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PubMed1998

Age and stage dependency of P300 latency alterations in non-demented Parkinson's disease patients without therapy.

Acoustic P300 was recorded from Fz, Cz and Pz by means of an 'odd-ball' paradigm in 44 non-demented de novo Parkinson's disease patients (PD) or PD patients under treatment withdrawal, and in 31 age-matched normal subjects, to evaluate whether a P300 latency increase was present in PD patients. The influence of age and disease stage on latency was successively verified by subgrouping PD patients according to different age ('young' and 'old') and disease stage ('early' or 'advanced'). PD patient data were compared to data of normal subjects subgrouped into 'young' and 'old' or, to eliminate the age-dependent shift of latency, this latter was adjusted to 60 years in all the examined subjects. A significant increase of latency has been found in Fz and Cz in the 'old' group of PD patients (n = 23) but not in the 'young' group (n = 21) utilising both methods. Moreover, a significant latency increase was also present in Fz and Cz in the group of 'advanced' PD patients (n = 8), but not in the group of 'early' PD patients (n = 36) utilising age-adjusted measurements. When the 'early' PD patient group was divided into 'young' (n = 20) and 'old' (n = 16), the 'early old' group displayed significantly increased latencies in Fz compared with normal subjects. Abnormal P300 latencies were observed, at least in one electrode, by analysing the raw data, in 5.0% of the 'early young', 43.7% of the 'early old' and up to 62.7% of the 'advanced' patients. Fz represented the site in which abnormal P300 latencies were most often observed. Moreover, in the total group of PD patients, the P300 delay was significant only on the frontal (Fz) site when compared with normal subjects. The reported findings were interpreted as if PD produces a sort of 'accelerated effect of age' on the cognitive functions, presumably produced by a mechanism different from that producing motor impairment since no clear correlation could be detected between P300 latency and motor score. The frontal impairment of P300 is in line with previous neuropsychological findings obtained in these patients. Considering that about 30% of PD patients develop dementia during their disease progression, a border-line or abnormal P300 latency observed at disease onset may represent a predictive marker of this evolution.

Adult↗
PubMed2000

Latency as a function of intensity in auditory neurons: influences of central processing.

The response latencies of sensory neurons typically shorten with increases in stimulus intensity. In the central auditory system this phenomenon should have a significant impact on a number of auditory functions that depend critically on an integration of precisely timed neural inputs. Evidence from previous studies suggests that the auditory system not only copes with the potential problems associated with intensity-dependent latency change, but that it also modifies latency change to shape the response properties of many cells for specific functions. This observation suggests that intensity-dependent latency change may undergo functional transformations along the auditory neuraxis. The goal of our study was to explore these transformations by making a direct, quantitative comparison of intensity-dependent latency change among a number of auditory centers from the lower brainstem to the thalamus. We found two main ways in which intensity-dependent latency change transformed along the neuraxis: (1) the range of latency change increased substantially and (2) one particular type of latency change, which has been suggested to be associated with sensitivity to temporally segregated stimulus components, occurred only at the highest centers tested, the midbrain and thalamus. Additional testing in the midbrain (inferior colliculus) indicated that inhibitory inputs are involved in shaping latency change. Our findings demonstrate that the central auditory system modifies intensity-dependent latency changes. We suggest that these changes may be functionally incorporated, actively enhanced, or modified to suit specific functions of the auditory system.

Animals↗
PubMed2003

The impact of motor activity on intracerebral ERPs: P3 latency variability in modified auditory odd-ball paradigms involving a motor task.

