, it’s not hard to imagine that the phase-locking explanation of perception could be at work here: astrocytes begin revving up blood supply if enough of the surrounding neurons are in sync (particularly pre- and post-synaptic neurons). That’s probably a gross simplification but one gets the idea.
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Terren wrote:
“For a causal relationship between perception and BOLD/LFP to manifest would require feedback from the deeper areas of the brain in which perception is manifest, to the specific areas of V1 (and presumably any sensory cortex that is not the current focus of perception) – feedback IOW to astrocytes that govern blood flow etc.”
Alfredo: I agree that this feedback is necessary.
“If such a mechanism did exist however, it’s not hard to imagine that the phase-locking explanation of perception could be at work here: astrocytes begin revving up blood supply if enough of the surrounding neurons are in sync (particularly pre- and post-synaptic neurons). That’s probably a gross simplification but one gets the idea.”
Alfredo: Yes, I think that large-scale oscillatory and firing gamma (maybe also alpha) synchrony facilitate neuron-astrocyte communication.
If feedback from conscious function to brain physiology involves astrocyte activity (and the result suggests that it does), two revolutionary ideas appear:
a) astrocytes are more involved in conscious processing than neurons;
b) the feedback of astrocytic activity on neurons (by means of glutamate or hormones), as well as the control of blood flow, are forms of “mental causation”, IOW ways of consciousness influencing brain physiology and behavior.Best
Alfredo
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First of all – thanks for bringing the paper to the attention to this group. It is discussion of this kind that motivates me to do this kind of research.
Concerning your questions and remarks: I agree it is too early to speculate about the actual physiological mechanisms.
This having said, we are about to publish a follow up paper including laminar LFP recordings that will help to narrow down some of the speculations.
Using this recording technique (laminar Current Source Density analysis) it becomes possible to locate the changes in synaptic activity reflected in the LFP within certain layers. This, combined with our knowledge of the cortical microcircuitry is a powerful tool to dissociate (sensory) thalamic inputs from horizontal or top-down feedback afferences.
I can’t give away our result at this time, but please hang in there. I promise to post a preprint as soon as this follow up study is accepted.
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Dear Alexander:
Many thanks for your message. Please insert the link for the preprint in the group’s References when possible.
Just a remark: local activation of astrocytes in V1 is necessary to produce the fMRI change. Would you like to compare your result with teh recent findings of Schummers et al. (please see the BPCC Notice “Astrocytes more sensitive to visual information than neurons”).Best
Alfredo
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Alfredo,
Tempting as it is to label this “mental causation”, I think it’s far more likely that this is mere correlation based on resource allocation. In essence, the feedback mechanism we’re discussing would simply be a “physiological heuristic” useful for efficient distribution of sugars and nutrients.
In other words, the brain makes a guess about where to allocate resources to neurons based on the fact that they are implicated in percpetion (if we’re paying attention to something, chances are we will keep paying attention to it, so feed those neurons).
That argument is compelling enough for me that I think making causative links to cognition based on blood flow etc are premature at best. I also fail to see how such a causative relationship between BOLD/LFP dynamics and cognition explains anything useful.
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An interesting finding. In terms of the retinoid model, the decrease in both low-frequency LFP and BOLD under flash suppression (phenomenal invisibility) would be the natural result of a power decay in the recurrent perceptual-signal loop between the retinoid structure and V1 (long loop = low-frequency signature). Under the same condition (suppression), the short recurrent loop within the synaptic matrix of V1 between its detection cells and its imaging matrix (see The Cognitive Brain Ch. 3) would conserve its normal high-frequency LFP. Without flash-suppression (phenomenal visibility), both low-frequency (because of the retinoid contribution) and high-frequency components (within V1) as well as BOLD would be at their normal level.
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14 Oct 2008 Astrocytes And Synaptic Plasticity
By mopping up excess neurotrophic factor from neuronal synapses, astrocytes may finely tune synaptic transmission to affect processes such as learning and memory, say Bergami et al.
The major cellular events of learning and memory are long-term potentiation (LTP) and long-term depression (LTD), both of which affect neurons’ ability to communicate with one another. Neurons that have undergone LTP display a stronger electrical response to the same level of a stimulus, whereas neurons that have gone through LTD display a weaker response. These changes are thought to result from modifications of the neuronal synapses, such as alterations in the density of postsynaptic receptors, or downstream signaling events.
