Blinks slow memory-guided saccades.

Memory-guided saccades are slower than visually guided saccades. The usual explanation for this slowing is that the absence of a visual drive reduces the discharge of neurons in the superior colliculus. We tested a related hypothesis: that the slowing of memory-guided saccades was due also to the more frequent occurrence of gaze-evoked blinks with memory-guided saccades compared with visually guided saccades. We recorded gaze-evoked blinks in three monkeys while they performed visually guided and memory-guided saccades and compared the kinematics of the different saccade types with and without blinks. Gaze-evoked blinks were more common during memory-guided saccades than during visually guided saccades, and the well-established relationship between peak and average velocity for saccades was disrupted by blinking. The occurrence of gaze-evoked blinks was associated with a greater slowing of memory-guided saccades compared with visually guided saccades. Likewise, when blinks were absent, the peak velocity of visually guided saccades was only slightly higher than that of memory-guided saccades. Our results reveal interactions between circuits generating saccades and blink-evoked eye movements. The interaction leads to increased curvature of saccade trajectories and a corresponding decrease in saccade velocity. Consistent with this interpretation, the amount of saccade curvature and slowing increased with gaze-evoked blink amplitude. Thus, although the absence of vision decreases the velocity of memory-guided saccades relative to visually guided saccades somewhat, the cooccurrence of gaze-evoked blinks produces the majority of slowing for memory-guided saccades.

Characterizing the spontaneous blink generator: an animal model.

Although spontaneous blinking is one of the most frequent human movements, little is known about its neural basis. We developed a rat model of spontaneous blinking to identify and better characterize the spontaneous blink generator. We monitored spontaneous blinking for 55 min periods in normal conditions and after the induction of mild dry eye or dopaminergic drug challenges. The normal spontaneous blink rate was 5.3 ± 0.3 blinks/min. Dry eye or 1 mg/kg apomorphine significantly increased and 0.1 mg/kg haloperidol significantly decreased the blink rate. Additional analyses revealed a consistent temporal organization to spontaneous blinking with a median 750 s period that was independent of the spontaneous blink rate. Dry eye and dopaminergic challenges significantly modified the regularity of the normal pattern of episodes of frequent blinking interspersed with intervals having few blinks. Dry eye and apomorphine enhanced the regularity of this pattern, whereas haloperidol reduced its regularity. The simplest explanation for our data is that the spinal trigeminal complex is a critical element in the generation of spontaneous blinks, incorporating reflex blinks from dry eye and indirect basal ganglia inputs into the blink generator. Although human subjects exhibited a higher average blink rate (17.6 ± 2.4) than rats, the temporal pattern of spontaneous blinking was qualitatively similar for both species. These data demonstrate that rats are an appropriate model for investigating the neural basis of human spontaneous blinking and suggest that the spinal trigeminal complex is a major element in the spontaneous blink generator.

Emotional valence and arousal effects on memory and hemispheric asymmetries.

This study examined predictions based upon the right hemisphere (RH) model, the valence-arousal model, and a recently proposed integrated model (Killgore & Yurgelun-Todd, 2007) of emotion processing by testing immediate recall and recognition memory for positive, negative, and neutral verbal stimuli among 35 right-handed women. Building upon methodologies of previous studies, we found that words presented to the right visual field/left hemisphere (RVF/LH) were recalled and recognized more accurately than words presented to the left visual field/right hemisphere (LVF/RH), and we found significant valence by visual field interactions. Some findings were consistent with one of the models evaluated whereas others were consistent with none of the models evaluated. Our findings suggest that an integration of the RH and valence-arousal models may best account for the findings with regard to hemispheric lateralization of memory for emotional stimuli.

Classical fear conditioning in the anxiety disorders: a meta-analysis.

Fear conditioning represents the process by which a neutral stimulus comes to evoke fear following its repeated pairing with an aversive stimulus. Although fear conditioning has long been considered a central pathogenic mechanism in anxiety disorders, studies employing lab-based conditioning paradigms provide inconsistent support for this idea. A quantitative review of 20 such studies, representing fear-learning scores for 453 anxiety patients and 455 healthy controls, was conducted to verify the aggregated result of this literature and to assess the moderating influences of study characteristics. Results point to modest increases in both acquisition of fear learning and conditioned responding during extinction among anxiety patients. Importantly, these patient-control differences are not apparent when looking at discrimination studies alone and primarily emerge from studies employing simple, single-cue paradigms where only danger cues are presented and no inhibition of fear to safety cues is required.