The P3 wave of event-related potentials was recorded with intracranial electrodes in 24 epileptic patients during the pre-surgical evaluation of epilepsy surgery. Three different cognitive auditory paradigms were used: (1) odd-ball paradigm with no output required (PGI) where patients had simply to recognize target tones, (2) odd-ball with motor response (PGII), where patients had to press a button in response to target tones, and (3) odd-ball with both counting task and motor response (PGIII), where patients had to recognize target tones, press a button in response to them, and count their number. The occurrence of P3 potential, its latency and amplitude, and the dependence of P3 latency on the task complexity were calculated. Identifiable P3 potentials in all the three paradigms were recorded from locations in mesial cortex (18 locations mesial temporal, eight locations mesial frontal, two locations mesial parietal) and lateral sites (eight sites lateral temporal, five lateral frontal, and two lateral parietal). P3 latency values ranged from 257 to 320 ms in all explored cortical areas when PGI was used; they significantly increased or decreased during PGII and PGIII, depending on the task and structure explored. In the mesial temporal cortex, the changes of P3 latency between paradigms were minimal. In the mesial parietal cortex, there was significant P3 delay in both PGII and PGIII relative to PGI. In the mesial frontal cortex, there was a significant latency decrease in PGII, and practically identical mean latency in PGI and PGIII. In all lateral cortices (temporal, frontal and parietal), there was always a P3 latency increase in PGII and PGIII relative to PGI, the most significant results being observed in the parietal and frontal lateral areas. The results support the multi-generator theory of P3. Prolongation of the mean P3 latency in lateral frontal and parietal cortices when the paradigm involved the execution of a motor task might reflect specific gating in this area during active movements, while the absence of modification in the temporal lobe may reflect minimal involvement of this region in motor planning or processing. The prolongation of mean P3 latency in practically all lateral structures in PGIII suggests that most cortical areas were involved in the cognitive functions needed for this test. The finding of reduction and subsequent prolongation of P3 latency in the mesial frontal cortex might reflect the unique specialization of this area and its specific involvement in motor processing.

Adolescent↗
PubMed2003

Long-latency motor evoked potentials in congenital hemiplegia.

OBJECTIVE: To investigate long-latency motor evoked potentials (MEPs) elicited by transcranial magnetic stimulation in congenital hemiplegia (CH) and to seek for correlation with paretic hand movement deficits. METHODS: MEPs were recorded from the first dorsal interosseous of both hands in 12 CH patients and 12 age-matched controls; dexterity and upper limb function were quantitatively assessed in both groups. RESULTS: In CH patients, long-latency MEPs, occurring much later than the commonly reported MEPs, were frequently observed in the paretic and non-paretic hands. Four distinct groups of long-latency MEPs were found, each cluster being identified by its mean latency, namely 35, 85, 160 and 225 ms. The residual dexterity of the paretic hand was correlated with the presence of contralateral MEPs with a 20 and 225 ms latency and was negatively correlated with ipsilateral MEPs, irrespective of their latency. In controls, only few MEPs with a latency of 225 ms were found in 4 out of 12 subjects. CONCLUSIONS: The pattern of MEPs found in CH patients differs dramatically from that reported in adult stroke patients, suggesting that long-latency MEPs are a rather distinctive consequence of early corticospinal lesions. The hypothesis that a given cluster of long-latency MEPs is mediated by a particular pathway appears very unlikely. Rather, we suggest that an exacerbation of cortical and/or spinal excitability is at the origin of these long-latency MEPs.

Adolescent↗
PubMed1992

Reduced latency of the visual evoked cortical response following cryogenic injury to the cerebral cortex--a neuroexcitatory phenomenon.

Changes in the latency of visual cortical evoked responses (VER) were studied in rats subjected to cryogenic injury of the cerebral cortex. Four hours after cold injury the animals revealed a significant reduction of VER latency, which lasted approximately one week, with maximal reduction in latency occurring after 3 days. A potential role of excitotoxic amino acids in this phenomenon was tested by direct application of glutamate to the exposed cerebral cortex of the control rat and by administration of MK-801, antagonist of the NMDA receptor, in rats subjected previously to cryogenic injury and displaying a significant reduction in the VER latency. The direct application of glutamate to the cortex resulted in a decrease of the VER latency similar in magnitude to that observed after cold injury and this effect could repeatedly be demonstrated after washing out the initial application of the glutamate. The administration of MK-801 in animals subjected previously to cryogenic injury produced, within 5 minutes, reversion of reduced VER latencies. The maximal prolongation of latency occurred 30 min after MK-801 administration and reached in some cases latency values greater than in controls. Reduced latencies, corresponding to those observed originally, reappeared within 2 to 4 hours. Our studies suggest that the described reductions in the VER latencies are related to cortical areas of hyperexcitation due to excessive release of neuroexcitatory transmitters.

