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Reactive inhibition is a phrase coined by Clark L. Hull in his 1943 book titled Principles of Behavior. He defined it as:
Whenever any reaction is evoked in an organism there is left a condition or state which acts as a primary negative motivation in that it has an innate capacity to produce a cessation of the activity which produced the state.
Reactive inhibition is typically studied in the context of drive reduction. Hull likens it to fatigue through which humans become tired over time and thus less accurate and precise within a given task. [1] There is significant debate whether the process of reactive inhibition is due to fatigue or some other process. Nevertheless, it is a factor researchers need to consider in analyses of sustained performance due to its possible role in the results and analysis of research. [2]
Hull goes on to further explain the decay of performance through the use of a decay formula which can estimate the rate of performance deterioration.
Hull explains:
I dissipates exponentially with time t:
With the passage of time since its formation IR spontaneously dissipates approximately as a simple decay function of the time t elapsed, i.e.,
- (Hull, 1951, p. 74).
Hull's decay formula is somewhat awkward and might give rise to confusion. For example, I'R does not refer to the derivative of IR. A more convenient way of writing the formula would be as follows:
with . is the inhibition at the beginning of the time interval [0,t]. Note that if one takes the natural logarithm of both sides one obtains:
where and . The last formula is used in inhibition theory. [3]
Reactive inhibition is distinct from proactive inhibition. Reactive inhibition occurs after an initial response has been activated and set to be carried out. In contrast, proactive inhibition determines whether or not the response process is activated in the future and occurs before initial activation. [4] Reactive inhibition is considered to be a bottom-up processing process and associated with “lower level mechanisms of inhibition”, whereas proactive inhibition is considered more top-down processing and dealing with “higher level mechanisms”. [5]
Reactive inhibition may be important in everyday life during a process in which a decline in performance can be detrimental such as driving a car during rush hour. [2] For example, Kathaus, Washcer, & Getzmann (2018) found that older adults who showed a tendency towards reactive inhibition, determined through electroencephalography measures, showed higher “driving lane variability” and more impairment. Although older adults matched younger adults in their lane keeping abilities, they were unable to change lanes as effectively when they relied on reactive inhibition. [6]
Another study also revolving around younger vs older adults in the realm of inhibition found that older adults had decreased reactive inhibition but sustain proactive inhibition overall. By using a smart phone app, participants played a game in which two apples were falling from either side of the tree. They were to tap either apple but not press one of the apples if that apple turned brown or “rotten”. This is similar to a Stop Signal Task as described below. Some of these trials were primed for a person to expect a change and others not. What was found was a decreased ability in older adults to inhibit an action when they were not primed thus indicating a deficit in reactive inhibition. [7]
Researchers have also studied reactive inhibition within the context of ADHD. [8] It is commonly accepted that decreased inhibition abilities are a prominent aspect of the symptoms associated with ADHD. [9] Within the context of the Stop Signal Task studies point to an inability to switch attention the signal switches from a go signal, to stop, which can be compared to environmental changes in the world. Further, it is proven that reactive inhibition in particular is affected in individuals with ADHD and related ADHD symptoms, and may not even have an impact on proactive inhibition at all. [10] The ability to inhibit can impact children’s learning abilities and is a lack of reactive inhibition is present in many learning disorders. [11]
Reactive inhibition is also related to repetition performance, including learning. For example, Torok et al. (2017) recorded learning capabilities in 180 adults using the Alternating Serial Reaction Time Test. Results showed reactive inhibition had a profound effect on performance. Specifically, they showed that significantly more learning had occurred than was perceived at the end of the task, for reactive inhibition had affected the individual over time. They concluded that reactive inhibition may affect one’s rate of learning due to how it causes progressive decline within a task. It was stated to be a feature of performance within 90% of the participants, and thus playing a significant role in results. These findings have caused some researchers to question existing psychological theories. [2] For example, Rickard, Pan, and Albarracín present evidence that even well accepted psychological findings such as memory consolidation during sleep may be incorrect. [12] The increase in “memory” that supposedly occurs after sleep may just be due to reactive inhibition. It may have existed at the end of learning before sleeping occurred, and thus caused seemingly lower memory scores.
