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Determinants of saccade latency: a non-exhaustive review
Because of the variability of saccadic latency distributions, many papers have focused on and investigated the factors that can affect the reaction times. These factors have often been categorized as either bottom-up factors, that is to say effects caused by the properties of the stimuli or its context, or top-down factors, such as goal-oriented saccades or expectation. This section provides a non-exhaustive review of the existing literature on this dichotomy.
Bottom-up factors have been extensively studied for decades, as they constitute a window for understanding how the visual processes work. One of the first factors that have been highlighted is the stimulus intensity. Wheeless, Cohen, and Boynton (1967) conducted a pioneer study manipulating the luminance of the target and its contrast with the background. After determining the foveal threshold (i.e., the minimum amount of luminance increment on a uniform background that can be detected by the individual during fixation), participants had to follow the target step of stimuli with varying luminance in either a high-contrast condition, in which the projection screen was not illuminated, or a low-contrast condition, in which the screen was illuminated with the same luminance as the target. The saccadic latency distributions changed drastically as a function of the luminance: the average reaction time increased up to 600ms for the lowest luminance and decreased down to 250ms with the highest luminance (Figure 7), an outcome that was observed regardless of the contrast condition. Their results were replicated by several studies with humans (e.g., Bell, Meredith, Van Opstal, & Munoz, 2006; Carpenter, 2004; Kalesnykas & Hallett, 1994; Ludwig, Gilchrist, & McSorley, 2004), monkeys (e.g., Boch, Fischer, & Ramsperger, 1984; Marino, Levy, & Munoz, 2015; Marino & Munoz, 2009) and express saccades (e.g., Boch et al., 1984; Marino et al., 2015). Interestingly, Ludwig et al. (2004) observed that the spatial frequency of Gabor patch targets also had an inversely proportional impact on reaction times. The suggested explanation for the decrease in latency as a function of luminance is that stimulus intensity reduces the processing time along the visual pathway (Barbur, Wolf, & Lennie, 1998; Boch et al., 1984).
Another issue emerged around the same time as stimulus intensity about the effect of stimulus temporal organization on saccadic latencies, and more precisely, the impact of a stimulus-onset-asynchrony (SOA). There are two kinds of SOA, either negative or positive. A negative SOA happens when the fixation stimulus is extinguished before the target stimulus onset and causes a gap effect. A positive SOA consists in the target stimulus appearing while the fixation stimulus remains on the screen, causing an overlap effect. Note that the classical step paradigm used to study saccadic latencies has a null SOA, where the fixation stimulus offset happens at the exact same time as the target stimulus onset. Saslow (1967) was the first to use what has been called subsequently the gap and overlap paradigms. He tested sixteen asynchronies from a negative SOA of 400ms to a positive SOA of 350ms with random amplitude and direction steps (4° or 8° and left or right). In comparison to the typical synchrony between the fixation-offset and target-onset (i.e., SOA = 0; step paradigm), triggering saccadic latency around 200ms, the author observed an increase in latency to about 250ms during the overlap and decreased to about 150ms during the gap (Figure 8).
The neural basis of saccades: what are the neuronal reasons for saccadic latencies to be so long?
Saccadic eye movements involve both sensory functions and motor skills and therefore require a sensory-motor interaction: the visual stimulation will be transformed into a motor command to produce a saccade toward that stimulus. Several areas responsible for sensory, attentional, intentional, mnemonic and motor processes are involved in the production of saccades. This section does not aim at reviewing all of these processes, but rather at evoking three of them –the frontal eye field, the superior colliculus and the reticular formation– in order to depict what and how underlying processes cause the latency of a saccade.