Animals↗
PubMedDate not supplied

Measurement of the lateral thoracic reflex latency in ponies.

Lateral thoracic nerve reflex latencies values were measured in ponies using a simple, non-invasive technique. The reflex was elicited using an external triggering hammer attached to an electrodiagnostic unit. The resulting evoked, compound muscle action potentials were recorded with electrodes, which were placed over the 6th ribs or 11th rib level with the axilla. Two superimposed repeats of 4 signal-averaged sweeps of 50 or 100 milliseconds were recorded and the estimated reflex pathway was measured for each subject in order to calculate the reflex latencies and latency velocities. Mean left and right 6th rib peak latencies were not significantly different from each other (P = .609), but left 6th rib latencies were shorter than those recorded from the 11th rib (P < .0001), substantiating the existence of an indirect (central) pathway to the reflex. The calculated left and right 6th rib latency velocities were not significantly different from each other (P = .58) but left 6th rib latency velocities were different from left 11th rib (P = .009). The calculated latency velocities were within the broad range for corticospinal tract motor conduction velocities and comparable to magnetic motor evoked latency velocities. The use of lateral thoracic reflex latency measurements to objectively identify the site of spinal cord lesions is discussed.

Animals↗
PubMed1983

Correlation of activity in neighbouring goldfish ganglion cells: relationship between latency and lag.

Pairs of retinal ganglion cells in the isolated goldfish retina were recorded simultaneously with a single electrode. Repeated flashes of light were delivered to evaluate the response latency of each of the units. The cross-correlation histogram for the maintained discharge of each pair of cells was examined, and its temporal relationships (lags) were compared with the differences in response latencies of the two units. There was a strong correlation between these measures; however, the differences between latencies were often at least twice as great as the lags. The differences between the times to the peaks of the responses of the two units were less reliably related to the lags of the pairs, although the correlation was positive and the differences in time-to-peak generally greater than the lags. The weaker relationship between the difference in time-to-peak and lag than between latency difference and lag is apparently a manifestation of a negative correlation between latency and rise time (from first response to peak). This indicates that cells with a longer latency compensate with a faster rise time. There was a negative correlation between the mean maintained rate of a neurone and its response latency. That is, cells with faster maintained discharge rates respond sooner than those with slower maintained rates. There was virtually no relationship between the lags or the differences in latency and the differences between the magnitudes of the responses to light. Thus, it is unlikely that differences in latency (or lags) could be attributed to unequal effectiveness of the stimuli for the two units. The relationship between differences in latency and lags did not depend on the response categorizations of the two units. Specifically, it did not matter whether the members of the pair were on centre, off centre or on-off centre; neither did it matter whether they were X-like or not-X-like neurones. Consideration of these data leads to the conclusion that there must be 'marked' pathways of differential conduction velocity through the retina.

Action Potentials↗
PubMed1984

Evidence from the use of vibration that the human long-latency stretch reflex depends upon spindle secondary afferents.

