The effect of staircase stopping accuracy and testing environment on stop-signal reaction time.

The stop-signal task is widely used in experimental psychology and cognitive neuroscience research, as well as neuropsychological and clinical practice for assessing response inhibition. The task requires participants to make speeded responses on a majority of trials, but to inhibit responses when a stop signal appears after the imperative cue. The stop-signal delay after the onset of the imperative cue determines how difficult it is to cancel an initiated action. The delay is typically staircased to maintain a 50% stopping accuracy for an estimation of stopping speed to be calculated. However, the validity of this estimation is compromised when participants engage in strategic slowing, motivated by a desire to avoid stopping failures. We hypothesized that maintaining stopping accuracy at 66.67% reduces this bias, and that slowing may also be impacted by the level of experimenter supervision. We found that compared with 50%, using a 66.67% stopping accuracy staircase produced slower stop-signal reaction time estimations (≈7 ms), but resulted in fewer strategic slowing exclusions. Additionally, both staircase procedures had similar within-experiment test-retest reliability. We also found that while individual and group testing in a laboratory setting produced similar estimations of stopping speed, participants tested online produced slower estimates. Our findings indicate that maintaining stopping accuracy at 66.67% is a reliable method for estimating stopping speed and can have benefits over the standard 50% staircase procedure. Further, our results show that care should be taken when comparing between experiments using different staircases or conducted in different testing environments.

Expected TMS excites the motor system less effectively than unexpected stimulation.

The brain's response to sensory input is modulated by prediction. For example, sounds that are produced by one's own actions, or those that are strongly predicted by environmental cues, elicit an attenuated N1 component in the auditory evoked potential. It has been suggested that this form of sensory attenuation to stimulation produced by one's own actions is the reason we are unable to tickle ourselves. Here we examined whether the neural response to direct stimulation of the brain is attenuated by prediction in a similar manner. Transcranial magnetic stimulation (TMS) applied over primary motor cortex can be used to gauge the excitability of the motor system. Motor-evoked potentials (MEPs), elicited by TMS and measured in peripheral muscles, are larger when actions are being prepared and smaller when actions are voluntarily suppressed. We tested whether the amplitude of MEPs was attenuated under circumstances where the TMS pulse can be reliably predicted, even though control of the relevant motor effector was never required. Self-initiation of the TMS pulse and reliable cuing of the TMS pulse both produced attenuated MEP amplitudes, compared to those generated programmatically in an unpredictable manner. These results suggest that predictive coding may be governed by domain-general mechanisms responsible for all forms predictive learning. The findings also have important methodological implications for designing TMS experiments that control for the predictability of TMS pulses.

Motor cortex dysfunction in problem gamblers.

Impairments in response inhibition have been implicated in gambling psychopathology. This behavioral impairment may suggest that the neural mechanisms involved in response inhibition, such as GABAA -mediated neurotransmission in the primary motor cortex (M1), are also impaired. The present study obtained paired-pulse transcranial magnetic stimulation markers of GABAA and glutamate receptor activity from the left M1 of three groups-problem gamblers (n = 17, 12 males), at-risk gamblers (n = 29, 19 males), and controls (n = 23, six males)-with each group matched for alcohol use, substance use, and attention-deficit hyperactivity disorder (ADHD) symptomology. Response inhibition was measured using the stop signal task. Results showed that problem gamblers had weaker M1 GABAA receptor activity relative to controls and elevated M1 glutamate receptor activity relative to at-risk gamblers and controls. Although there were no differences in response inhibition between the groups, poorer response inhibition was correlated with weaker M1 GABAA receptor activity. These findings are the first to show that problem gambling is associated with alterations in M1 GABAA and glutamate-mediated neurotransmission.

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 GABAA-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 GABAA-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.

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.

Timing of interfering events in one-trial serial overshadowing of a taste aversion.

This set of experiments examined the question of when a stimulus would be most effective in overshadowing the acquisition of long-delay taste aversion learning. In Experiment 1 rats drank sucrose, the target solution, followed by a hydrochloric acid (HCl) solution before lithium injection some time later; HCl was presented either early or late in the interval. The late condition produced greater overshadowing than the early condition. The importance of the HCl-injection interval was confirmed by Experiment 2, in which the sucrose-injection interval was varied. Experiment 3 found that even placement in a different context - an event that normally produces little overshadowing of a CTA - produced one-trial overshadowing of a sucrose aversion as long as the context was novel and exposure to it occurred immediately before lithium injection. No current theoretical account of one-trial overshadowing predicts that a late event produces more overshadowing than an early event. This result can, however, be accommodated within a modified version of the Rescorla-Wagner model.