The triggering of voluntary saccades is essentially based on a network of frontal areas. The frontal eye field (FEF) in the prefrontal cortex is known to disengage fixations and is involved in saccade triggering for exploration of the visual environment (Johnston & Everling, 2011; Pierrot-Deseilligny, Rivaux, Gaymard, Müri, & Vermersch, 1995), since its lesion is associated with an increase of saccadic latencies (Rivaud, Müri, Gaymard, Vermersch, & Pierrot-Deseilligny, 1994; Schiller, Sandell, & Maunsell, 1987). The FEF enables the production of voluntary saccades via projections to the superior colliculus, which will integrate visual information, as well as other sensory information and turn them into a driving command. These areas also project to basal ganglia, which is a key structure in controlling the production of voluntary movements (Hikosaka, Takikawa, & Kawagoe, 2000). The basal ganglia control the production of saccades by maintaining a tonic inhibition of the superior colliculus and they contribute to the initiation of saccades by removing this inhibition. The superior colliculus (SC) plays a central role in the sensorimotor integration associated with the production of saccades (King, 2004) because it receives afferences from sensory and sensorimotor areas and projects on pre-motor and motor structures of the brainstem circuitry. It is part of the final common route to reactive saccades and voluntary saccades for the production of rapid eye movements. The lesion of the SC will not prevent saccade production but induces a latency increase and accuracy impairment (Hanes & Wurtz, 2001; Schiller et al., 1987). Finally, the saccadic generator allowing the production of horizontal saccades is localized at the level of the reticular formation of the brainstem. The reticular formation is a set of interconnected nuclei that are located throughout the brainstem whose functions are modulatory and premotor. It generates an activation that is transmitted to the motor neurons of the oculomotor nuclei whose role is to activate the extraocular agonist muscles and inhibit the antagonists to produce a saccade in a given direction.
The modulation of saccadic amplitude as an illustration of saccadic plasticity
The spatial allocation of saccades concerns the direction of the displacement but also the accuracy and its precision, which are quantified through the saccadic amplitude. Usually, saccades are hypometrics (i.e., undershooting the target) with some saccadic endpoint variability. Classically, this variation is viewed as the outcome of neural noise occurring during sensorimotor processing (Faisal, Selen, & Wolpert, 2009; van Beers, 2007). However, in behavior analysis theory, variability is regarded as an operant essential to learning that might be placed under the control of reinforcement (e.g., Neuringer, 2002; Page & Neuringer, 1985). To further support the plasticity of the saccadic system, Paeye and Madelain (2011) probed the extent of control one can have over saccadic amplitude variability. Participants were required to make saccades toward a target horizontally stepping with an amplitude ranging from 9.5° to 14.2° while their saccadic amplitude gain was recorded. The gain is defined as the ratio between the saccadic amplitude and the target displacement; when the eye lands exactly on the target, the gain is equal to one; if the eye undershoots, the gain is inferior to 1 and if the eye overshoots, the gain is superior to 1. The saccadic gain is used to normalize saccadic amplitude when using several target amplitudes, which would otherwise prevent a direct comparison. During baseline, the saccadic gain was on average equal to 1 with some variability (standard deviation, i.e., SD, around 0.05) for all participants (Figure 19C-D). During learning, the authors induced high levels of variability while keeping constant the median gain by reinforcing the least frequent amplitudes with the contingent presentation of an auditory stimulus. Importantly, the post-saccadic target position was stabilized on the fovea so that the only variable inducing the changes in variability would be the tone (this was done by extinguishing the target during the eye flight and displaying it at the eye location after the saccade). Figure 19A and Figure 19B represent the saccadic gain distribution for one participant and illustrate well the large variability that was induced by the contingent presentation of an auditory stimulus on specific saccadic amplitude variations and disappeared once repetition was reinforced (recovery).
Table of contents :
