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PubMed2006

The utility of pudendal nerve terminal motor latencies in idiopathic incontinence.

PURPOSE: Pudendal nerve terminal motor latency testing has been used to test for pudendal neuropathy, but its value remains controversial. We sought to clarify the relationship of pudendal nerve terminal motor latency to sphincter pressure and level of continence in a cohort of patients with intact anal sphincters and normal pelvic floor anatomy. METHODS: We reviewed 1,404 consecutive patients who were evaluated at our pelvic floor laboratory for fecal incontinence. From this group, 83 patients had intact anal sphincters on ultrasound and did not have internal or external rectal prolapse during defecography. These patients were evaluated by pudendal nerve terminal motor latency testing, a standardized questionnaire, and anorectal manometry, which measured resting and squeeze anal pressures. Incontinence scores were calculated by using the American Medical Systems Fecal Incontinence Score. Values were compared by using the Fisher's exact test and Wilcoxon's rank-sum test; and significance was assigned at the P < 0.05 level. RESULTS: 1) Using a 2.2-ms threshold, 28 percent of patients had prolonged pudendal nerve terminal motor latency unilaterally and 12 percent bilaterally. 2) At a 2.4-ms threshold, 18 percent of patients had prolonged pudendal nerve terminal motor latency unilaterally and 8 percent bilaterally. 3) Bilaterally prolonged pudendal nerve terminal motor latency was significantly associated with decreased maximum mean resting pressure and increased Fecal Incontinence Score, but not decreased maximum mean squeeze pressure, at both 2.2-ms and 2.4-ms thresholds. 4) Unilaterally prolonged pudendal nerve terminal motor latency was not associated with maximum mean resting pressure, maximum mean squeeze pressure, or fecal incontinence score at either threshold. CONCLUSIONS: The majority of incontinent patients with intact sphincters have normal pudendal nerve terminal motor latency. Bilaterally but not unilaterally prolonged pudendal nerve terminal motor latency is associated with poorer function and physiology in the incontinent patient with an intact sphincter.

Aged↗
PubMed2004

Determining abnormal interocular latencies of multifocal visual evoked potentials.

PURPOSE: To describe methods for measuring interocular latency differences of multifocal visual evoked potentials (mfVEP) and for determining regions with abnormal interocular latencies in patients. METHODS: The mfVEPs from 100 individuals with normal visual fields and normal fundus examinations were analyzed. Individuals ranged in age from 21.6 to 92.4 years. The stimulus was a 60 sector, pattern-reversing dartboard display. Each sector had 16 checks, 8 white (200 cd/m2) and 8 black (< 1 cd/m2). Interocular latency was measured as the temporal shift producing the best cross-correlation value between the corresponding responses of each eye. The 'corrected interocular latency' was defined as the difference between this shift and the mean interocular latency (shift) for a particular sector and recording channel. RESULTS: The variability of the corrected interocular latency decreased as the signal-to-noise ratio (SNR) of the mfVEP responses increased. For example, the 95% confidence intervals decreased from over 16 ms to under 4 ms as SNR increased. Grouping and summing the responses also lead to an increase in SNR and a decrease in the confidence interval. The results of various cluster criteria were also derived. A cluster criterion (e.g. two or more contiguous points within a hemisphere exceeding a given confidence interval), can serve to increase the specificity for detection of eyes or individuals with abnormal interocular latencies. For example, while 21% of the eyes had 3 or more points exceeding the 5% confidence interval, only 1.8% of the eyes had a cluster of 3 or more of these points. Finally, interocular latency was only weakly correlated with age (r = 0.26). CONCLUSION: In testing for abnormalities in interocular latencies, the confidence interval should be based upon the SNR of the response. Grouping and summing responses to increase SNR or employing a cluster test may also prove useful.

Acute Disease↗
PubMed1987

Latency of gustatory neural impulses initiated in frog tongue.

