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PubMed1997

The abundant latency-associated transcripts of herpes simplex virus type 1 are bound to polyribosomes in cultured neuronal cells and during latent infection in mouse trigeminal ganglia.

During herpes simplex virus type 1 (HSV-1) latency, limited viral transcription takes place. This transcription has been linked to the ability of the HSV-1 genome to reactivate and consists of abundant 2.0- and 1.5-kb collinear latency-associated transcripts (LATs), spanned by minor hybridizing RNA (mLAT). The 1.5-kb LAT is derived from the 2.0-kb LAT by splicing, and both transcripts contain two large overlapping open reading frames. The molecular action mechanisms of the latency-associated gene expression are unknown, and no HSV-1 latency-encoded proteins have been convincingly demonstrated. We have cloned the entire latency-associated transcriptionally active HSV-1 DNA fragment (10.4 kb) under control of a constitutive promoter and generated a neuronal cell line (NA4) stably transfected with the viral LAT's region. NA4 cells produced the 2.0- and the 1.5-kb LATs. Northern blotting and reverse transcription-PCR analysis of RNA from NA4 cells and from trigeminal ganglia of mice latently infected with HSV-1 revealed that the two abundant LAT species were present in the polyribosomal RNA fractions. After addition of EDTA, which causes dissociation of mRNA-ribosome complexes, both LATs could be detected only in subpolyribosomal, but not in polyribosomal fractions. These results show that (i) HSV-1 LATs are bound to polyribosomes during latency in vivo, as well as in neuronal cells in vitro, and therefore might be translated, and that (ii) the NA4 cell line is a suitable tool with which to look for HSV-1 latency-encoded gene products.

Animals↗
PubMed2000

Rta of murine gammaherpesvirus 68 reactivates the complete lytic cycle from latency.

Herpesviruses are characterized as having two distinct life cycle phases: lytic replication and latency. The mechanisms of latency establishment and maintenance, as well as the switch from latency to lytic replication, are poorly understood. Human gammaherpesviruses, including Epstein-Barr virus (EBV) and human herpesvirus-8 (HHV-8), also known as Kaposi's sarcoma-associated herpesvirus (KSHV), are associated with lymphoproliferative diseases and several human tumors. Unfortunately, the lack of cell lines to support efficient de novo productive infection and restricted host ranges of EBV and HHV-8 make it difficult to explore certain important biological questions. Murine gammaherpesvirus 68 (MHV-68, or gammaHV68) can establish de novo lytic infection in a variety of cell lines and is also able to infect laboratory mice, offering an ideal model with which to study various aspects of gammaherpesvirus infection. Here we describe in vitro studies of the mechanisms of the switch from latency to lytic replication of MHV-68. An MHV-68 gene, rta (replication and transcription activator), encoded primarily by open reading frame 50 (ORF50), is homologous to the rta genes of other gammaherpesviruses, including HHV-8 and EBV. HHV-8 and EBV Rta have been shown to play central roles in viral reactivation from latency. We first studied the kinetics of MHV-68 rta gene transcription during de novo lytic infection. MHV-68 rta was predominantly expressed as a 2-kb immediate-early transcript. Sequence analysis of MHV-68 rta cDNA revealed that an 866-nucleotide intron 5' of ORF50 was removed to create the Rta ORF of 583 amino acids. To test the functions of MHV-68 Rta in reactivation, a plasmid expressing Rta was transfected into a latently infected cell line, S11E, which was established from a B-cell lymphoma in an MHV-68-infected mouse. Rta induced expression of viral early and late genes, lytic replication of viral DNA, and production of infectious viral particles. We conclude that Rta alone is able to disrupt latency, activate viral lytic replication, and drive the lytic cycle to completion. This study indicates that MHV-68 provides a valuable model for investigating regulation of the balance between latency and lytic replication in vitro and in vivo.

Animals↗
PubMed2002

Antibody to a lytic cycle viral protein decreases gammaherpesvirus latency in B-cell-deficient mice.