Pathological Gambling and Motor Impulsivity: A Systematic Review with Meta-Analysis.

Motor impulsivity, which is an impairment in withholding and cancelling inappropriate responses, may account for the inability for pathological gamblers (PGs) to inhibit their urges to gamble. The aim of this systematic review was to perform a quantitative and qualitative synthesis of existing studies in order to assess whether PGs without comorbid substance use disorder have elevated motor impulsivity, relative to healthy controls. An exhaustive literature search led to the identification of 20 studies which met inclusion criteria. A meta-analysis was then conducted on the following measures: stop signal reaction time from the stop signal task; commission errors, omission errors, and Go reaction time from the Go/No-Go task; and the motor impulsiveness subscale of the Barratt Impulsiveness Scale (BIS-Motor). The results revealed a moderate to large mean effect size of stop signal reaction time, small to moderate mean effect sizes for commission errors, omission errors and Go reaction time, and a large mean effect size for the BIS-Motor. Significant heterogeneity in effect sizes was observed on most behavioural measures, but not for the BIS-Motor or omission errors on the Go/No-Go task. Overall, these results suggest that motor impulsivity may be one of the features of PG psychopathology, accounting for their poor inhibitory control over gambling behaviours. Moreover, other deficits in sustained attention, or more generally in executive/cognitive control, may be present in PGs. We discuss the implications, limitations of existing research, and suggested avenues for future studies, particularly the need to acknowledge heterogeneity amongst PGs and amongst different behavioural measures.

Single tactile afferents outperform human subjects in a vibrotactile intensity discrimination task.

We simultaneously compared the sensitivity of single primary afferent neurons supplying the glabrous skin of the hand and the psychophysical amplitude discrimination thresholds in human subjects for a set of vibrotactile stimuli delivered to the receptive field. All recorded afferents had a dynamic range narrower than the range of amplitudes across which the subjects could discriminate. However, when the vibration amplitude was chosen to be within the steepest part of the afferent's stimulus-response function the response of single afferents, defined as the spike count over the vibration duration (500 ms), was often more sensitive in discriminating vibration amplitude than the perceptual judgment of the participants. We quantified how the neuronal performance depended on the integration window: for short windows the neuronal performance was inferior to the performance of the subject. The neuronal performance progressively improved with increasing spike count duration and reached a level significantly above that of the subjects when the integration window was 250 ms or longer. The superiority in performance of individual neurons over observers could reflect a nonoptimal integration window or be due to the presence of noise between the sensory periphery and the cortical decision stage. Additionally, it could indicate that the range of perceptual sensitivity comes at the cost of discrimination through pooling across neurons with different response functions.

Benzodiazepine administration prevents the use of error-correction mechanisms during fear extinction.

Three experiments examined the effect of systemic administration of the benzodiazepine midazolam on extinction and re-extinction of conditioned fear. Experiment 1 demonstrated that midazolam administration prior to extinction of a conditioned stimulus (CS) impaired that extinction when rats were subsequently tested drug free; however, extinction was spared if rats were extinguished, reconditioned, and re-extinguished under midazolam. Experiment 2 provided a replication of this effect within-subjects; rats were conditioned to two CSs (A and B), extinguished to one (A-), reconditioned to both, and then extinguished/re-extinguished to both stimuli in compound (AB-), under either vehicle or midazolam. On the drug-free test, rats given midazolam froze more to the CS that had been extinguished (B) than the one that been re-extinguished (A). The final experiment examined whether extinction under midazolam was regulated by prediction error. Rats were trained with three CSs (A, B, C) and extinguished to two (A-, C-). These stimuli then underwent additional extinction under midazolam or vehicle, with one CS now presented in compound with the non-extinguished CS (AB-, C-). Rats were then tested for fear of A relative to C. Rats given vehicle showed a deepening of extinction to A relative to C, as is predicted from error-correction models; however, rats given midazolam failed to show any such discrepancy in responding. The results are interpreted to indicate that the drug reduced prediction error during extinction by reducing fear, and rats were able to re-extinguish fear via a retrieval mechanism that is independent of prediction error.

