While emotional dysregulation is a broad construct, the current paper adopts a narrow approach to facilitate translational neuroscience research on pediatric anxiety. The paper first presents data on an adapted version of the antisaccade task and then integrates these data into a research framework. Data on an adapted version of the antisaccade task were collected in 57 youth, including 35 seeking treatment for an anxiety disorder. Associations were examined between performance on the antisaccade task and (a) age, (b) performance on other cognitive-control tasks (i.e., the stop-signal delay and flanker tasks), and (c) level of anxiety symptoms. Better performance on the antisaccade task occurred in older relative to younger subjects and correlated with better performance on the flanker task. Across the 57 youth, higher levels of anxiety correlated with shorter latency for correct antisaccades. These data can be placed within a three-step framework for translational neuroscience research. In the first step, a narrow index of emotion dysregulation is targeted. In the second step, this narrow index is linked to other correlated indicators of the same underlying narrow latent construct. In the third and final step, associations are examined with clinical outcomes and response to treatment.

Latency hinders a mobile robot teleoperator's ability to perform remote tasks. However, this effect is not well modeled. This paper develops a model for teleoperator steering behavior as a PD controller based on projected lateral displacement, which was tuned to reflect user performance determined by a 31-subject user study under constant and variable latency (having mean latencies between 0 and 750 ms). Additionally, we determined that operator performance under variable latency could be mapped to the expected performance of an equivalent constant latency. We then tested additional latency distributions in simulation and demonstrated equivalent steering performance among several different latency distributions.

Bovine herpesvirus 1 (BHV-1) causes a variety of diseases and is globally distributed. It infects via mucosal epithelium, leading to rapid lytic replication and latent infection, primarily in sensory ganglia. Large amounts of virus can be excreted by the host on primary infection or upon recrudescence of latent infection, resulting in disease spread. The bovine immune response to BHV-1 is rapid, robust, balanced, and long-lasting. The innate immune system is the first to respond to the infection, with type I interferons (IFNs), inflammatory cytokines, killing of infected host cells, and priming of a balanced adaptive immune response. The virus possesses a variety of immune evasion strategies, including inhibition of type I IFN production, chemokine and complement binding, infection of macrophages and neutrophils, and latency. BHV-1 immune suppression contributes to the severity of its disease manifestations and to the bovine respiratory disease complex, the leading cause of cattle death loss in the USA.

This study was conducted to investigate the pattern of plasma carotenoid concentration (PCC) in lambs switching from a low to a high dietary carotenoid level. A total of 12 Romane lambs were individually penned indoors and fed a low dietary carotenoid level for 23 days (period 1) and then a high dietary carotenoid level for 15 days (period 2). At the beginning of period 2, the lambs were 15 weeks old and weighed 29.9 kg (s.d. 2.7) on average. Lambs were fed daily (dry matter) 0.558 kg alfalfa pellets, 0.181 kg straw and 0.181 kg barley. Plasma content of total carotenoids was measured daily in period 2 by spectrophotometry. PCC (μg/l) varied with the animal (P < 0.001) and with time elapsed since the beginning of alfalfa distribution (P < 0.001). Mean PCC was 8 μg/l (s.d. 3.3) at the beginning of period 2, then increased curvilinearly with the time elapsed since the beginning of alfalfa distribution. As early as 24 h on the alfalfa diet, PCC was already higher than before the switch (P < 0.001). Mean PCC continued to increase until day 6 on average and reached a plateau thereafter. We propose a monomolecular function to model this pattern, the equation obtained on the mean data being: PCC = 97 (s.e. 2.2) × (1−exp(−0.3378 (s.e. 0.0282)×d)), where r2 = 0.997, r.s.d. = 4.47, n = 15 and d = day. The percentage of variance explained by the model ranged between 95.9% and 99.2%, depending on the animal. The parameters of the monomolecular function varied among animals, confirming the interindividual variability in animal response. Plateau for PCC was reached slightly earlier for the six lambs with the lowest values of the asymptote than for the six lambs with the highest values of the asymptote.

Retinal ganglion cells (RGCs) are highly sensitive to changes in contrast, which is crucial for the detection of edges in a visual scene. However, in the natural environment, edges do not just vary in contrast, but edges also vary in the degree of blur, which can be caused by distance from the plane of fixation, motion, and shadows. Hence, blur is as much a characteristic of an edge as luminance contrast, yet its effects on the responses of RGCs are largely unexplored.

We examined the responses of rabbit RGCs to sharp edges varying by contrast and also to high-contrast edges varying by blur. The width of the blur profile ranged from 0.73 to 13.05 deg of visual angle. For most RGCs, blurring a high-contrast edge produced the same pattern of reduction of response strength and increase in latency as decreasing the contrast of a sharp edge. In support of this, we found a significant correlation between the amount of blur required to reduce the response by 50% and the size of the receptive fields, suggesting that blur may operate by reducing the range of luminance values within the receptive field. These RGCs cannot individually encode for blur, and blur could only be estimated by comparing the responses of populations of neurons with different receptive field sizes. However, some RGCs showed a different pattern of changes in latency and magnitude with changes in contrast and blur; these neurons could encode blur directly.