The electromyographic activity of flexor pollicis longus has been recorded in normal human subjects on moving the tip of the thumb with the proximal phalanx clamped. Ramp and hold displacements (stretches) were compared with high-frequency sinusoidal movement (vibration). The subject exerted a constant flexor force between stimuli and made no voluntary response to them. On stretching the muscle by forcibly extending the thumb at various constant velocities the usual combination of short-latency (ca. 25-30 ms) and long-latency (ca. 40 ms) components of response were observed. The short-latency response progressively predominated as the velocity was increased (60-900 deg s-1, 9 deg joint displacement). One subject still showed only a long-latency response with the fastest stretch, arguing that it is a distinct reflex entity. On commencing vibration (143 Hz, 3 deg movement peak-to-peak) a short-latency response was regularly obtained, but any long-latency response was always small in relation to that elicited by stretch. This was equally so when the short-latency responses to the two types of stimulation were matched by using appropriate parameters of stimulation. The time course of the vibration response did not change appreciably with change of amplitude of vibration, so that its temporal profile was always quite different from that of the stretch response. The observed differences are in accordance with the hypothesis that the spindle group II afferents produce the long-latency excitation, with the time lost peripherally in afferent conduction rather than centrally. In relation to the strength of their Ia excitatory actions, stretch is known to excite secondary afferents more powerfully than does vibration. The findings are not readily accommodated on the hypothesis that the long-latency response is a transcortical reflex elicited by the initial Ia input, since vibration should then also have had a powerful long-latency action. Similar responses to vibration were obtained when it was applied percutaneously to the tendon of flexor pollicis longus 6 cm above the wrist. Also, those elicited by thumb vibration persisted largely unchanged when the thumb was anaesthetized. This confirms that they were dependent upon the excitation of receptors in flexor pollicis longus, presumably the Ia afferents, rather than upon cutaneous or joint receptors in the thumb. The stretch responses also depended upon muscle receptors, since they too survived anaesthesia.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed1987

Long latency EMG responses in hand and leg muscles: cerebellar disorders.

Electromyographic responses to stretches of hand muscles (first dorsal interosseus) and leg muscles (triceps surae, tibialis anterior) were investigated in patients with cerebellar disorders of different locations. Stimuli consisted of short dorsiflexions of the index finger during background force and in tilting (toe up) of a movable platform on which the subject stood. The most important findings were increased long latency responses in upper and lower extremities. For hand muscles it was the late part of the long latency complex, which was increased. For leg muscles it was the long latency response in the anterior tibialis muscle, the antagonist of the stretched triceps surae. The medium latency response in the triceps surae was unaffected. Latencies of the early segmental reflexes and the long latency responses were normal except for cases with peripheral neuropathy (moderate increase in latency of all EMG responses) and diseases affecting both the peripheral nerves and the dorsal columns (for example Friedreich's ataxia). The latter leads to a pronounced delay of the short latency response and a massive delay of the long latency complex in the first dorsal interosseus and of the long latency response in the anterior tibialis muscle.

Atrophy↗
PubMed2003

Relation between the rate of tumour cell proliferation and latency time in radiation associated breast cancer.

BACKGROUND: Patients with possible radiation induced cancer could be used to study if the rate of tumour cell proliferation is related to latency time. Such a finding could help researcher to find time periods when other initiating risk factors operate. METHODS: Seventeen women with breast cancer, with a prior history of radiation treatment towards the parts or the whole breast, exclusive of the primary treatment of a breast cancer were identified. Most women had received treatment for benign disorders as hemangiomas, shoulder pain or skin infections. Three patients had been treated with mantle radiation for Hodgkin's disease prior to developing breast cancer. DNA analysis were performed, on remaining tumour tissue after hormone receptor analysis had been done, measuring the fraction of tumour cells in S-phase. Latency time (time between diagnosis and previous radiation treatment) was calculated and related to the S-phase fraction. RESULTS: A significant inverse relationship between latency time and S-phase was found (p < 0.0025), indicating that tumours with a high S-phase had a short latency time and vice versa. Among the possible radiation induced tumours, median S-phase was 14%, comparable with a median latency time of 22 years. Very high S-phase values were associated with short latency times (eg a S-phase of 35% would be compatible with a latency time of 7 years). CONCLUSION: Our preliminary results indicate that S-phase is related to latency time and that the median latency time maybe as long as 22 years. Our data may also explain why breast cancer is rare before 30 years of age and if patients are diagnosed at early ages, tumours often show high S-phase values and bad prognostic signs. We postulate that these results from radiation induced breast cancer may be used to extrapolate possible latency times in patients with non radiation induced breast tumours in order to isolate possible time periods for research after other initiating events.