The sequencing of trials during partial reinforcement affects subsequent extinction.

If a conditioned stimulus or response has been inconsistently ("partially") reinforced, conditioned responding will take longer to extinguish than if responding had been established by consistent ("continuous") reinforcement. This partial reinforcement extinction effect (PREE) is one of the best-known phenomena in associative learning but defies ready explanation by associative models which assume that a partial reinforcement schedule will produce weaker conditioning that should be less resistant to extinction. The most popular explanation of the PREE is that, during partial reinforcement, animals learn that recent nonreinforced (N) trials are associated with subsequent reinforcement (R), and therefore the presence of N trials during extinction serves to promote generalization of conditioning to extinction. According to sequential theory (Capaldi, 1966), animals can encode whole sequences (runs) of N trials and associate their memory of the sequence with subsequent R. The length of these N sequences during conditioning affects how long the animal will continue to respond during extinction. The present experiment used Pavlovian magazine approach conditioning with rats to test two predictions of this theory. Consistent with sequential theory, the PREE was sensitive to the length of the N sequence: conditioning with long sequences (runs of 3-5 N trials) produced a stronger PREE than conditioning with short sequences (runs of 1 or 2) even when the total number of N and R trials was held constant. Surprisingly, there was no PREE among rats trained with the short sequences. Moreover, contrary to the theory's prediction, interrupting the long N sequences with reinforced trials of a different conditioned stimulus did not affect the subsequent PREE. I conclude that uncertainty about reinforcement, rather than the memory of N sequences per se, is a key factor in the development of the PREE. (PsycInfo Database Record (c) 2024 APA, all rights reserved).

Learning about trial sequences disrupts the partial reinforcement extinction effect in classical conditioning.

The partial reinforcement extinction effect (PREE) refers to the phenomenon that conditioned responding extinguishes more slowly if subjects had been inconsistently ("partially") reinforced than if they had been reinforced on every trial ("continuously" reinforced). One largely successful account of the PREE, known as sequential theory (Capaldi, 1966), suggests that, when subjects are partially reinforced, they learn that memories of sequences of nonreinforced trials are associated with subsequent reinforcement. This association helps to maintain responding (i.e., delay extinction) when the subjects experience nonreinforced trials during extinction. Sequential theory's explanation of the PREE hinges on subjects learning sequences of nonreinforced trials during acquisition. However, direct evidence for such sequential learning is not available in previous studies of the PREE where animals are trained with multiple sequences of different lengths that are randomly intermixed and, therefore, cannot anticipate whether a given trial will be reinforced during acquisition. The current study conducted two experiments that trained rats with a single fixed trial sequence to provide evidence of sequential learning during conditioning, and then observe its effect on the PREE. Under one condition the rats did learn about the fixed sequence but did not subsequently show a PREE, whereas other rats that did show a PREE had not learned the trial sequences during conditioning. Therefore, contrary to sequential theory's prediction, our result suggests that learning about the trial sequence is neither necessary nor sufficient for the PREE. We suggest that the PREE may instead depend on uncertainty about whether the conditioned stimulus will be reinforced. (PsycInfo Database Record (c) 2024 APA, all rights reserved).

Correlated physiological and perceptual effects of noise in a tactile stimulus.

We investigated connections between the physiology of rat barrel cortex neurons and the sensation of vibration in humans. One set of experiments measured neuronal responses in anesthetized rats to trains of whisker deflections, each train characterized either by constant amplitude across all deflections or by variable amplitude ("amplitude noise"). Firing rate and firing synchrony were, on average, boosted by the presence of noise. However, neurons were not uniform in their responses to noise. Barrel cortex neurons have been categorized as regular-spiking units (putative excitatory neurons) and fast-spiking units (putative inhibitory neurons). Among regular-spiking units, amplitude noise caused a higher firing rate and increased cross-neuron synchrony. Among fast-spiking units, noise had the opposite effect: It led to a lower firing rate and decreased cross-neuron synchrony. This finding suggests that amplitude noise affects the interaction between inhibitory and excitatory neurons. From these physiological effects, we expected that noise would lead to an increase in the perceived intensity of a vibration. We tested this notion using psychophysical measurements in humans. As predicted, subjects overestimated the intensity of noisy vibrations. Thus the physiological mechanisms present in barrel cortex also appear to be at work in the human tactile system, where they affect vibration perception.

