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Justin A. Harris
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Journal Articles
Publisher: Journals Gateway
Journal of Cognitive Neuroscience (2020) 32 (10): 1984–2000.
Published: 01 October 2020
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Abstract
View articletitled, Stop Signal Task Training Strengthens GABA-mediated Neurotransmission within the Primary Motor Cortex
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for article titled, Stop Signal Task Training Strengthens GABA-mediated Neurotransmission within the Primary Motor Cortex
We have recently shown that the efficiency in stopping a response, measured using the stop signal task, is related to GABA A -mediated short-interval intracortical inhibition (SICI) in the primary motor cortex. In this study, we conducted two experiments on humans to determine whether training participants in the stop signal task within one session (Experiment 1) and across multiple sessions (Experiment 2) would increase SICI strength. For each experiment, we obtained premeasures and postmeasures of stopping efficiency and resting-state SICI, that is, during relaxed muscle activity (Experiment 1, n = 45, 15 male participants) and SICI during the stop signal task (Experiment 2, n = 44, 21 male participants). In the middle blocks of Experiment 1 and the middle sessions of Experiment 2, participants in the experimental group completed stop signal task training, whereas control participants completed a similar task without the requirement to stop a response. After training, the experimental group showed increased resting-state SICI strength (Experiment 1) and increased SICI strength during the stop signal task (Experiment 2). Although there were no overall behavioral improvements in stopping efficiency, improvements at an individual level were correlated with increases in SICI strength at rest (Experiment 1) and during successful stopping (Experiment 2). These results provide evidence of neuroplasticity in resting-state and task-related GABA A -mediated SICI in the primary motor cortex after response inhibition training. These results also suggest that SICI and stopping efficiency are temporally linked, such that a change in SICI between time points is correlated with a change in stopping efficiency between time points.
Journal Articles
Publisher: Journals Gateway
Journal of Cognitive Neuroscience (2019) 31 (9): 1343–1353.
Published: 01 September 2019
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Abstract
View articletitled, Motor Memory: Revealing Conditioned Action Tendencies Using Transcranial Magnetic Stimulation
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for article titled, Motor Memory: Revealing Conditioned Action Tendencies Using Transcranial Magnetic Stimulation
Action tendencies can be elicited by motivationally salient stimuli (e.g., appetitive rewards) or objects that support utilization behaviors. These action tendencies can benefit behavioral performance through speeded RTs in response tasks and improve detection accuracy in attentional capture tasks. However, action tendencies can be counterproductive when goals change (e.g., refraining from junk foods or abstaining from alcohol). Maintaining control over cue-elicited action tendencies is therefore critical for successful behavior modification. To better understand this relationship, we used transcranial magnetic stimulation to investigate the neural signatures of action tendencies in the presence of previously trained response cues. Participants were presented with a continuous letter stream and instructed to respond quickly to two target letters using two different response keys. Following this training phase, the target letters were embedded in a new task (test phase), and we applied transcranial magnetic stimulation to the motor cortex and measured motor evoked potentials as an index of corticospinal excitability (CSE). We found that CSE could be potentiated by a former response cue trained within a single experimental session, even when participants were instructed to withhold responses during the test phase. Critically, attention to the previously trained response cue was required to elicit the primed modulation in CSE, and successful control of this activity was accompanied by CSE suppression. These findings suggest that well-trained response cues can come to prime a conditioned action tendency and provide a model for understanding how the implementation of cognitive control can override action automaticity.
Journal Articles
Publisher: Journals Gateway
Journal of Cognitive Neuroscience (2008) 20 (4): 734–740.
Published: 01 April 2008
Abstract
View articletitled, The Functional Effect of Transcranial Magnetic Stimulation: Signal Suppression or Neural Noise Generation?
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for article titled, The Functional Effect of Transcranial Magnetic Stimulation: Signal Suppression or Neural Noise Generation?
Transcranial magnetic stimulation (TMS) is a popular tool for mapping perceptual and cognitive processes in the human brain. It uses a magnetic field to stimulate the brain, modifying ongoing activity in neural tissue under the stimulating coil, producing an effect that has been likened to a “virtual lesion.” However, research into the functional basis of this effect, essential for the interpretation of findings, lags behind its application. Acutely, TMS may disable neuronal function, thereby interrupting ongoing neural processes. Alternatively, the effects of TMS have been attributed to an injection of “neural noise,” consistent with its immediate and effectively random depolarization of neurons. Here we apply an added-noise paradigm to test these alternatives. We delivered TMS to the visual cortex and measured its effect on a simple visual discrimination task, while concurrently manipulating the level of image noise in the visual stimulus itself. TMS increased thresholds overall; and increasing the amount of image noise systematically increased discrimination thresholds. However, these two effects were not independent. Rather, TMS interacted multiplicatively with the image noise, consistent with a reduction in the strength of the visual signal. Indeed, in this paradigm, there was no evidence that TMS independently added noise to the visual process. Thus, our findings indicate that the “virtual lesion” produced by TMS can take the form of a loss of signal strength which may reflect a momentary interruption to ongoing neural processing.
Journal Articles
Publisher: Journals Gateway
Journal of Cognitive Neuroscience (2001) 13 (6): 800–812.
Published: 15 August 2001
Abstract
View articletitled, Object Orientation Agnosia: A Failure to Find the Axis?
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for article titled, Object Orientation Agnosia: A Failure to Find the Axis?
A dissociation between the ability to recognize misoriented objects and to determine their orientation has been reported in a small number of patients with vascular lesions. In this article, we describe a 57-year-old man with probable Alzheimer's disease who shows the same dissociation. Neuro-imaging findings indicated marked hypometabolism in the posterior cortical regions, particularly the postero-superior parietal lobes. Clinically, the patient had good object recognition accompanied by severely impaired spatial abilities. The experimental investigations comprised a variety of tasks in which he identified misoriented objects, evaluated the orientation of single objects, or discriminated the orientation of simultaneously presented items. Results revealed that his object recognition was independent of orientation and was largely mediated by salient features. With respect to orientation judgements, the patient displayed a profound inability to judge the orientation of nonupright objects, but remarkably intact (though largely implicit) knowledge of the upright orientation. Strikingly, his orientation judgements were also more accurate for upside-down objects than for other orientations (i.e., 90°). We interpret these results as evidence that judgements about object orientation are facilitated when the orientation of the principal axis of the object matches that of an internal representation. We propose that the inability to determine other orientations may be due to the failure of an “axis-finding” mechanism implemented in the posterior parietal lobes, that translates between object-centered and eye-centered coordinates appropriate for guiding visual scanning.