Adult↗
PubMed1985

[Latency behavior of early acoustic evoked potentials in inner ear hearing loss].

In 101 patients suffering from sensory hearing loss the latency of the auditory evoked brain stem potentials was investigated. In case of minor and moderate pancochlear deafness latency is found to be within normal range. In severe pancochlear hearing loss above 80 dB latency is significantly delayed. In basocochlear hearing disorders the latency-delay is depending on the extent of the frequency loss and on the degree of pure tone threshold shift. If the patient is suffering from a high frequency hearing loss, normal latency will be found in the higher stimulus levels whereas within low levels latency tends to be delayed depending on the cut-off frequency. A general prolongation of latency across all sound pressure levels will take place in cases with steep forms of high frequency hearing loss. For the purpose of investigating the wave-I-latency we used an earcanal electrode in some patients. It can be shown, that in cochlear hearing disorders the latency of wave V is delayed to the same extent as the latency of wave V. After discussing model studies reference values of wave-V-delay as a function of the degree of high frequency disorders are listed

Audiometry, Pure-Tone↗
PubMed2002

Methylation of the EBV genome and establishment of restricted latency in low-passage EBV-infected 293 epithelial cells.

Epstein-Barr virus (EBV) encodes multiple latency programs: a growth-transforming program (type III) latency program and restricted-latency (types I and II) programs. During type III latency, EBV expresses six nuclear antigens, all of which are encoded by a single complex transcriptional unit driven by two linked promoters, Cp and Wp, while restricted viral latency is characterized by the expression of a single nuclear antigen, EBNA1, whose expression is driven from a distinct transcription unit under the control of the Qp promoter. EBV infection of the 293 epithelial cell line frequently leads to the establishment of a type I/II latent infection. Here we report that during the initial stages of virus infection of the 293 cell line, both Cp and Wp are active. However, analysis of four established, low-passage EBV-infected 293 cell lines revealed that three of these exhibited Qp-driven transcription of the EBNA 1 gene and little or no detectable Cp and Wp activity, while the fourth cell line exhibited Cp activity. Notably, all four cell lines contained the necessary transcription factors to drive transcription initiation from Cp and Wp when transiently transfected with unmethylated reporter constructs. Furthermore, in the cell lines exhibiting restricted EBV latency the viral genomes were extensively methylated around Cp and Wp, but not Qp. In contrast, in the cell line exhibiting Cp activity the viral genomes were hypomethylated around Cp, Wp, and Qp. Taken together, these results provide evidence that the establishment of a restricted latent infection in the 293 epithelial cell line is not due to a failure to initiate the growth-transforming (type III) latency program, but rather may arise from a selection against the type III latency program. Furthermore, these results are consistent with the hypothesis that methylation of Cp and Wp is required for entry into the type I or II latency programs.

Cell Line, Transformed↗
PubMed1999

Latency analysis in epidemiologic studies of occupational exposures: application to the Colorado Plateau uranium miners cohort.

BACKGROUND: Latency effects are an important factor in assessing the public health implications of an occupational or environmental exposure. Usually, however, latency results as described in the literature are insufficient to answer public health related questions. Alternative approaches to the analysis of latency effects are warranted. METHODS: A general statistical framework for modeling latency effects is described. We then propose bilinear and exponential decay latency models for analyzing latency effects as they have parameters that address questions of public health interest. Methods are described for fitting these models to cohort or case-control data; statistical inference is based on standard likelihood methods. APPLICATION: A latency analysis of radon exposure and lung cancer in the Colorado Plateau uranium miners cohort was performed. We first analyzed the entire cohort and found that the relative risk associated with exposure increases for about 8.5 years and thereafter decreases until it reaches background levels after about 34 years. The hypothesis that the relative risk remains at its peak level is strongly rejected (P < 0.001). Next, we investigated the variation in the latency effects over subsets of the cohort based on attained age, level and rate of exposure, and smoking. Age was the only factor for which effect modification was demonstrated (P = 0.014). We found that the decline in effect is much steeper at older ages (60+ years) than younger. CONCLUSION: The proposed methods can provide much more information about the exposure-disease latency effects than those generally used.

