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Area V5 of the primate brain—past, present, future
Lectures
Ll
BRAIN MECHANISMS OF PERCEPTION. Vernon B. Mountcastle, The Johns Hopkins University, Baltimore, Maryland, USA.
A central dogma of Neuroscience emphasizes the fusion of acquired and rational knowledge, a monistic view of the mind/brain relation, mechanistic not mentalistic concepts of perception, and objective methods in sensory and perceptual research. This research is congruent with the philosophical concept of Emergent Materialism. That is, that a large-numbered, dynamically active system like a brain possesses properties not explicable in terms of the properties of its individual elements, the neurons. Perception is an emergent process of the brain, one of the many that compose what is traditionally called mind, which I designate by the active verb, to mind. It is the major theme of my lecture that perceptions vary greatly in content and complexity, from those virtually isomorphic with external reality to those that are central neural constructions. I shall first describe one of the quasi-isomorphic class, the sense of flutter, a mechanoreceptive component of somatic sensibility. I shall show the identity of the human and monkey capacities for frequency discrimination in this sense; illustrate the critical neural discriminandum in the postcentral gyrus of the discriminating monkey; describe the propagation of that signal from the primary sensory cortex through the distributed system linking it to the contralateral motor cortex, and specify the composition there of neuronal signals for differential motor response. I shall then turn to an emergent function of developed brains, their capacity to construct and update images of surrounding space, and to identify the spatial relations between objects in that space. These perceptual functions are ordinarily executed at preconscious levels, as witness the usually unnoticed role of the visual flow fields in guiding locomotion; they can be brought to conscious perception by directed attention. Lesion studies in humans and monkeys indicate that the parietal lobe system plays an essential role in these aspects of visuospatial perception, and the visual guidance of pointing, reaching, and locomotion. The functional properties of several classes of neurons in the posterior parietal homotypical cortex of the monkey mimic many of the functions attributed to the parietal system, and mirror the defects seen in man and monkey after parietal lobe lesions. I shall describe only the parietal visual neurons (PVNs), whose properties are not predictable from those of neurons in the multi-staged, transcortical system linking the striate and parietal areas. Those properties are constructed within the parietal system itself. PVNs are well-suited to signal events in the visual flow fields during locomotion. Moreover, population analysis reveals that ensembles of PVNs provide an accurate signal of the direction of moving visual stimuli, even though each single neuron provides only an imprecise signal of that direction: it is of a central construction not derivable from the properties of single neurons.
L2
AREA V5 OF THE PRIMATE BRAIN-PAST, PRESENT, FUTURE S. Zeki, University College London, London WClE 6BT, England
We identified Area V5 as a specific visual area of the monkey brain, specialized for visual motion, in the early 1970s. Since then, it has provided us with profound and unhoped for insights into the organization of the visual brain. Using the technique of position emission tomography (PET), co-registered with images derived from magnetic resonance (MRI), my colleagues and I have been able to locate VS in the human brain and, using the same techniques, to show that it is active, not only when humans see objective motion but also when they see ‘illusory’ motion, i.e. motion that is not there objectively but only phenomenally. In addition, and with the same methods, we have shown that area V5 is absent in a patient suffering from the syndrome of cerebral akinetopsia, i.e. visual motion imperception. We have extended these studies to show that area VS can mediate a simple and relatively crude but conscious motion vision, without pre- or post-processing by Vl, since it is active when a patient blinded by a lesion in Vl reports having seen a high contrast stimulus in motion, whose direction of motion he is able to discriminate correctly. More recently, we have used the technique of transcranial magnetic stimulation (TMS) to show that impulses delivered to V5 can lead to severe transient akinetopsia whereas stimulation of Vl is not so effective in producing the same transient syndrome. The fact that TMS of VS is only effective when delivered at delays of -20 to + 10 ms before or after onset of the visual stimulus whereas TMS of Vl is partially effective only at delays of 60-70 ms after the onset of visual stimulation led us to hypothesize that there is a fast parallel pathway that reaches VS before Vl, and at delays of no more than 30 ms, a latency which is compatible with direct recording from monkey VS. We have recently conhrmed this by using our PET results to locate and record the activity evoked at the scalp when humans view a visual stimulus in motion, using the combined techniques of electro-encephalography (EEG) and magneto-encephalography (MEG). The results have shown that there are indeed parallel pathways leading to Vl and V5, that the fast pathway to V5 is only present with fast moving stimuli (in excess of 6” s-i) and that, consequently, the parallelism we speak of is a dynamic one, dependent upon the properties of the visual stimulus. These findings explain why patients with lesions in Vl who have residual vision for motion can only detect fast motion and why a patient with a lesion in VS can only detect very slow motion. Thus, from simple beginnings based on anatomical observations and electrophysiological recordings in monkeys, V5 has provided us with insights into profound questions which include conscious visual perception. Such a rapid progress has even encouraged us to look at the role of V5 in kinetic art.