While antiviral antibody plays a key role in resistance to acute viral infection, the contribution of antibody to the control of latent virus infection is less well understood. Gammaherpesvirus 68 (gammaHV68) infection of mice provides a model well suited to defining contributions of specific immune system components to the control of viral latency. B cells play a critical role in regulating gammaHV68 latency, but the mechanism(s) by which B cells regulate latency is not known. In the experiments reported here, we determined the effect of passively transferred antibody on established gammaHV68 latency in B-cell-deficient (B-cell(-/-)) mice. Immune antibody decreased the frequency of cells reactivating ex vivo from latency in splenocytes (>10-fold) and peritoneal cells (>100-fold) and the frequency of cells carrying latent viral genome in splenocytes (>5-fold) and peritoneal cells (>50-fold). This effect required virus-specific antibody and was observed when total and virus-specific serum antibody concentrations in recipient B-cell(-/-) mice were <8% of those in normal mice during latent infection. Passive transfer of antibody specific for the lytic cycle gammaHV68 RCA protein, but not passive transfer of antibody specific for the v-cyclin protein or the latent protein M2, decreased both the frequency of cells reactivating ex vivo from latency and the frequency of cells carrying the latent viral genome. Therefore, antibody specific for lytic cycle viral antigens can play an important role in the control of gammaherpesvirus latency in immunocompromised hosts. Based on these findings, we propose a model in which ongoing productive replication is essential for maintaining high levels of latently infected cells in immunocompromised hosts. We confirmed this model by the treatment of latently infected B-cell(-/-) mice with the antiviral drug cidofovir.

Animals↗
PubMed2003

Maintenance of gammaherpesvirus latency requires viral cyclin in the absence of B lymphocytes.

Gammaherpesviruses establish a life-long chronic infection that is tightly controlled by the host immune response. We previously demonstrated that viruses lacking the gammaherpesvirus 68 (gammaHV68) viral cyclin (v-cyclin) exhibited a severe defect in reactivation from latency and persistent replication. In this analysis of chronic infection, we demonstrate that the v-cyclin is required for gammaHV68-associated mortality in B-cell-deficient mice. Furthermore, we identify the v-cyclin as the first gene product required for maintenance of gammaherpesvirus latency in vivo in the absence of B lymphocytes. While the v-cyclin was necessary for maintenance of latency in the absence of B cells, maintenance of v-cyclin-deficient viruses was equivalent to that of wild-type gammaHV68 in the presence of B cells. These results support a model in which maintenance of chronic gammaHV68 infection requires v-cyclin-dependent reactivation and reseeding of non-B-cell latency reservoirs in the absence of B cells and raise the possibility that B cells represent a long-lived latency reservoir maintained independently of reactivation. These results highlight distinct mechanisms for the maintenance of chronic infection in immunocompetent and B-cell-deficient mice and suggest that the different latency reservoirs have distinct gene requirements for the maintenance of latency.

Animals↗
PubMed2004

Role of NF-kappa B in cell survival and transcription of latent membrane protein 1-expressing or Epstein-Barr virus latency III-infected cells.

Epstein-Barr virus (EBV) latency III infection converts B lymphocytes into lymphoblastoid cell lines (LCLs) by expressing EBV nuclear and membrane proteins, EBNAs, and latent membrane proteins (LMPs), which regulate transcription through Notch and tumor necrosis factor receptor pathways. The role of NF-kappa B in LMP1 and overall EBV latency III transcriptional effects was investigated by treating LCLs with BAY11-7082 (BAY11). BAY11 rapidly and irreversibly inhibited NF-kappa B, decreased mitochondrial membrane potential, induced apoptosis, and altered LCL gene expression. BAY11 effects were similar to those of an NF-kappa B inhibitor, Delta N-I kappa B alpha, in effecting decreased JNK1 expression and in microarray analyses. More than 80% of array elements that decreased with Delta N-I kappa B alpha expression decreased with BAY11 treatment. Newly identified NF-kappa B-induced, LMP1-induced, and EBV-induced genes included pleckstrin, Jun-B, c-FLIP, CIP4, and I kappa B epsilon. Of 776 significantly changed array elements, 134 were fourfold upregulated in EBV latency III, and 74 were fourfold upregulated with LMP1 expression alone, whereas only 28 were more than fourfold downregulated by EBV latency III. EBV latency III-regulated gene products mediate cell migration (EBI2, CCR7, RGS1, RANTES, MIP1 alpha, MIP1 beta, CXCR5, and RGS13), antigen presentation (major histocompatibility complex proteins and JAW1), mitogen-activated protein kinase pathway (DUSP5 and p62Dok), and interferon (IFN) signaling (IFN-gamma R alpha, IRF-4, and STAT1). Comparison of EBV latency III LCL gene expression to immunoglobulin M (IgM)-stimulated B cells, germinal-center B cells, and germinal-center-derived lymphomas clustered LCLs with IgM-stimulated B cells separately from germinal-center cells or germinal-center lymphoma cells. Expression of IRF-2, AIM1, ASK1, SNF2L2, and components of IFN signaling pathways further distinguished EBV latency III-infected B cells from IgM-stimulated or germinal-center B cells.

