I heard a cool talk by Christopher Moore today:
Perception, Cortical Dynamics, and the Hemo-Neural Hypothesis.
"Abstract
Our laboratory studies how rapid changes in neural organization, on millisecond to second timescales, underlie rapid changes in perceptual capability. Our focus is on understanding how activity-dependent dynamics in primary sensory cortex impact sensation.
To test cellular- and circuit-level hypotheses, we conduct studies in rodent barrel cortex and, to a more limited degree, monkey cortex. To test the relevance of these findings to humans, we conduct parallel neuroimaging studies during perceptual task performance.
Establishing Key Features of Our Model, the Vibrissa Barrel Cortex
In the first part of the seminar, I will briefly review experiments conducted to define basic principles of barrel cortex organization, a key model for our studies of cortical dynamics. We recently discovered 2 new cortical feature maps, of vibrissa motion frequency and direction. We also conducted the first studies of the detailed input to the system, the vibrissa motions believed to relay surface information. Recent experiments in awake behaving rats have confirmed a key prediction of our 'resonance hypothesis,' that vibrissa length predicts the frequencies transmitted during active sensation.
Activity-Dependent Dynamics: Modulation of Neural Sensitivity by Frequency
In the second part of the seminar, I will discuss our studies of frequency-dependent dynamics. Our studies of barrel cortex suggested that during conditions of lower frequency afferent input, the neocortex is in a higher-gain mode, more optimal for perceptual detection. In contrast, sensory stimulation of vibrissae at 5-25 Hz leads to suppression of this cortical circuit, and is predicted to impair detection. These studies led to the prediction that the amplitude of the SI response predicts detection, and that internally-generated rhythmic activity in the thalamo-cortical circuit at 5-25 Hz (in the range of 'alpha' and 'beta' states) predicts suppression of the evoked response and of detection.
Our recent human studies of detection using MEG confirmed these predictions. To link these human data to our single-neuron and circuit level analyses, we developed a biophysically realistic, laminated cortical model of SI. Activity in this model predicts the human MEG response, including the suppression of this response with increased pre-stimulus activity in the alpha and beta bands.
Ongoing studies will test the hypothesis that frequency-dependent recruitment of specific interneuron sub-types is a central mechanism underlying the observed dynamics. A key tool in these studies will be genetically-engineered mice developed in the Tsai laboratory. Parallel experiments are examining, in awake rats, changes in neural sensitivity in specific cell types and in behavioral detection probability as a function of ongoing thalamo-cortical oscillations.
Activity-Dependent Dynamics: Modulation of Neural Sensitivity by Hemodynamics
In the third part of the seminar, I will present the hypothesis that hemodynamics play an active role in information processing. Specifically, we are testing the prediction that functional hyperemia, the activity-related increase in local blood flow that is the source of the fMRI 'BOLD' signal, acts as a neuromodulator, shaping local neural sensitivity. To test this hypothesis, we induce hyperemia by selective means while recording in barrel cortex. Our preliminary data using intracellular recording show that hyperemia is correlated with depolarization of neurons (N=6/9) and of glia (N=4/5).
If supported by the data, this hypothesis provides a novel use for hemodynamics in the brain. It further suggests that the widely-used technique of fMRI is measuring part of the computational process, and not simply a 'secondary' marker. This hypothesis also indicates a different etiology for clinical disorders such as cerebrovascular epilepsy, and potentially novel strategies for the remediation of these maladies.
In addition to our electrophysiological studies, ongoing work is testing this hypothesis using 2-photon imaging of neurons and astrocytes during hyperemia induction. With the Boyden lab, we are also developing methods for the transfection of light-activated channels into smooth muscles, providing a novel and highly selective means of blood flow regulation."
cos's stepmom published a book, "Adobe Photoshop Forensics":
http://cos.livejournal.com/51951.html
Perception, Cortical Dynamics, and the Hemo-Neural Hypothesis.
"Abstract
Our laboratory studies how rapid changes in neural organization, on millisecond to second timescales, underlie rapid changes in perceptual capability. Our focus is on understanding how activity-dependent dynamics in primary sensory cortex impact sensation.
To test cellular- and circuit-level hypotheses, we conduct studies in rodent barrel cortex and, to a more limited degree, monkey cortex. To test the relevance of these findings to humans, we conduct parallel neuroimaging studies during perceptual task performance.
Establishing Key Features of Our Model, the Vibrissa Barrel Cortex
In the first part of the seminar, I will briefly review experiments conducted to define basic principles of barrel cortex organization, a key model for our studies of cortical dynamics. We recently discovered 2 new cortical feature maps, of vibrissa motion frequency and direction. We also conducted the first studies of the detailed input to the system, the vibrissa motions believed to relay surface information. Recent experiments in awake behaving rats have confirmed a key prediction of our 'resonance hypothesis,' that vibrissa length predicts the frequencies transmitted during active sensation.
Activity-Dependent Dynamics: Modulation of Neural Sensitivity by Frequency
In the second part of the seminar, I will discuss our studies of frequency-dependent dynamics. Our studies of barrel cortex suggested that during conditions of lower frequency afferent input, the neocortex is in a higher-gain mode, more optimal for perceptual detection. In contrast, sensory stimulation of vibrissae at 5-25 Hz leads to suppression of this cortical circuit, and is predicted to impair detection. These studies led to the prediction that the amplitude of the SI response predicts detection, and that internally-generated rhythmic activity in the thalamo-cortical circuit at 5-25 Hz (in the range of 'alpha' and 'beta' states) predicts suppression of the evoked response and of detection.
Our recent human studies of detection using MEG confirmed these predictions. To link these human data to our single-neuron and circuit level analyses, we developed a biophysically realistic, laminated cortical model of SI. Activity in this model predicts the human MEG response, including the suppression of this response with increased pre-stimulus activity in the alpha and beta bands.
Ongoing studies will test the hypothesis that frequency-dependent recruitment of specific interneuron sub-types is a central mechanism underlying the observed dynamics. A key tool in these studies will be genetically-engineered mice developed in the Tsai laboratory. Parallel experiments are examining, in awake rats, changes in neural sensitivity in specific cell types and in behavioral detection probability as a function of ongoing thalamo-cortical oscillations.
Activity-Dependent Dynamics: Modulation of Neural Sensitivity by Hemodynamics
In the third part of the seminar, I will present the hypothesis that hemodynamics play an active role in information processing. Specifically, we are testing the prediction that functional hyperemia, the activity-related increase in local blood flow that is the source of the fMRI 'BOLD' signal, acts as a neuromodulator, shaping local neural sensitivity. To test this hypothesis, we induce hyperemia by selective means while recording in barrel cortex. Our preliminary data using intracellular recording show that hyperemia is correlated with depolarization of neurons (N=6/9) and of glia (N=4/5).
If supported by the data, this hypothesis provides a novel use for hemodynamics in the brain. It further suggests that the widely-used technique of fMRI is measuring part of the computational process, and not simply a 'secondary' marker. This hypothesis also indicates a different etiology for clinical disorders such as cerebrovascular epilepsy, and potentially novel strategies for the remediation of these maladies.
In addition to our electrophysiological studies, ongoing work is testing this hypothesis using 2-photon imaging of neurons and astrocytes during hyperemia induction. With the Boyden lab, we are also developing methods for the transfection of light-activated channels into smooth muscles, providing a novel and highly selective means of blood flow regulation."
http://cos.livejournal.com/51951.html