Is cortical inhibition in primary motor cortex related to executive control?

Recent research using paired-pulse transcranial magnetic stimulation (TMS) has shown that the speed with which people can stop an action is linked to GABAergic inhibitory activity in the motor system. Specifically, a significant proportion of the variance in stop signal reaction time (SSRT; a widely used measure of inhibitory control) is accounted for by short-interval cortical inhibition (SICI). It is still unclear whether this relationship reflects a broader link between GABAergic processes and executive functions, or a specific link between GABAergic processes and motor stopping ability. The current study sought to replicate the correlation between SSRT and SICI while investigating whether this association generalises to other measures of inhibitory control and working memory, and to long-interval cortical inhibition (LICI). Participants completed a battery of inhibition (Stop-Signal, Stroop, Flanker) and working memory (n-back, Digit Span, and Operation Span) tasks. We replicated the correlation between SICI and SSRT but found no other correlations between behavioural measures of executive control and the two cortical measures of inhibition. These findings indicate that the relationship between SSRT and SICI is specific to a particular property of response inhibition and likely reflects the function of local inhibitory networks mediated by GABAA.

Improving visual sensitivity with subthreshold transcranial magnetic stimulation.

We probed for improvement of visual sensitivity in human participants using transcranial magnetic stimulation (TMS). Stimulation of visual cortex can induce an illusory visual percept known as a phosphene. It is known that TMS, delivered at intensities above the threshold to induce phosphenes, impairs the detection of visual stimuli. We investigated how the detection of a simple visual stimulus is affected by TMS applied to visual cortex at or below the phosphene threshold. Participants performed the detection task while the contrast of the visual stimulus was varied from trial to trial according to an adaptive staircase procedure. Detection of the stimulus was enhanced when a single pulse of TMS was delivered to the contralateral visual cortex 100 or 120 ms after stimulus onset at intensities just below the phosphene threshold. No improvement in visual sensitivity was observed when TMS was applied to the visual cortex in the opposite hemisphere (ipsilateral to the visual stimulus). We conclude that TMS-induced neuronal activity can sum with stimulus-evoked activity to augment visual perception.

Normalization between stimulus elements in a model of Pavlovian conditioning: showjumping on an elemental horse.

Harris and Livesey. Learning & Behavior, 38, 1-26, (2010) described an elemental model of associative learning that implements a simple learning rule that produces results equivalent to those proposed by Rescorla and Wagner (1972), and additionally modifies in "real time" the strength of the associative connections between elements. The novel feature of this model is that stimulus elements interact by suppressively normalizing one another's activation. Because of the normalization process, element activity is a nonlinear function of sensory input strength, and the shape of the function changes depending on the number and saliences of all stimuli that are present. The model can solve a range of complex discriminations and account for related empirical findings that have been taken as evidence for configural learning processes. Here we evaluate the model's performance against the host of conditioning phenomena that are outlined in the companion article, and we present a freely available computer program for use by other researchers to simulate the model's behavior in a variety of conditioning paradigms.

The learning curve, revisited.

The nature of the operations that support learning should be evident in the form or shape of the learning curve. For example, models that describe learning as an iterative error-correction process expect that the amount learned on each trial follows a decelerating (negatively inflected) function. That prediction is broadly consistent with the shape of the acquisition and extinction curves derived from mean measures of response strength. However, such evidence can be flawed because group means may not accurately portray the response curves of individual subjects in a conditioning experiment. Moreover, such evidence relies on strong assumptions about the way that what has been learned is expressed in responding. The current work presents a new analytical approach to reveal the rate of change in responding across the course of conditioning in individual animals. When applied to the conditioning and extinction data from a large sample of rats, this analysis confirms that responses are acquired and extinguish gradually and, in both cases, follow a decelerating learning curve. That is, changes in responding are largest at the start of conditioning or extinction and get progressively smaller as responding approaches an asymptote. However, rather than conforming to the specific shape predicted by an error-correction process, the results suggest that the amount learned increases according to a logarithmic function such that responding during conditioning and extinction is proportional to the log of the number of trials. The implications of these findings for models of associative learning are discussed. (PsycInfo Database Record (c) 2022 APA, all rights reserved).