Apoptosis↗
PubMed2000

Molecular circuitry regulating herpes simplex virus type 1 latency in neurons.

Herpes simplex virus (HSV) type 1 (HSV-1) enters nerve endings during a primary infection, is transported to sensory ganglia, and establishes latency within nuclei of a subpopulation of neurons. The latent state is characterized by absence of detectable HSV-1 antigen, minimal transcription of productive cycle genes, and high expression of 1.5- and 2-kb viral transcripts, termed the major latency-associated transcripts (LATs), within nuclei of a subpopulation of infected neurons. Transcription within the HSV-1 LAT genomic locus has been reported to both facilitate the establishment of latency in additional neurons and to increase the frequency of spontaneous and induced viral reactivation in animal model systems. More recent evidence suggests some possible mechanisms that may explain the relationship between LATs and both reactivation and establishment of latency. This review summarizes general aspects of latency, but focuses on the structure, expression, and function of LATs, and the interaction between host transcriptional regulators and viral gene expression that may impact latency and reactivation. A model that incorporates evidence from a number of experimental studies is proposed that summarizes the involvement of the LAT locus in the biology of HSV-1 latency.

Animals↗
PubMed1993

Latency--a reappraisal.

This paper discusses the specific metapsychology and developmental tasks of the latency period. It offers a Kleinian view of the phase and compares it with other current psychoanalytic theories. The emphasis is on the importance of ego and superego growth and integration during latency resulting in better contact with both external and internal reality. Character formation, social integration and learning are discussed as the specific developmental tasks of the period. Freud's original formulation that the latency period is a consequence of the resolution of the Oedipus complex is evaluated in the light of contemporary developments. I draw on the ideas of Klein and others such as Loewald, Burgner, Holder, Tyson to describe it as a process of progressive and more complex elaboration throughout latency, interconnected with superego development. This process of gradual working through is considered to be a fundamental feature of the period. This model of progressive maturation is illustrated with clinical material. The clinical concept of pseudo-latency is used to distinguish between the developmental achievement represented by the establishment of the latency organisation in contrast to a defensive structure (pseudo-latency) which hides pathology.

Child↗
PubMed1997

P3 latency change in aging and Parkinson disease.

OBJECTIVE: To evaluate whether age-related slowing of mental processing assessed by event-related potentials is more prominent in patients with Parkinson disease (PD) than in age-matched control subjects. DESIGN: Consecutive case series of patients with PD and an age-matched control group. SETTING: A university hospital in Nishinomiya, Japan. STUDY PARTICIPANTS: Twenty-eight nondemented patients with PD and 28 age-matched control subjects. MAIN OUTCOME MEASURES: The P3 component of the event-related potentials was elicited during a visual semantic discrimination task. The relation of the P3 latency and the reaction time (RT) to age within each group was evaluated using correlation and regression analysis. The relationship among the P3 latency, the RT, and age was also assessed by dividing both groups into younger (age < 60 years) and older (age > or = 60 years) subgroups. RESULTS: The P3 latency and the RT of patients with PD were significantly longer than those of the control subjects (P < .01 and P < .02, respectively). There was a significant correlation between the P3 latency and age in both the parkinsonian and control groups (P < .01 and P < .05, respectively). The slope (b = 3.54 ms/y) of the P3 latency vs age was steeper among the patients with PD than among the control subjects (b = 1.66 ms/y) at the Pz site. The P3 latency in the older parkinsonian group (n = 16) was significantly prolonged compared with that in the older control group (n = 16) (P < .01), while no difference was found between the younger patients (n = 12) and the younger control group (n = 12). Similar trends were found for the RTs (P < .05). Neither the P3 latency nor the RT was correlated with any variable (eg, medication, mental status, illness duration, or motor disability). CONCLUSION: The results provide evidence that patients with PD experience excessive cognitive slowing with advancing age.

