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Basal ganglia: beyond sensorimotor control
1148
BIOL PSYCHIATRY
Correspondence
1997:41:1147
Basal Ganglia: Beyond Sensorimotor Control To the Editors: Lidsky called for schizophrenia researchers to consider seriously that the basal ganglia (BG) may have a role in precipitating psychotic symptoms in addition to their well-known function of sensorimotor control. This reminds the writer (a designer of computer/robot systems circa 1960-1980) that some 20 years ago my colleagues and I developed circuitry emulating BG functions so that we could teach sophisticated robots (through operant conditioning) to identify behaviorally relevant (Lidsky's term) objects or events in the environment. One robot application, for example, was to identify component parts of a machine in a parts tray, even if the parts are jumbled together, and remove and assemble them correctly. Our view was that key elements of the BG were self-quenching circuits similar to electronic components known as differentiators; that is, inputs triggered a burst of activity that rapidly inhibited itself unless input was maintained or augmented by another input. This feature was needed to allow the machine to learn when to continue or inhibit specific motor behavior depending on the immediate consequences or context, and when to change behavioral set. Necessarily, the robotic BG mediated selective attention and saccades. Through operant conditioning, BG functions became inextricably associated with the robot's preprogrammed or learned repertoire of behaviorally relevant objects/events and correct responses to them. In highly simplified summary, the robotic BG received and encoded behavioral patterns specified by cortical and thalamic circuits (the robot had analogous units) and also received signals from a unit which corresponded to the limbic system and detected reward and punishment qualities of sensory stimuli. (The anatomy here is dated. Neuroanatomists have since then been debating the dorsal and ventral subdivisions of the BG, connections between limbic and thalamic structures, and distinctions between movements initiated by emotional or motivational stimuli--the dorsal striatopallidal system--versus those initiated by cognitive activities--the ventral striatopallida] system; how-
ever, these specifics do not affect the conceptual basis of this discussion.) An associated short-term memory provided visuospatial orientation (context) through a feedback loop. As a result of its operant conditioning and self-quenching action, the robotic BG could selectively implement different learned behaviors. The self-quenching action ensured that, under the influence of a sustained input from the limbic unit, only one of many competing response patterns would emerge from the BG as a set of commands to units corresponding to the motor cortex, cerebellum, and reflex motor units. It was relatively easy to build units that implemented behavior specified by our emulators of cortical, thalamic, and limbic inputs and that continued the behavior only if initial input results produced a sustaining input from the limbic-mesencephalic unit. These were crude engineering features, of course. Of conceptual interest, however, is that through operant conditioning the functions of the robotic BG became inseparable from intentional behavior and short-term memory to which it was linked in feedback loops. (If, as is often reported, short-term contextual memory corresponds to dorsolateral prefrontal circuits, then BG dysfunction may lead to prefrontal dysfunction, and vice versa.) Robotic BG dysfunction clearly would affect selective attention or saccades; obviously, however, the dysfunction could originate in BG or contextual memory circuits themselves, or it could be the result of systematic or randomly erratic behavior of the limbic unit. To determine the source of a dysfunction, a technician would interrupt the feedback connections and test each unit separately. Dysfunction localized to BG might leave them unable to adequately process limbic inputs and thus blunt or eliminate the robot's interest in objects/events that previously were behaviorally relevant. Dysfunction of limbic units, in human terms, would be analogous to a lack of emotional salience or behavioral relevance in sensory inputs.
Robert Bernhard Princeton. New Jersey PII S0006-3223 (97)00090-5
BIOL PSYCHIATRY
Correspondence
1997:41:1147
Basal Ganglia: Beyond Sensorimotor Control To the Editors: Lidsky called for schizophrenia researchers to consider seriously that the basal ganglia (BG) may have a role in precipitating psychotic symptoms in addition to their well-known function of sensorimotor control. This reminds the writer (a designer of computer/robot systems circa 1960-1980) that some 20 years ago my colleagues and I developed circuitry emulating BG functions so that we could teach sophisticated robots (through operant conditioning) to identify behaviorally relevant (Lidsky's term) objects or events in the environment. One robot application, for example, was to identify component parts of a machine in a parts tray, even if the parts are jumbled together, and remove and assemble them correctly. Our view was that key elements of the BG were self-quenching circuits similar to electronic components known as differentiators; that is, inputs triggered a burst of activity that rapidly inhibited itself unless input was maintained or augmented by another input. This feature was needed to allow the machine to learn when to continue or inhibit specific motor behavior depending on the immediate consequences or context, and when to change behavioral set. Necessarily, the robotic BG mediated selective attention and saccades. Through operant conditioning, BG functions became inextricably associated with the robot's preprogrammed or learned repertoire of behaviorally relevant objects/events and correct responses to them. In highly simplified summary, the robotic BG received and encoded behavioral patterns specified by cortical and thalamic circuits (the robot had analogous units) and also received signals from a unit which corresponded to the limbic system and detected reward and punishment qualities of sensory stimuli. (The anatomy here is dated. Neuroanatomists have since then been debating the dorsal and ventral subdivisions of the BG, connections between limbic and thalamic structures, and distinctions between movements initiated by emotional or motivational stimuli--the dorsal striatopallidal system--versus those initiated by cognitive activities--the ventral striatopallida] system; how-
ever, these specifics do not affect the conceptual basis of this discussion.) An associated short-term memory provided visuospatial orientation (context) through a feedback loop. As a result of its operant conditioning and self-quenching action, the robotic BG could selectively implement different learned behaviors. The self-quenching action ensured that, under the influence of a sustained input from the limbic unit, only one of many competing response patterns would emerge from the BG as a set of commands to units corresponding to the motor cortex, cerebellum, and reflex motor units. It was relatively easy to build units that implemented behavior specified by our emulators of cortical, thalamic, and limbic inputs and that continued the behavior only if initial input results produced a sustaining input from the limbic-mesencephalic unit. These were crude engineering features, of course. Of conceptual interest, however, is that through operant conditioning the functions of the robotic BG became inseparable from intentional behavior and short-term memory to which it was linked in feedback loops. (If, as is often reported, short-term contextual memory corresponds to dorsolateral prefrontal circuits, then BG dysfunction may lead to prefrontal dysfunction, and vice versa.) Robotic BG dysfunction clearly would affect selective attention or saccades; obviously, however, the dysfunction could originate in BG or contextual memory circuits themselves, or it could be the result of systematic or randomly erratic behavior of the limbic unit. To determine the source of a dysfunction, a technician would interrupt the feedback connections and test each unit separately. Dysfunction localized to BG might leave them unable to adequately process limbic inputs and thus blunt or eliminate the robot's interest in objects/events that previously were behaviorally relevant. Dysfunction of limbic units, in human terms, would be analogous to a lack of emotional salience or behavioral relevance in sensory inputs.
Robert Bernhard Princeton. New Jersey PII S0006-3223 (97)00090-5