Reactive inhibition is often not recognized as a factor of performance in learning based experiments and thus can lead to incorrect results. [13] The presence of reactive inhibition can result in decreased performance over time and thus decrease the level of supposed learning. If tested at a later time, however, when reactive inhibition is not present one may see true measures of learning.
Reactive inhibition within experimental settings is most commonly measured through the stop-signal task (SST). In the SST, a “go-signal” is presented to the participant to indicate that he or she should complete an action. Then, in some instances, a “stop-signal” is also presented to the participant indicate he or she should abandon the previously initiated action. This stop signal is presented within hundreds of milliseconds of receiving the go signal. [14] What is important within this task is the stop signal reaction time, which indicates how long it takes reactive inhibition to be triggered and thus for the action to be ceased. [4] Shorter times indicate a person has better reactive inhibition skills, and thus able to more quickly switch from the activation of some response to the abandoning of that goal through reactive inhibition. [15]
Due to the simplicity of the SST some modern researchers are against its use to make broader assumptions about inhibition. The SST’s demands on attention and inhibition are relatively low and simple in nature, unlike many real life situations, which makes them distrusting of its results. [16] However, the SST is thought to be more indicative by many of reactive inhibition as opposed to proactive. [17] In addition, reactive inhibition is thought to involve mechanisms that are not context dependent but generally the same amongst many conditions in which contexts are changing and the original “go-signal” explicitly or implicitly stated. [18]
Reactive inhibition is negatively affected by Parkinson's disease. [19] People with Parkinson’s disease have difficulty inhibiting their behaviors. It is proposed that levels of Dopamine are directly associated with one’s ability to inhibit. Proper inhibition is believed to be successful at some desired level of dopamine. Using the simon task, researchers showed that inhibitory processes were significantly depleted in Parkinson’s patients who were withdrawing from their medications, and thus experiencing low levels of dopamine. Performance has been also depleted among high levels of dopamine, indicating that there is an ideal middle ground level of dopamine in which reactive inhibition is most successful. These results suggest an association between dopamine levels and reactive inhibition. [20]
Reactive inhibition appears to be related to the subthalamic nucleus (STN), particularly within the active inhibition of “overriding the behavior”. [21] The STN is in charge of sending a signal to “inhibit thalamo-cortical activation”. Thus reaction then causes GABA driven inhibitory signals to be sent to the thalamus which inhibits the behavior. [22] Although reactive inhibition is supported by early STN activity relative to the time of responses, proactive inhibition is defined by more continuous STN activity. [21]
One study has also shown that significant damage to the prefrontal cortex, particularly the right superior medial frontal region, can result in a lack of inhibitory control. When this particular region was damaged patients relied more on last second reactive inhibition to avoid performing inappropriate behaviors. [23]
A neurotransmitter is a signaling molecule secreted by a neuron to affect another cell across a synapse. The cell receiving the signal, or target cell, may be another neuron, but could also be a gland or muscle cell.
The substantia nigra (SN) is a basal ganglia structure located in the midbrain that plays an important role in reward and movement. Substantia nigra is Latin for "black substance", reflecting the fact that parts of the substantia nigra appear darker than neighboring areas due to high levels of neuromelanin in dopaminergic neurons. Parkinson's disease is characterized by the loss of dopaminergic neurons in the substantia nigra pars compacta.
Dopamine is a neuromodulatory molecule that plays several important roles in cells. It is an organic chemical of the catecholamine and phenethylamine families. Dopamine constitutes about 80% of the catecholamine content in the brain. It is an amine synthesized by removing a carboxyl group from a molecule of its precursor chemical, L-DOPA, which is synthesized in the brain and kidneys. Dopamine is also synthesized in plants and most animals. In the brain, dopamine functions as a neurotransmitter—a chemical released by neurons to send signals to other nerve cells. Neurotransmitters are synthesized in specific regions of the brain, but affect many regions systemically. The brain includes several distinct dopamine pathways, one of which plays a major role in the motivational component of reward-motivated behavior. The anticipation of most types of rewards increases the level of dopamine in the brain, and many addictive drugs increase dopamine release or block its reuptake into neurons following release. Other brain dopamine pathways are involved in motor control and in controlling the release of various hormones. These pathways and cell groups form a dopamine system which is neuromodulatory.