Adult↗
PubMed1987

Latencies of visually guided saccades in unilateral hemispheric cerebral lesions.

Latencies of lateral visually guided saccades were studied in 60 patients without hemianopia who had unilateral focal lesions clearly visible on computed tomographic (CT) scan that were variously located in both cerebral hemispheres. Significantly asymmetrical latencies were found in 29 patients whose lesions had damaged the deep and posterior frontal region near the corpus callosum and/or, just inferior to this region, the anterior part of the internal capsule. In the 31 other patients, including those with lesions of the frontal eye fields (FEF), latencies were not significantly asymmetrical and the lesions spared the entire region just described. These topographical features suggest that the asymmetry of latencies is due to damage in a certain portion of the efferent pathways descending from the FEF. A significant increase in bilateral latency was observed in most patients whose lesions had damaged the posterior part of the parietal cortex and/or the underlying white matter. The parietal lobe could therefore exert an excitatory bilateral action on the triggering of visually guided saccades, probably mediated via the superior colliculus. A significant decrease in the bilateral or ipsilateral latency was often found in patients whose lesions had damaged the FEF or the underlying white matter. The frontal lobe could therefore exert a predominantly inhibitory bilateral action on this triggering, probably also mediated via the superior colliculus. However, an increase in contralateral latency in some patients with subcortical frontal lesions indicates that the FEF also probably have an excitatory action. This action could be transmitted directly (or indirectly via the superior colliculus) to the reticular premotor structures by tracts decussating partly through the corpus callosum.

Adult↗
PubMedDate not supplied

Nerve conduction velocity and evoked potential latencies in streptozotocin-diabetic rats: effects of treatment with an angiotensin converting enzyme inhibitor.

BACKGROUND: Diabetes mellitus is associated with deficits in cerebral function. Vascular disorders may play a role in the pathogenesis and provide a potential target for treatment. The present study examined if prevention and intervention treatment with the angiotensin converting enzyme inhibitor enalapril could improve peripheral and central neurophysiological deficits in streptozotocin-diabetic rats. METHODS: Sciatic nerve conduction velocities were measured prior to diabetes induction and again every three weeks. In the prevention study, the final nerve conduction measurements were performed at 15 weeks and in the intervention study at 24 weeks. Brain stem auditory and visual evoked potential latencies were measured every 3 weeks from 10 weeks after diabetes induction. In the prevention study, the final evoked potential measurements were performed at 16 weeks and in the intervention study at 25 weeks. Treatment with the angiotensin converting enzyme inhibitor enalapril was started directly after diabetes induction (prevention treatment) and after 15 weeks of diabetes (intervention treatment). RESULTS: Nerve conduction velocity, brain stem auditory and visual evoked potential latencies were impaired in diabetic rats. Enalapril prevented deficits in nerve conduction velocity (p < 0.001), brain stem auditory evoked potential latencies (p < 0.01) and visual evoked potential latencies (p < 0.005). Enalapril intervention treatment had no effect on nerve conduction velocity and on visual evoked potential latencies, but improved brain stem auditory evoked potential latencies (p < 0.05) after 10 weeks of treatment. CONCLUSION: Enalapril partially prevents the development of neurophysiological alterations in the peripheral and central nervous system and partially reverses deficits in brain stem auditory evoked potential latencies in STZ-diabetic rats.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed2003

Conduction latency along CA3 hippocampal axons from rat.