We also tested whether the response of a RGC to a blurred edge was linear, that is, whether the response of a neuron to a sharp edge was equal to the response to a blurred edge plus the response to the missing spatial components that were the difference between a sharp and blurred edge. Brisk-sustained cells were more linear; however, brisk-transient cells exhibited both linear and nonlinear behavior.

In the frog Xenopus laevis, the isthmotectal projection, which relays input from the ipsilateral eye, exhibits anatomical reorganization following surgical eye rotation performed during tadpole stages while the isthmotectal projection in the frog Rana pipiens fails to show reorganization. This plasticity has been shown to be dependent upon activation of the N-methyl-D-aspartate (NMDA) receptor located on tectal cell dendrites. The reorganization process in Xenopus is hypothesized to employ a Hebbian mechanism requiring correlated firing of ipsilateral and contralateral inputs to a given tectal cell; when an ipsilateral axon synapses onto a tectal cell that receives input from a contralateral axon with a matching receptive-field location, the correlation in activity triggers stabilization of the ipsilateral synapse. However, in neither Xenopus nor Rana do ipsilateral and contralateral inputs begin to fire simultaneously in response to a given visual stimulus; the ipsilateral input is delayed because it reaches the tectum indirectly, through a polysynaptic relay via the opposite tectum and nucleus isthmi. The objective of this experiment was to test whether there is a significant difference in this intertectal delay between Xenopus laevis and Rana pipiens in order to determine whether intertectal delay could be a contributing factor in this species-specific ability to exhibit visual plasticity. We have found that intertectal delay is 26.16 ms longer in Rana pipiens (36.53 ms) than in Xenopus laevis (10.37 ms).

Using two microelectrodes, recordings were made from pairs of like-signed cells at different depths in single layers (A or Al) of the cat's lateral geniculate nucleus (LGN). The cells were chosen to have near or overlapping receptive fields so that they could be stimulated simultaneously with a single spot or bar of light. Under these controlled conditions, paired X cells (n = 32 pairs) showed differences in latency from less than 10 to about 80 ms, but no latency differences were observed between paired Y cells (n = 3 pairs). Within XY pairs (n = 11) the Y cells responded faster than the X cells. A separate analysis of previously reported, singly recorded X cells (n= 131) also showed wide differences in X cell latencies.

The results confirm that temporal differences in signalling occur within the X pathway in the cat LGN (Mastronarde, 1981, 1987a; Humphrey & Weller, 1988a) and they show explicitly that the differences occur simultaneously, in single layers and at single retinotopic loci. No consistent relationship was found between timing and depth, but the possibility of weak, depth-dependent trends is considered in the Discussion.

Averaged grating-evoked cortical potentials were recorded from area 17 of awake cats. Peak latency of early components of the visual-evoked potential (VEP) response to stimulus onset increased as a function of spatial frequency, while amplitude tended to be largest at intermediate spatial frequencies. Latency increased and amplitude generally decreased to lower spatial-frequency stimuli (<0.25 cycle/deg) in the presence of a uniform flickering field (UFF). The UFF had a relatively small or opposite effect on peak latency and amplitude for higher spatial-frequency stimuli (>0.50 cycle/deg). The VEP response to stimulus offset was present only at low spatial frequencies and was virtually eliminated by the presence of the UFF. The effects were similar whether the target and UFF background were simultaneously presented or briefly separated; however, the UFF had no effect when the two were spatially separated. The effects of the UFF background on VEP onset response increased with increasing temporal frequency from 2–8 Hz; offset responses were affected similarly at all temporal frequencies. These effects are similar to those observed in humans and suggest that two spatio-temporally tuned mechanisms contribute to the early VEP response. In the cat, the mechanisms seem to correspond to X and Y cells in the dorsal lateral geniculate nucleus.

Infection of cattle by bovine herpesvirus type 1 (BHV-1) can lead to upper respiratory tract disorders, conjunctivitis, genital disorders and immune suppression. BHV-1-induced immune suppression initiates bovine respiratory disease complex (BRDC), which costs the US cattle industry approximately 3 billion dollars annually. BHV-1 encodes at least three proteins that can inhibit specific arms of the immune system: (i) bICP0 inhibits interferon-dependent transcription, (ii) the UL41.5 protein inhibits CD8+ T-cell recognition of infected cells by preventing trafficking of viral peptides to the surface of the cells and (iii) glycoprotein G is a chemokine-binding protein that prevents homing of lymphocytes to sights of infection. Following acute infection of calves, BHV-1 can also infect and induce high levels of apoptosis of CD4+ T-cells. Consequently, the ability of BHV-1 to impair the immune response can lead to BRDC. Following acute infection, BHV-1 establishes latency in sensory neurons of trigeminal ganglia (TG) and germinal centers of pharyngeal tonsil. Periodically BHV-1 reactivates from latency, virus is shed, and consequently virus transmission occurs. Two viral genes, the latency related gene and ORF-E are abundantly expressed during latency, suggesting that they regulate the latency-reactivation cycle. The ability of BHV-1 to enter permissive cells, infect sensory neurons and promote virus spread from sensory neurons to mucosal surfaces following reactivation from latency is also regulated by several viral glycoproteins. The focus of this review is to summarize the biology of BHV-1 and how this relates to BRDC.