Secretion of the neurotrophic factor BDNF (brain-derived neurotrophic factor) has been implicated in long-term synaptic modification, and the function of BDNF on synaptic strength depends on its particular form: in its pro-BDNF form it is believed to promote LTD, and in its mature form it prompts LTP. Neurons were thought to secrete pro-BDNF, which then matured into BDNF in the synaptic space. However, a recent study suggests that only mature BDNF is secreted, pro-BDNF being processed intracellularly.
To get to the bottom of things, Bergami et al. investigated the fate of both forms after LTP induction in brain slices from the rat cortex. By fluorescent immunohistochemistry they showed that that neurons indeed secrete both mature and pro-BDNF, but that a large amount of the pro-BDNF is immediately taken up by astrocytes.
Astrocytes, previously thought to be unimportant in neuronal transmission, have recently been implicated in long-term modulation of neuronal synapses. For example, they release the neurotransmitter glutamate into the synapse prompting LTP. By specifically mopping up pro-BDNF, astrocytes seem to have another means to assist in LTP. However, while it’s likely that most pro-BDNF gets degraded inside astrocytes, say the authors, some gets recycled and re-released, suggesting that astrocytes in fact fine-tune synaptic plasticity.
Bergami, M., et al. 2008. J. Cell Biol. doi:10.1083/jcb.200806137. -
Dear Bob:
Many thanks for the Abstract. You can also find other Sub-Forums about Astrocytes in this Forum.
Best
Alfredo
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Hello, I´m Manuel Fontoira.
It would be fascinating that astrocytes were involved in this chain of events, as a part of the process.
Can I speak about another point of your post?
At first I was surprised by this discrepancy you stated:
“Human functional magnetic resonance imaging (fMRI) studies of
perceptual suppression have revealed a robust drop in V1 activity when a stimulus
is subjectively invisible. In contrast, monkey single-unit recordings have failed
to demonstrate such perception-locked changes in V1”.I was surprised because in my own thinking game, I had come up with the prediction of a no-discrepancy in these grounds, as I stated here: http://neuronalintegration.es.tl/ (in point 5, paragraph 13, where I wrote: Another prediction is a peak in energy consumption in the brain during the presence of the subjectivity in the area involved (the reason is that the brain should be doing, during the effectiveness of the subjectivity, something it was not doing while subjectivity did not take place, but without giving up doing what it was doing until that point: becoming coherent between single signals).
But inmediatly you make it clear that: “To investigate the basis of
this discrepancy, we measured both the blood oxygen level-dependent (BOLD)
response and several electrophysiological signals in two behaving monkeys. We
found that all signals were in good agreement during conventional stimulus
presentation, showing strong visual modulation to presentation and removal of a
stimulus. During perceptual suppression, however, only the BOLD response and the
low-frequency local field potential (LFP) power showed decreases, whereas the
spiking and high-frequency LFP power were unaffected. These results demonstrate
that the coupling between the BOLD and electrophysiological signals in V1 is
context dependent, with a marked dissociation occurring during perceptual
suppression”.And this is logical, and coherent with my previous ideas and predictions about this matter in particular.
So, appart from astrocytes (if I may, and forgive me for changing slightly the subject of this post of yours), your post seems to me very interesting not for what you miss (the possible role of astrocytes) but for what you´ve found, which helps me to further understand my own hypothesis about the mind´s clockwork.
Furthermore: I would like to see more investigation in single signals during perception (investigations I can´t do). In particular, I´d like to see the demonstration of the presence of transient coherent activity between single signals of compatible neurons of V1 and V2 during perception, and the absence of this hypothetical (and new) type of neuronal activity during de absence of perception too (being coherence no synchronization, phase coincidence, but a constant phase difference).
What I try to say is that, astrocytes could be a part of the clockwork, but not the key to understand the perception. And the lacking part of the machine, could very well be this type of neuronal activity I´m predicting here and now (that I´ve explained in more detail in the link I´ve left, that I repeat now: http://neuronalintegration.es.tl/).
What do you think of this?
Thank you
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