Does the time-span of conditioning affect spontaneous recovery after extinction?

Gold-standard psychological treatments such as exposure therapy are significantly undermined by high relapse rates. Although exposure-based treatments are capable of extinguishing maladaptive behaviours, these behaviours often spontaneously re-emerge over time - a phenomenon known in experimental research as spontaneous recovery. Understanding the factors that underlie this process is essential to improving long-term treatment outcomes. One factor that is yet to be properly examined is the effect of the total span of time across which behaviours are learned. To date, only one study by Gallistel & Papachristos (2020) has explored this in mice. Their findings suggest that long spans of acquisition learning result in greater spontaneous recovery compared to short spans. We investigated the effect of conditioning span across 5 experiments using rats. Contrary to Gallistel & Papachristos, our results found no difference in recovery between rats conditioned over a long span versus a short span, following short, intermediate and long delay intervals. This suggests that the span of conditioning does not affect the magnitude of recovery, nor the rate at which recovery emerges. Unexpectedly, conditioning span did appear to influence the strength of responding during acquisition, such that longer conditioning spans led to higher levels of responding. This finding could indicate that the learning process operates over a long time period beyond the original training episode. However, further research is needed to establish whether conditioning span influences the strength of what is learned, or instead the performance of a conditioned response.

Delaying extinction weakens the partial reinforcement extinction effect.

Conditioned responding that has been extinguished can spontaneously return when the conditioned stimulus (CS) is first presented after an extended delay. This spontaneous recovery of responding suggests that the memory of nonreinforced experience with the CS is impaired over the delay period. Rescorla (2007) provided evidence that this effect of time on nonreinforcement is not specific to extinction. He showed that a delay period can also reverse the reduction of responding established by a partial reinforcement schedule. Here we describe a series of experiments that attempted to confirm Rescorla's finding and additionally assessed the impact of the delay on another well-known consequence of partial reinforcement-the partial reinforcement extinction effect (PREE). Like Rescorla, we used a Pavlovian conditioning procedure with rats, measuring magazine activity during a CS that signaled food. Unlike Rescorla, we did not find that responding acquired under partial reinforcement spontaneously increased after a delay; however, we did observe a significant reduction in the PREE after that delay. We conclude that the passage of time has a selective effect on the retrieval of memories of nonreinforcement. Therefore, time produces spontaneous recovery by impairing retrieval of extinction memories but also weakens the PREE by impairing retrieval of memories of nonreinforcement that were acquired during partial reinforcement. (PsycInfo Database Record (c) 2022 APA, all rights reserved).

The effect of TMS on visual motion sensitivity: an increase in neural noise or a decrease in signal strength?

The underlying mechanisms of action of transcranial magnetic stimulation (TMS) are still a matter of debate. TMS may impair a subject's performance by increasing neural noise, suppressing the neural signal, or both. Here, we delivered a single pulse of TMS (spTMS) to V5/MT during a motion direction discrimination task while concurrently manipulating the level of noise in the motion stimulus. Our results indicate that spTMS essentially acts by suppressing the strength of the relevant visual signal. We suggest that TMS may induce a pattern of neural activity that complements the ongoing activation elicited by the sensory signal in a manner that partially impoverishes that signal.

Pre-exposure enhances recovery of conditioned responding after extinction.

Four experiments used a within-subjects design with rats to study the effects of preexposure on the restoration of fear responses (freezing) to an extinguished conditioned stimulus (CS). In each experiment, rats were preexposed to one CS (A), but not to another (B), and then were exposed to pairings of each of these CSs with an aversive unconditioned stimulus (US). In each experiment, there was less freezing to A than to B across extinction, showing a latent inhibitory effect of preexposure. There was no differential recovery to A and B following either a US reexposure (Experiment 1) or a delay interval (Experiment 2). However, when a delay interval included US reexposure, there was greater recovery to the preexposed CS, A, than to the nonpreexposed CS, B (Experiments 1, 3, and 4). These results suggest that the effects of US reexposure and delay combine to affect recovery from the depressive effects of CS-alone exposure. The results are consistent with the view that US reexposure produces better mediated conditioning of CSs that are strongly associated with the context. The results may additionally reflect an effect of preexposure on the learning produced by extinction.