Air Pollutants, Radioactive↗
PubMed1989

The role of joint biomechanics in determining stretch reflex latency at the normal human ankle.

In order to study the influence of biomechanical factors on the timing of stretch reflex activity in the ankle extensor musculature, well defined, small amplitude and relatively rapid dorsiflexing stretch was applied to the ankle of seated normal human subjects at a series of angles within the range of physiological movement. If the ankle musculature was relaxed, a single reflex component appeared in the Triceps surae (TS) EMG with a latency compatible with a predominantly monosynaptic pathway. The latency of this response could be prolonged by applying stretch from an initially plantarflexed position and, similarly, decreased by applying stretch from a dorsiflexed position. A decrease in latency of 5-30 ms could be achieved by altering the pre-displacement ankle angle from 105 to 75 degrees. Intermediate changes in the start angle led to intermediate changes in latency. This trend was highly linear. If stretch was applied while the subject maintained a low level contraction in the TS, however, this shift in latency was abolished, with the earliest reflex components appearing with a latency obtained in the relaxed state at or close to maximum dorsiflexion. It is suggested that this shift in latency results from the properties of the long, compliant tendon through which joint movements are transmitted to the TS muscle. This shift in latency caused by passive alteration in the ankle angle at which a reflex was evoked should be taken into account when classifying reflexes arising from a mechanical input, or when using latency determinations as evidence for the involvement of particular pathways in their genesis.

Adult↗
PubMed1993

Latency in the inositol lipid transduction pathway: the role of cellular events in responses to thyrotropin-releasing hormone in Xenopus oocytes.

To dissect the cellular events responsible for the prolonged latency of the response to thyrotropin-releasing hormone (TRH) in Xenopus oocytes we interfered with different steps of the signal transduction pathway. Preincubation of oocytes with cis-vaccenic acid (a membrane-fluidizing agent) shortened the latency, suggesting a contribution of membranal processes. TRH-induced depletion of cellular calcium stores prolonged latency (up to threefold), which returned to control levels upon repletion of the stores. Injection of D-2,3-diphosphoglycerate (PGA), which inhibits inositol (1,4,5)-trisphosphate (InsP3) dephosphorylation, alone evoked a small, prolonged depolarizing current and significantly shortened the latency of the response to TRH. Injection of guanosine 5'-O-(2-thiodiphosphate) (GDP beta S), which inactivates guanine nucleotide-binding regulatory proteins, decreased the amplitude of the response and increased latency. Injection of guanosine 5-O-(3-thiotriphosphate) (GTP gamma S) immediately before the challenge with TRH did not shorten the latency of the response. Decreasing the effective receptor density with chlordiazepoxide, an antagonist of the TRH receptor, resulted in an extension of latency, whereas the expression of a large number of TRH receptors by injection of RNA transcribed from cloned receptor DNA (10-100 ng/oocyte) shortened the latency to below 2 s. Our results suggest that the latency of the response to TRH reflects the activation of a late step in the signal transduction sequence, most likely the release of calcium by InsP3. We propose that this process is kinetically controlled by an early rate-limiting event, involving the activation of a guanine nucleotide-binding protein by the TRH receptor.

2,3-Diphosphoglycerate↗
PubMed2004

The relationship of saccadic peak velocity to latency: evidence for a new prosaccadic abnormality in schizophrenia.