Relatively few physiological studies have been carried out on intrahippocampal axons. We have recorded compound potentials from fiber groups and the activity of individual axons at 22-25 degrees C to characterize the conduction in subsets of the broad fan-shaped CA3 pyramidal axonal tree, including the Schaffer collaterals and longitudinal branches. The same wide axonal branching was indicated by antidromic activation of individual CA3 pyramidal cells. The average compound action potential latency from the CA3 to the CA1 area (Schaffer collaterals) increased by 4.16 +/- 0.06 ms/mm separation between the stimulation and registration electrodes. The impulses spread 31% faster in the 45-degree oblique temporal than in the transverse direction across CA1. The latency of the longitudinal axons in the CA3 area increased by 6.19 +/- 0.19 ms/mm. More impressive than these direction-dependent differences in latency were the large differences between individual axons running in the same direction. For both the longitudinal axons and the Schaffer collaterals, there was a broad distribution of antidromic latencies for a given distance between the stimulation and recording points. Typically, the fastest impulses arrived in half the time of the slowest. The distribution of compound action potential latencies between two points in the tissue could be made narrower by surgical restriction of the thickness and width of the preparation. By comparison, the cerebellar parallel fibers showed a narrower distribution of their latencies than the Schaffer collaterals. Because the cerebellar fibers run more straight than Schaffer collaterals, this suggested that some of the latency differences of the latter were due to differences in the path length of the axons. One consequence of our findings is that synchronous firing of neighboring CA3 pyramidal cells does not necessarily give synchronous inputs to common target CA1 neurons.

Action Potentials↗
PubMed2005

The correlation between blood oxygenation level-dependent signal strength and latency.

PURPOSE: To investigate the relationship between signal strength and latency of the blood oxygenation level-dependent (BOLD) signal. MATERIALS AND METHODS: Several correlation analyses were performed on data obtained in a functional magnetic resonance imaging (fMRI) experiment, where subjects were presented with a simple visual stimulus. The BOLD signal strength was correlated with both the phase shift of the spectral density matrix and time-to-peak calculated from trial-averaged time courses. Correlation coefficients were calculated for visual stimuli of 2, 6, and 15 seconds in duration. RESULTS: Analyzing all functional runs for the same subject separately, i.e., including for each run all significantly activated voxels, we observed that correlations between phase shift and signal strength, as well as between time-to-peak and signal strength, decreased with increasing stimulus length. However, when analyses were restricted to voxels found activated in all functional runs, we observed similar correlations between BOLD signal strength and latency in all runs, independent of the length of stimulation. This result was again obtained for both latency measures: the spectral density phase shift and time-to-peak. CONCLUSION: For both latency measures, phase shift and time-to-peak, a high correlation between BOLD signal strength and latency was observed. We have shown that this correlation is independent of the length of visual stimulation. Thus, the correlation between BOLD signal strength and latency seems to be an inherent property of the BOLD response that is independent of the length of stimulation and can be observed using different methods for determining signal latency.

Adult↗
PubMed1994

H reflex latency in the healthy elderly.

The purpose of this study was to evaluate prospectively and analyze the relationship of tibial nerve H reflex latency to age, sex, leg length, and skin temperature in a large healthy elderly population. The H reflex was recorded bilaterally in 92% of 103 carefully screened individuals aged 60-88 years. The mean H reflex latency was 30.8 (SD = 2.6) and 30.7 (SD = 2.6) ms for right and left legs, respectively. A high correlation (r = 0.55, P < 0.05) was present between H reflex latency and leg length. No significant correlation existed for H reflex latency and age. The upper normal limit for the difference between right and left H reflex latencies was 1.8 ms. This limit is greater than that reported in the literature for younger individuals due to a larger standard deviation. These findings suggest that aging increases the between-leg variability of H reflex latency in individuals. This greater difference must be taken into account when using side-to-side H reflex latency comparison to detect unilateral pathology in the elderly.

Aged↗
PubMed2002

Effects of glibenclamide, metformin and insulin on the incidence and latency of death by oubain-induced arrhythmias in mice.

