Publications by authors named "Eric B Knudsen"

During decision-making, neurons in the orbitofrontal cortex (OFC) sequentially represent the value of each option in turn, but it is unclear how these dynamics are translated into a choice response. One brain region that may be implicated in this process is the anterior cingulate cortex (ACC), which strongly connects with OFC and contains many neurons that encode the choice response. We investigated how OFC value signals interacted with ACC neurons encoding the choice response by performing simultaneous high-channel count recordings from the two areas in nonhuman primates.

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We make complex decisions using both fast judgments and slower, more deliberative reasoning. For example, during value-based decision-making, animals make rapid value-guided orienting eye movements after stimulus presentation that bias the upcoming decision. The neural mechanisms underlying these processes remain unclear.

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People with damage to the orbitofrontal cortex (OFC) have specific problems making decisions, whereas their other cognitive functions are spared. Neurophysiological studies have shown that OFC neurons fire in proportion to the value of anticipated outcomes. Thus, a central role of the OFC is to guide optimal decision-making by signalling values associated with different choices.

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The hippocampus is thought to encode a "cognitive map," a structural organization of knowledge about relationships in the world. Place cells, spatially selective hippocampal neurons that have been extensively studied in rodents, are one component of this map, describing the relative position of environmental features. However, whether this map extends to abstract, cognitive information remains unknown.

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Neuronal oscillations in the frontal cortex have been hypothesized to play a role in the organization of high-level cognition. Within the orbitofrontal cortex (OFC), there is a prominent oscillation in the theta frequency (4-8 Hz) during reward-guided behavior, but it is unclear whether this oscillation has causal significance. One methodological challenge is that it is difficult to manipulate theta without affecting other neural signals, such as single-neuron firing rates.

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Acute neurophysiology in the behaving primate typically relies on traditional manufacturing approaches for the instrumentation necessary for recording. For example, our previous approach consisted of distributing single microelectrodes in a fixed plane situated over a circular patch of frontal cortex using conventionally-milled recording grids. With the advent of robust, multisite linear probes, and the introduction of commercially-available, high-resolution rapid prototyping systems, we have been able to improve upon traditional approaches.

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Single neuron and local field potential signals recorded in the primary motor cortex have been repeatedly demonstrated as viable control signals for multi-degree-of-freedom actuators. Although the primary source of these signals has been fore/upper limb motor regions, recent evidence suggests that neural adaptation underlying neuroprosthetic control is generalizable across cortex, including hindlimb sensorimotor cortex. Here, adult rats underwent a longitudinal study that included a hindlimb pedal press task in response to cues for specific durations, followed by brain machine interface (BMI) tasks in healthy rats, after rats received a complete spinal transection and after the BMI signal controls epidural stimulation (BMI-FES).

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Background: In rat models of spinal cord injury, at least 3 different strategies can be used to promote long-term cortical reorganization: (1) active exercise above the level of the lesion; (2) passive exercise below the level of the lesion; and (3) serotonergic pharmacotherapy. Whether and how these potential therapeutic strategies-and their underlying mechanisms of action-interact remains unknown. Methods In spinally transected adult rats, we compared the effects of active exercise above the level of the lesion (treadmill), passive exercise below the level of the lesion (bike), serotonergic pharmacotherapy (quipazine), and combinations of the above therapies (bike+quipazine, treadmill+quipazine, bike+treadmill+quipazine) on long-term cortical reorganization (9 weeks after the spinal transection).

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Neural encoding of the passage of time to produce temporally precise movements remains an open question. Neurons in several brain regions across different experimental contexts encode estimates of temporal intervals by scaling their activity in proportion to the interval duration. In motor cortex the degree to which this scaled activity relies upon afferent feedback and is guided by motor output remains unclear.

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Physical exercise promotes neural plasticity in the brain of healthy subjects and modulates pathophysiological neural plasticity after sensorimotor loss, but the mechanisms of this action are not fully understood. After spinal cord injury, cortical reorganization can be maximized by exercising the non-affected body or the residual functions of the affected body. However, exercise per se also produces systemic changes - such as increased cardiovascular fitness, improved circulation and neuroendocrine changes - that have a great impact on brain function and plasticity.

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Cortical reorganization plays a significant role in recovery of function after injury of the central nervous system. The neural mechanisms that underlie this reorganization may be the same as those normally responsible for skilled behaviors that accompany extended sensory experience and, if better understood, could provide a basis for further promoting recovery of function after injury. The work presented here extends studies of spontaneous cortical reorganization after spinal cord injury to the role of rehabilitative strategies on cortical reorganization.

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The gradual buildup of neural activity over experimentally imposed delay periods, termed climbing activity, is well documented and is a potential mechanism by which interval time is encoded by distributed cortico-thalamico-striatal networks in the brain. Additionally, when multiple delay periods are incorporated, this activity has been shown to scale its rate of climbing proportional to the delay period. However, it remains unclear whether these patterns of activity occur within areas of motor cortex dedicated to hindlimb movement.

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Epidural electrical stimulation (EES) has often been used to restore stereotypic locomotor movements after spinal cord injury (SCI). However, restoring freeform movement requires specific force generation and independently controlled limbs for changing environments. Therefore, a second stimulus location would be advantageous, controlling force separately from locomotor movements.

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Behavioral tasks utilized as models for decoding neural activity for use in brain-machine interfaces are constrained primarily to forelimb tasks or locomotion. We present here our methodology for training adult rats in a novel skilled hindlimb 'reaching' task in which the animal is trained to make different types of hindlimb movements. 6 adult Long-Evans rats were trained to make variable duration (<1 or >1.

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