The basal ganglia (BG) or basal nuclei are a group of subcortical nuclei found in the brains of vertebrates. In humans and other primates, differences exist, primarily in the division of the globus pallidus into external and internal regions, and in the division of the striatum. Positioned at the base of the forebrain and the top of the midbrain, they have strong connections with the cerebral cortex, thalamus, brainstem and other brain areas. The basal ganglia are associated with a variety of functions, including regulating voluntary motor movements, procedural learning, habit formation, conditional learning, eye movements, cognition, and emotion.
Dopaminergic pathways in the human brain are involved in both physiological and behavioral processes including movement, cognition, executive functions, reward, motivation, and neuroendocrine control. Each pathway is a set of projection neurons, consisting of individual dopaminergic neurons.
Dopamine receptors are a class of G protein-coupled receptors that are prominent in the vertebrate central nervous system (CNS). Dopamine receptors activate different effectors through not only G-protein coupling, but also signaling through different protein interactions. The neurotransmitter dopamine is the primary endogenous ligand for dopamine receptors.
Hypokinesia is one of the classifications of movement disorders, and refers to decreased bodily movement. Hypokinesia is characterized by a partial or complete loss of muscle movement due to a disruption in the basal ganglia. Hypokinesia is a symptom of Parkinson's disease shown as muscle rigidity and an inability to produce movement. It is also associated with mental health disorders and prolonged inactivity due to illness, amongst other diseases.
The pars compacta (SNpc) is one of two subdivisions of the substantia nigra of the midbrain ; it is situated medial to the pars reticulata. It is formed by dopaminergic neurons. It projects to the striatum and portions of the cerebral cortex. It is functionally involved in fine motor control.
Medium spiny neurons (MSNs), also known as spiny projection neurons (SPNs), are a special type of inhibitory GABAergic neuron representing approximately 90% of neurons within the human striatum, a basal ganglia structure. Medium spiny neurons have two primary phenotypes : D1-type MSNs of the direct pathway and D2-type MSNs of the indirect pathway. Most striatal MSNs contain only D1-type or D2-type dopamine receptors, but a subpopulation of MSNs exhibit both phenotypes.
The reward system is a group of neural structures responsible for incentive salience, associative learning, and positively-valenced emotions, particularly ones involving pleasure as a core component. Reward is the attractive and motivational property of a stimulus that induces appetitive behavior, also known as approach behavior, and consummatory behavior. A rewarding stimulus has been described as "any stimulus, object, event, activity, or situation that has the potential to make us approach and consume it is by definition a reward". In operant conditioning, rewarding stimuli function as positive reinforcers; however, the converse statement also holds true: positive reinforcers are rewarding.The reward system motivates animals to approach stimuli or engage in behaviour that increases fitness. Survival for most animal species depends upon maximizing contact with beneficial stimuli and minimizing contact with harmful stimuli. Reward cognition serves to increase the likelihood of survival and reproduction by causing associative learning, eliciting approach and consummatory behavior, and triggering positively-valenced emotions. Thus, reward is a mechanism that evolved to help increase the adaptive fitness of animals. In drug addiction, certain substances over-activate the reward circuit, leading to compulsive substance-seeking behavior resulting from synaptic plasticity in the circuit.
Synaptic gating is the ability of neural circuits to gate inputs by either suppressing or facilitating specific synaptic activity. Selective inhibition of certain synapses has been studied thoroughly, and recent studies have supported the existence of permissively gated synaptic transmission. In general, synaptic gating involves a mechanism of central control over neuronal output. It includes a sort of gatekeeper neuron, which has the ability to influence transmission of information to selected targets independently of the parts of the synapse upon which it exerts its action.
In psychology, impulsivity is a tendency to act on a whim, displaying behavior characterized by little or no forethought, reflection, or consideration of the consequences. Impulsive actions are typically "poorly conceived, prematurely expressed, unduly risky, or inappropriate to the situation that often result in undesirable consequences," which imperil long-term goals and strategies for success. Impulsivity can be classified as a multifactorial construct. A functional variety of impulsivity has also been suggested, which involves action without much forethought in appropriate situations that can and does result in desirable consequences. "When such actions have positive outcomes, they tend not to be seen as signs of impulsivity, but as indicators of boldness, quickness, spontaneity, courageousness, or unconventionality." Thus, the construct of impulsivity includes at least two independent components: first, acting without an appropriate amount of deliberation, which may or may not be functional; and second, choosing short-term gains over long-term ones.