This study was performed to investigate possible effects of glibenclamide, insulin and metformin on the death latency and incidence caused by a cardiac glycoside, oubain. Mice of both sexes were injected with oubain (i.p. 20 mg x kg (-1), glibenclamide (s.c. 0.1-10 mg x kg (-1), insulin (s.c. 0.3-3 U kg (-)) and metformin (i.p. 200 mg x kg (-1)) and combinations of the last three drugs with oubain. Death latency was measured and lethality incidence was calculated. Death was assessed by visual observation. Plasma glucose level was evaluated from the tail blood. Glibenclamide (0.1 mg x kg (-)) prolonged the latency from 11.3 plus minus 1.2 to 15.8 plus minus 1.8 min but failed to decrease the incidence of death. At higher doses (1--10 mg x kg (-1)) it had no effects on the latency or the incidence. 0.3 U kg (-1)insulin decreased the incidence from 73.7 to 33.3% ( P< 0.05) without affecting the latency. However the higher dose (3 U kg (-1)) did not have any effects on the incidence or the latency. Oubain increased blood glucose level from 114.1 plus minus 3.8 (control) to 152.1 plus minus 5.3 mg x dl (-1). Metformin (200 mg x kg (-1)) did not affect either the latency or the incidence of death. While metformin did not decrease plasma glucose, insulin and higher doses of glibenclamide (1--10 mg x kg (-1)) markedly lowered glucose in blood. However, at the dose of 0.1 mg x kg (-1)glibenclamide did not alter the glucose level in the blood but prevented oubain from increasing it. Insulin (0.3 U kg (-1)) and, to some extent, glibenclamide (0.1 mg x kg (-)) but not metformin could be effective antiarrhythmic agents against oubain-induced arrhythmias.

Animals↗
PubMed1993

Neuronal control of herpes simplex virus latency.

Herpes simplex virus (HSV) is a common neurotropic virus, and latent infection of sensory ganglion neurons readily occurs in humans and in experimentally infected animals. During HSV latency, infectious virus and viral antigen are not detected, and HSV transcription is limited to specific RNA termed latency-associated transcript (LAT). In the present study, the effect of altered nervous system function on HSV latent infection was investigated in dorsal root ganglia (drg) of experimentally infected mice. Latent infection of lumbar drg was established by footpad inoculation of HSV. During latency, sciatic neurectomy was performed in order to modify the in vivo function of latently infected neurons, and HSV LAT and HSV DNA in drg were investigated. Neurectomy has been used in many neurobiological studies to alter neuronal RNA and protein expression. After neurectomy there was a marked decrease in the number of LAT-positive neurons and in the amount of ganglion LAT. This was determined by in situ and RNA (Northern) blot hybridization. The neurectomy-related decrease of HSV LAT was apparent 9-10 days after neurectomy and was more marked after 21 days. The decrease was noted both in drg latently infected with standard thymidine kinase-positive (TK+) HSV and in ganglia infected with mutant TK- HSV. Since TK- HSV is largely reactivation defective, it is concluded that the neurectomy-induced decrease of LAT was probably not the result of in vivo HSV reactivation. It is acknowledged, however, that abortive reactivation by TK- HSV may occur, and decrease of latency may have resulted from neuronal or other host mechanisms subsequent to this. In order to investigate residual HSV latency, in addition to viral transcription, HSV DNA in drg was evaluated by polymerase chain reaction techniques. Decrease of HSV DNA was noted after neurectomy in drg latently infected with either TK+ or TK- HSV. It is suggested that the decrease in LAT expression detected was due to the change in neuronal transcription which is part of the neurectomy-induced axon reaction. Decreased HSV LAT may have led to decreased HSV DNA and latency. The decrease in the molecular markers of HSV latency following neurectomy emphasized the importance of neuronal control mechanisms in the pathogenesis of HSV latent infection.

Animals↗
PubMed1993

The latency of the cat vestibulo-ocular reflex before and after short- and long-term adaptation.

Latencies of normal and adapted feline vestibulo-ocular reflex (VOR) were studied in five cats by applying +/- 20 degrees/s horizontal head velocity steps (4000 degrees/s2 acceleration) and measuring the elicited horizontal or vertical reflex eye responses. Normal VOR latency was 13.0 ms +/- 1.9 SD. Short-term adaptation was then accomplished by using 2 h of paired horizontal sinusoidal vestibular stimulation and phase-synchronized vertical optokinetic stimulation (cross-axis adaptation). For long-term adaptation, cats wore x 0.25 or x 2.2 magnifying lenses for 4 days. The cats were passively rotated for 2 h/day and allowed to walk freely in the laboratory or their cages for the remainder of the time. The latency of the early (primary) adaptive response was 15.2 ms +/- 5.2 SD for cross-axis adaptation and 12.5 ms +/- 3.9 SD for lens adaptation. This short-latency response appeared within 30 min after beginning the adaptation procedure and diminished in magnitude overnight. A late (secondary) adaptive response with latency of 76.8 ms +/- 7.0 SD for cross-axis adaptation and 68.1 ms +/- 8.8 SD for lens adaptation appeared after approximately 2 h of adaptation. It had a more gradual increase in magnitude than the primary response and did not diminish in magnitude overnight. These data suggest that brainstem VOR pathways are a site of learning for adaptive VOR modification, since the primary latency is short and has a similar latency to that of the normal VOR.