Ll
BRAIN MECHANISMS OF PERCEPTION. Vernon B. Mountcastle, The Johns Hopkins University, Baltimore, Maryland, USA.
A central dogma of Neuroscience emphasizes the fusion of acquired and rational knowledge, a monistic view of the mind/brain relation, mechanistic not mentalistic concepts of perception, and objective methods in sensory and perceptual research. This research is congruent with the philosophical concept of Emergent Materialism. That is, that a large-numbered, dynamically active system like a brain possesses properties not explicable in terms of the properties of its individual elements, the neurons. Perception is an emergent process of the brain, one of the many that compose what is traditionally called mind, which I designate by the active verb, to mind. It is the major theme of my lecture that perceptions vary greatly in content and complexity, from those virtually isomorphic with external reality to those that are central neural constructions. I shall first describe one of the quasi-isomorphic class, the sense of flutter, a mechanoreceptive component of somatic sensibility. I shall show the identity of the human and monkey capacities for frequency discrimination in this sense; illustrate the critical neural discriminandum in the postcentral gyrus of the discriminating monkey; describe the propagation of that signal from the primary sensory cortex through the distributed system linking it to the contralateral motor cortex, and specify the composition there of neuronal signals for differential motor response. I shall then turn to an emergent function of developed brains, their capacity to construct and update images of surrounding space, and to identify the spatial relations between objects in that space. These perceptual functions are ordinarily executed at preconscious levels, as witness the usually unnoticed role of the visual flow fields in guiding locomotion; they can be brought to conscious perception by directed attention. Lesion studies in humans and monkeys indicate that the parietal lobe system plays an essential role in these aspects of visuospatial perception, and the visual guidance of pointing, reaching, and locomotion. The functional properties of several classes of neurons in the posterior parietal homotypical cortex of the monkey mimic many of the functions attributed to the parietal system, and mirror the defects seen in man and monkey after parietal lobe lesions. I shall describe only the parietal visual neurons (PVNs), whose properties are not predictable from those of neurons in the multi-staged, transcortical system linking the striate and parietal areas. Those properties are constructed within the parietal system itself. PVNs are well-suited to signal events in the visual flow fields during locomotion. Moreover, population analysis reveals that ensembles of PVNs provide an accurate signal of the direction of moving visual stimuli, even though each single neuron provides only an imprecise signal of that direction: it is of a central construction not derivable from the properties of single neurons.
L2
AREA V5 OF THE PRIMATE BRAIN-PAST, PRESENT, FUTURE S. Zeki, University College London, London WClE 6BT, England
We identified Area V5 as a specific visual area of the monkey brain, specialized for visual motion, in the early 1970s. Since then, it has provided us with profound and unhoped for insights into the organization of the visual brain. Using the technique of position emission tomography (PET), co-registered with images derived from magnetic resonance (MRI), my colleagues and I have been able to locate VS in the human brain and, using the same techniques, to show that it is active, not only when humans see objective motion but also when they see ‘illusory’ motion, i.e. motion that is not there objectively but only phenomenally. In addition, and with the same methods, we have shown that area V5 is absent in a patient suffering from the syndrome of cerebral akinetopsia, i.e. visual motion imperception. We have extended these studies to show that area VS can mediate a simple and relatively crude but conscious motion vision, without pre- or post-processing by Vl, since it is active when a patient blinded by a lesion in Vl reports having seen a high contrast stimulus in motion, whose direction of motion he is able to discriminate correctly. More recently, we have used the technique of transcranial magnetic stimulation (TMS) to show that impulses delivered to V5 can lead to severe transient akinetopsia whereas stimulation of Vl is not so effective in producing the same transient syndrome. The fact that TMS of VS is only effective when delivered at delays of -20 to + 10 ms before or after onset of the visual stimulus whereas TMS of Vl is partially effective only at delays of 60-70 ms after the onset of visual stimulation led us to hypothesize that there is a fast parallel pathway that reaches VS before Vl, and at delays of no more than 30 ms, a latency which is compatible with direct recording from monkey VS. We have recently conhrmed this by using our PET results to locate and record the activity evoked at the scalp when humans view a visual stimulus in motion, using the combined techniques of electro-encephalography (EEG) and magneto-encephalography (MEG). The results have shown that there are indeed parallel pathways leading to Vl and V5, that the fast pathway to V5 is only present with fast moving stimuli (in excess of 6” s-i) and that, consequently, the parallelism we speak of is a dynamic one, dependent upon the properties of the visual stimulus. These findings explain why patients with lesions in Vl who have residual vision for motion can only detect fast motion and why a patient with a lesion in VS can only detect very slow motion. Thus, from simple beginnings based on anatomical observations and electrophysiological recordings in monkeys, V5 has provided us with insights into profound questions which include conscious visual perception. Such a rapid progress has even encouraged us to look at the role of V5 in kinetic art.