The external globus pallidus combines with the internal globus pallidus (GPi) to form the globus pallidus, an anatomical subset of the basal ganglia. Globus pallidus means "pale globe" in Latin, indicating its appearance. The external globus pallidus is the segment of the globus pallidus that is relatively further (lateral) from the midline of the brain.
The internal globus pallidus, and the external globus pallidus (GPe) make up the globus pallidus. In rodents its homologue is known as the entopeduncular nucleus. The GPi is one of the output nuclei of the basal ganglia. The GABAergic neurons of the GPi send their axons to the ventral anterior nucleus (VA) and the ventral lateral nucleus (VL) in the dorsal thalamus, to the centromedian complex, and to the pedunculopontine complex.
In psychology and neuroscience, executive dysfunction, or executive function deficit is a disruption to the efficacy of the executive functions, which is a group of cognitive processes that regulate, control, and manage other cognitive processes. Executive dysfunction can refer to both neurocognitive deficits and behavioural symptoms. It is implicated in numerous psychopathologies and mental disorders, as well as short-term and long-term changes in non-clinical executive control. Executive dysfunction is the mechanism underlying ADHD paralysis, and in a broader context, it can encompass other cognitive difficulties like planning, organizing, initiating tasks and regulating emotions. It is a core characteristic of ADHD and can elucidate numerous other recognized symptoms.
Basal ganglia disease is a group of physical problems that occur when the group of nuclei in the brain known as the basal ganglia fail to properly suppress unwanted movements or to properly prime upper motor neuron circuits to initiate motor function. Research indicates that increased output of the basal ganglia inhibits thalamocortical projection neurons. Proper activation or deactivation of these neurons is an integral component for proper movement. If something causes too much basal ganglia output, then the ventral anterior (VA) and ventral lateral (VL) thalamocortical projection neurons become too inhibited, and one cannot initiate voluntary movement. These disorders are known as hypokinetic disorders. However, a disorder leading to abnormally low output of the basal ganglia leads to reduced inhibition, and thus excitation, of the thalamocortical projection neurons which synapse onto the cortex. This situation leads to an inability to suppress unwanted movements. These disorders are known as hyperkinetic disorders.
Blocq's disease was first considered by Paul Blocq (1860–1896), who described this phenomenon as the loss of memory of specialized movements causing the inability to maintain an upright posture, despite normal function of the legs in the bed. The patient is able to stand up, but as soon as the feet are on the ground, the patient cannot hold himself upright nor walk; however when lying down, the subject conserved the integrity of muscular force and the precision of movements of the lower limbs. The motivation of this study came when a fellow student Georges Marinesco (1864) and Paul published a case of parkinsonian tremor (1893) due to a tumor located in the substantia nigra.
Inhibitory control, also known as response inhibition, is a cognitive process – and, more specifically, an executive function – that permits an individual to inhibit their impulses and natural, habitual, or dominant behavioral responses to stimuli in order to select a more appropriate behavior that is consistent with completing their goals. Self-control is an important aspect of inhibitory control. For example, successfully suppressing the natural behavioral response to eat cake when one is craving it while dieting requires the use of inhibitory control.
Gordon Logan is the Centennial Professor of Psychology at Vanderbilt University. A cognitive and mathematical psychologist, Logan is well known for his work on cognitive control and inhibition of cognitive and motor activity, divided attention and the nature of the human brain’s processing limitations, and the fundamental characterization of attention deficit hyperactivity disorder ADHD. He has also done extensive research on the hierarchical control of skilled copytyping, which he views as a useful model for hierarchically organized complex human skills in general. He collaborates on research that applies mathematical models to neural and behavioral data.
The cortico-basal ganglia-thalamo-cortical loop is a system of neural circuits in the brain. The loop involves connections between the cortex, the basal ganglia, the thalamus, and back to the cortex. It is of particular relevance to hyperkinetic and hypokinetic movement disorders, such as Parkinson's disease and Huntington's disease, as well as to mental disorders of control, such as attention deficit hyperactivity disorder (ADHD), obsessive–compulsive disorder (OCD), and Tourette syndrome.