Antisaccades have not only longer latencies but also lower peak velocities than prosaccades. It is not known whether these latency and velocity differences are related. Studies of non-human primates suggest that prosaccade peak velocity declines as latency from target appearance increases. We examined whether a similar relationship between peak velocity and latency existed in human saccades, whether it accounted for the difference in peak velocity between antisaccades and prosaccades, and whether it was affected by schizophrenia, a condition that affects antisaccade performance. Sixteen control and 21 schizophrenia subjects performed prosaccade and antisaccade trials in the same test session. In both groups antisaccades had lower peak velocities than prosaccades. Latency did not influence the peak velocities of antisaccades in either subject group. At short latencies, the peak velocities of prosaccades were also similar in the two groups. However, while prosaccade peak velocities declined minimally with increasing latency in control subjects, those in the schizophrenia group declined significantly until they reached a value similar to antisaccade peak velocities. We conclude that, in normal subjects, the effect of latency on prosaccade peak velocity is minimal and cannot account for the lower velocity of antisaccades. In schizophrenia, we hypothesize that the latency-related decline in prosaccade peak velocity may reflect either an increased rate of decay of the effect of the transient visual signal at the saccadic goal, or a failure of the continuing presence of the target to sustain neural activity in the saccadic system.

Adult↗
PubMed2005

Differential effects of target probability on saccade latencies in gap and warning tasks.

Saccade latencies are significantly reduced by extinguishing a foveal fixation stimulus before the appearance of a saccade target. It has been shown recently that this "fixation offset effect" (FOE) can be modulated by varying target probability. Cortico-collicular top-down effects have been assumed to mediate this strategic FOE modulation. Here, we have investigated strategic FOE modulation in 14 healthy human subjects performing gap and warning tasks. In the former task, the central fixation point was extinguished 200 ms before target onset. In the latter task, the central fixation point changed its colour 200 ms before target onset, but remained illuminated until the target appeared. Target probability was varied block-wise between 25 and 75%. In both tasks, mean latencies decreased with increasing target probability. However, in contrast with what can be expected from preceding studies, we found no differential modulation of mean latencies by target probability between tasks. Instead, we observed differential probability-dependent changes in latency distributions. In the gap task, discrete changes of saccade latencies were found, with a probability-dependent change in frequency of express and regular latencies. By contrast, in the warning task a shift of the entire latency distribution towards longer latencies with low target probability was found. We conclude that strategic modulation of saccade latencies by target probability may be mediated by two distinct neural mechanisms. Selection of either mechanism seems to depend critically on activation of the fixation system.

Adult↗
PubMed2006

Overlapping visual response latency distributions in visual cortices and LP-pulvinar complex of the cat.

The visual system of the cat is considered to be organized in both a serial and parallel manner. Studies of visual onset latencies generally suggest that parallel processing occurs throughout the dorsal stream. These studies are at odds with the proposed hierarchies of visual areas based on termination patterns of cortico-cortical projections. In previous studies, a variety of stimuli have been used to compute latencies, and this is problematic as latencies are known to depend on stimulus parameters. This could explain the discrepancy between latency and neuroanatomical based studies. Therefore, the first aim of the present study was to determine whether latencies increased along the hierarchy of visual areas when the same stimuli are used. In addition, the effect of stimulus complexity was assessed. Visual onset latencies were calculated for area 17, PMLS, AMLS, and AEV neurons. Latencies were also computed from neurons in the lateral posterior (LP)-pulvinar complex given the importance of this extrageniculate complex in cortical intercommunication. Latency distributions from all regions overlapped substantially, and no significant difference was present, regardless of the type of stimulus used. The onset latencies in the LP-pulvinar complex were comparable to those seen in cortical areas. The data suggest that the initial processing of information in the visual system is parallel, despite the presence of a neuroanatomical hierarchy. Simultaneous response onsets among cortical areas and the LP-pulvinar suggest that the latter is more than a simple relay station for information headed to cortex. The data are consistent with proposals of the LP-pulvinar as a center for the integration and distribution of information from/to multiple cortical areas.

Animals↗