ACKNOWLEDGEMENT
ABSTRACT
PREFACE
CONCEPTS & THEORETICAL FRAMEWORK
CHAPTER 1: SACCADIC EYE MOVEMENTS AND DECISION
1.1. Vision: a selective review
1.1.1. The visual field and visual perception
1.1.2. Eye movements
1.2. Saccadic eye movements
1.2.1. Characteristics of saccades: amplitude, duration, peak velocity, latency
1.2.2. Determinants of saccade latency: a non-exhaustive review
1.2.3. The neural basis of saccades: what are the neuronal reasons for saccadic latencies to be so long?
1.2.4. A common sensorimotor model: saccadic decision-making
CHAPTER 2: THE PLASTICITY OF THE SACCADIC SYSTEM AND THE EFFECTS OF REINFORCEMENT: SACCADE AS AN OPERANT RESPONSE
2.1. Effect of reinforcement on spatial allocation of saccades
2.1.1. Target selection according to behavior analysis
2.1.2. The modulation of saccadic amplitude as an illustration of saccadic plasticity
2.1.3. The discriminative control of saccadic adaptation: differential saccadic responses can be placed under stimulus control
2.2. Effect of reinforcement on temporal allocation of saccades
2.2.1. Using reinforcement on saccades incidentally impacts the temporal dimension of saccades
2.2.2. Reinterpreting the conventional determinants of saccade latency as antecedent stimulus
2.2.3. Direct effect of reinforcement contingencies on saccadic latencies
GENERAL QUESTION
STUDY 1: CONTROL OF SACCADIC LATENCY IN A DYNAMIC ENVIRONMENT:
ALLOCATION OF SACCADES IN TIME FOLLOWS THE MATCHING LAW
CHAPTER 3: CHOICE OF SACCADIC LATENCY
I. CONTEXT
II. METHODS
2.1. Participants
2.2. Apparatus
2.3. Procedure
2.4. Acquisition and data analysis
III. RESULTS
IV. DISCUSSION
4.1. SRTs and the matching law
4.2. SRTs and reinforcement
4.3. SRTs are not a function of reward expectancy
4.4. Effects of a dynamic environment on saccades
4.5. Costs and benefits of saccades
4.6. Conclusion
STUDY 2: REINFORCEMENT REDUCES THE SIZE-LATENCY PHENOMENON: A COSTBENEFIT EVALUATION OF SACCADE TRIGGERING
CHAPTER 4: SACCADIC LATENCY DEPENDS ON BENEFICIAL CONSEQUENCES
I. CONTEXT
II. METHODS
2.1. Participants
2.2. Apparatus
2.3. Procedure
2.4. Acquisition and data analysis
III. RESULTS
IV. DISCUSSION
4.1. The size-latency phenomenon is not a function of uncertainty
4.2. A cost-benefit evaluation of saccade latencies
4.3. Saccade latencies and arbitrary reinforcement
4.4. Conclusion
STUDY 3: DISCRIMINATIVE CONTROL OF SACCADIC REACTION TIMES USING A NOVEL LATENCY-CONTINGENT PARADIGM
CHAPTER 5: STIMULUS CONTROL OF SACCADIC LATENCY
I. CONTEXT
II. METHODS
2.1. Participants
2.2. Apparatus
2.3. Procedure
2.4. Acquisition and data analysis
III. RESULTS
IV. DISCUSSION
4.1. Inducing and maintening discriminative control of latencies
4.2. Reinforcers
4.3. Saccadic latencies and Discriminative control
4.4. Saccadic latency and Associative learning
4.5. Conclusion
STUDY 4 (PILOT): CLASSICAL CONDITIONING OF SACCADIC LATENCIES USING GAP AND OVERLAP PARADIGMS
CHAPTER 6: ASSOCIATIVE LEARNING OF SACCADIC LATENCY
I. CONTEXT
II. METHODS
2.1. Participants
2.2. Apparatus
2.3. Procedure
2.4. Acquisition and data analysis
III. RESULTS
IV. DISCUSSION
4.1. SRTs and classical conditioning
4.2. Gap and overlap as unconditional stimuli
4.3. Saccades and associative learning
4.4. Conclusion
DISCUSSION & PERSPECTIVES
CHAPTER 7: DOES SACCADIC LATENCY DEPEND ON A FUNCTIONAL RELATION?
1. SCOPE OF THE MAIN EXPERIMENTAL RESULTS
2. TEMPORAL CONTROL OF SACCADIC LATENCIES
2.1. Reaction times are an operant dimension of saccades
2.2. Saccadic latencies and decision
2.3. Temporal discrimination
3. PLASTICITY OF THE SACCADIC SYSTEM AND ITS IMPLICATION FOR EYE MOVEMENTS
4. LIMITS AND RESEARCH PROSPECTS
5. CONCLUSION
REFERENCES .