We measured the latency of 35 cells from V1 in two rhesus monkeys, to dynamic random dot stimuli monocular and binocularly presented. Mean latencies after non-dominant eye stimulation (97.9 ms) were longer than those for dominant eye (78.2 ms) and binocular (70.7 ms) stimulation. Differences between latencies for dominant eye and binocular stimulation were not statistically significant. For dominant eye, there was a significant statistical correlation between dominance strength and latency (R = −0.36; p = 0.03). We failed to find significant statistical differences between latencies for cells with temporal and nasal dominant receptive-field. We conclude that, in V1, the response latency is largely determined by the dominant eye, whereas interocular interactions do not seem to play a relevant role regarding response latency.

Given that the action potential output of retinal ganglion cells (RGCs) determines the nature of the visual information that is transmitted from the retina, an understanding of their intrinsic impulse firing characteristics is critical for an appreciation of the overall processing of visual information. Recordings from RGCs within an isolated whole-mount retina preparation showed that their normal impulse firing from the resting membrane potential (RMP) was linearly correlated in its frequency with the stimulus intensity. In addition to describing the relationship between the magnitude of the current injection and the resulting impulse frequency (F/I relationship), we have characterized the properties of individual action potentials when they are elicited from the RMP. In contrast, hyperpolarizing below the RMP revealed that RGCs displayed a time dependent anomalous rectification, manifested by the appearance of a depolarizing sag in their voltage response. When an adequate period of hyperpolarization was terminated, a fast phasic period of “rebound excitation” was observed, characterized by a brief phasic burst of impulse activity. When compared to equivalent action potential firing evoked by depolarizing from the RMP, rebound spiking was associated with a lower threshold and shorter latency for impulse activation as well as a prominent, phasic, burst-like doublet, or triplet of impulses. The rebound action potential had a more positive voltage overshoot and displayed a higher peak rate of rise in its upstroke than those correspondingly generated by depolarizing current pulses from the RMP. Blocking sodium spikes with TTX confirmed that the preceding hyperpolarization led to the recruitment and subsequent generation of a transient depolarizing voltage overshoot, which we have termed the net depolarizing overshoot (NDO). We propose that the NDO boosts the generation of sodium spikes by triggering rebound spikes on its upstroke and crest, thus accounting for the observed voltage dependent change in the firing pattern of RGCs.

Herpes simplex virus type 1 (HSV-1) and type 2 (HSV-2) are ubiquitous human pathogens. They share with other herpesviruses the ability to establish lifelong latent infection of the host. Periodic reactivation from latency is responsible for most of the clinical disease burden of HSV infection. This review focuses on what we have learned from molecular studies in model systems of HSV latency, and the implications these findings have for treating recurrent HSV disease.

The ventral intraparietal area (VIP) is located at the end of the dorsal stream. Its neurons are known to have receptive-field characteristics similar to those of MT and MST neurons, but little is known about the temporal characteristics of VIP cells' responses. How fast are directionally selective responses evoked in the ventral intraparietal area after viewing optic flow patterns, and what are the temporal properties of these neuronal responses? To examine these questions, we recorded the activity of 37 directionally selective ventral intraparietal area (VIP) neurons in two awake macaque monkeys in response to optic flow stimuli with presentation times ranging from 17 ms to 2000 ms. We found a minimum response latency of 45 ms, and a median latency of 152 ms. Of all neurons, 10% showed early response components only (response latency < 150 ms and no activity in 500–2000 ms interval after stimulus onset), 55% only late response components (response latency >150 ms and sustained activity in 500–2000 ms interval), and 35% both early and late response components. Early responses appeared to very brief stimulus presentations (33-ms duration), while the late responses required longer stimulus durations. The directional selectivity was independent of optic flow duration in all cells. These results suggest that only a subset of neurons in area VIP may contribute to the fast processing of optic flow, while showing that the temporal properties of VIP responses clearly differ from the temporal characteristics of neurons in areas MT and MST.

The effect of visual stimulus significance on saccade latency and accuracy in gaze shifts was investigated. Stimulus significance refers to the temporal proximity of an imperative stimulus. It was hypothesized that stimulus significance serves as a cue that influences the observer's expectancy for a forthcoming event. Twenty-one undergraduate students participated in two experiments involving monitoring of visual events. Stimuli were a sequence of 1,000 single-digit integers presented one at a time at 9° of visual angle to the left or right of a fixation point in random order. The subject was required to make a manual response after the presentation of a sequence of two odd integers. The probability of the subsequent integer being odd, a “target,” after the presentation of an odd integer was 0.75. The integer after a target was always an even integer. When stimulus location was unpredictable (Experiment 1), latency of visually guided saccades to the target was shorter (p < .01) than to the nontarget stimuli. Under the condition of predictable stimulus location (Experiment 2), anticipatory saccades to the target occurred earlier (p < .01), more frequently (p < .01), and more accurately (p < .05). Our results suggest that both timing and accuracy of gaze shift are affected by the observer's expectation of future events.