Adaptation, Physiological↗
PubMed1995

Independent contributions of the orienting of attention, fixation offset and bilateral stimulation on human saccadic latencies.

In a series of experiments we examined the effects of the endogenous orienting of visual attention on human saccade latency. Three separate manipulations were performed: the orienting of visual attention, the prior offset of fixation (gap paradigm) and the bilateral presentation of saccade targets. Each of these manipulations was shown to make an independent contribution to saccade latency. In experiments 1 and 2 subjects were instructed to orient their attention covertly to a location by a verbal pre-cue; targets could appear in the attended hemifield (valid) or in the non-attended hemifield (invalid) together with a no-instruction (neutral) condition. Saccades were made under fixation gap and overlap conditions, to either single target or two bilaterally presented targets which appeared at equal and opposite eccentricities in both hemifields. The results showed a large increase (cost) of saccade latency to invalid targets and a small non-significant decrease (benefit) of saccade latency to valid targets. The cost associated with invalid targets replicates the "meridan crossing effect" shown in manual reaction time experiments and is consistent with the hemifield inhibition and premotor models of attentional orienting. The use of a "gap" procedure produced a generalised facilitation of saccade latency, which was not modified by the prior orienting of visual attention. The magnitude of the gap effect was similar for saccades made to attended and non-attended stimulis. This suggests that the gap effect may be due to ocular motor disengagement, or a warning signal effect, rather than to the prior disengagement of visual attention. When two targets were presented simultaneously, one in each hemifield, saccade latency was slowed compared with the single target condition. The magnitude of this slowing was unaffected by the prior orienting of visual attention or by the fixation condition. The slowing was examined in more detail in experiment 3, by presenting targets with brief offset delays. The latency increase was maximal if the two targets were presented simultaneously and decreased if the distractor appeared at short intervals (20-80 ms) before or after the saccade target onset. If the non-attended stimulus was presented at greater intervals (160, 240 ms) before the saccade target, then a facilitation effect was observed. This demonstrates that the onset of a distractor in the non-attended hemifield can have both an inhibitory and a facilitatory effect on a saccade production.

Attention↗
PubMed1995

Latency measurement of rectoanal reflexes.

PURPOSE: Latency values of rectoanal reflexes may be altered in disorders of the pelvic floor. Evaluation of this relatively uninvestigated aspect of rectoanal reflexes may have diagnostic implications in patients with disorders of defecation. METHODS: We studied the latency of rectoanal inhibitory and excitatory reflexes to sequential balloon distention of the rectum with 60 ml and 120 ml of air in 14 normal controls (mean age, 41.5 (range, 19-66) years), in 14 patients with fecal incontinence (FI) (mean age, 44.2 (range, 28-72) years), and in 14 patients with slow transit constipation (STC) (mean age, 40.6 (range 22-68) years). RESULTS: The mean latency of inhibition (FI = 5.3 seconds; STC = 4.6 seconds; controls = 5.1 seconds) was remarkably similar for the three groups (P = 0.19). The mean latency of excitation in the proximal anal canal (FI = 2.8 seconds; STC = 2.5 seconds; controls = 2.8 seconds) was comparable in the three groups (P = 0.58). The mean latency of excitation in the distal anal canal (FI = 4.8 seconds; STC = 2.6 seconds; controls = 2.7 seconds) was prolonged in patients who were incontinent compared with the other two groups (P < 0.01). CONCLUSIONS: Proximal rectoanal excitation and inhibitory reflexes, when present, have a constant latency, irrespective of the underlying condition. The different latency values for proximal and distal rectoanal excitatory reflexes in patients with FI may indicate disparate denervation damage to the external anal sphincter.

Adult↗