Latencies of gustatory neural impulses evoked by stimulation of the bullfrog tongue with the 4 basic taste substances (NaCl, acetic acid, quinine-HCl(Q-HCl), sucrose), CaCl2 and water were studied by recording antidromic impulses conducted to the fungiform papillae. Mean latencies of the impulses ranged from 58 to 107 ms when very strong stimuli, such as 2 M NaCl, 0.1 M acetic acid, 0.1 M Q-HCl, 2 M sucrose and 1 M CaCl2, were applied. Mean latency in response to water was 2.41 s. The time required for arrival of an applied taste stimulus on the taste receptor membrane was a mean of 20.1 ms. The time required for antidromic conduction from the impulse initiation site to the recording site was a mean of 2.4 ms. Electrical stimulation of the fungiform papilla with a strong intensity produced the impulse with a long and fluctuating latency. The mean minimum latency of the fluctuating impulse, from which the conduction time was subtracted, was 5.3 ms. Mechanical destruction of the taste disk situated at the top of the fungiform papilla resulted in a disappearance of the fluctuating impulse, suggesting that this was initiated synaptically via a depolarization of taste cells by electrical current. The minimum 5.3-ms latency was likely to be the time required from the onset of taste cell depolarization to the initiation of an impulse at the first node of Ranvier of myelinated gustatory fiber. These results indicate that the latencies of 58-107 ms by strong taste stimulation were composed of the 30- to 79-ms latency of taste cell receptor potential and the remaining 28 ms latency, which was the sum of the time of stimulant diffusion, the time from taste cell depolarization to the first impulse and the time of impulse conduction.

Animals↗
PubMed1978

VEP latency and RT as power functions of luminance in the peripheral visual field.

Behavioral correlates of P1 latency of visual evoked potentials (VEPs) were investigated using visual reaction time (RT) as a measure at the fovea, 20 degrees and 40 degrees nasal retinal eccentricities along the horizontal meridian of the right eye. Three luminances of the target in steps of 1 log units were used: 26, 260 and 2600 cd/m2. As luminance increased VEP latency and RT decreased. Further, as eccentricity increased VEP latency and RT increased. The highest product-moment coefficient of correlation (r = 0.998) was found between RT and P1 latency in the fovea, whereas the coefficient of correlation was found to be slightly small in the peripheral loci. The data (both VEPs and RTs) were fitted by the power function of the form: T = kLB + T0 where T, k, L T0 and B indicate VEP latency (or RT, scaling constant, luminance, asymptotic latency and exponent of the power function, respectively. This shows how the VEP latency and the RT can be related to luminance with exponent B. It was found that psychophysical power law governs VEP latency as well as RT with an exponent of about -0.32. It was suggested that both RT AND P1 latencies of VEP originate in the similar nonlinear visual system.

Adult↗
PubMed1995

Is "memory-scanning" time in the Sternberg paradigm reflected in the latency of event-related potentials?

The time taken to scan short term memory for a target (probe) digit in the Sternberg paradigm is thought to be reflected in the latency of a major positive wave in the associated event-related potentials. In the present study we have recorded and analysed reaction time and event-related potentials to a digit probe identification task in 37 healthy subjects. Using methods similar to those of earlier studies, we have confirmed the previously reported relationship between memory set size and the apparent latency of the major positive wave. However, analysis of the responses of individual subjects showed that increasing set size had no consistent effects on this wave. One-third of the subjects showed no latency change with increasing set size. In the other subjects, possible latency changes were invariably associated with wave form changes, suggesting that impression of latency shifts may arise from a comparison of non-analogous waves. We suggest that the most significant effect of increasing set size, in the majority of subjects, is a negative amplitude shift which overlaps and distorts a variable section of the major positive wave. In these subjects, an apparent shift in the latency of the major positive wave could be attributed to a combination of attenuation of earlier contributions and relative preservation of later subpeaks, with the result that the dominant positive waves at different levels of memory load are not analogous. By contrast, reaction time increased with set size in all subjects, irrespective of the presence or absence of associated wave form changes. Whereas the reaction time changes with increasing memory load in our study support the original concept of memory scanning, we found no consistent relationship between the latency of event-related potentials generated by this digit probe identification task and memory load. While the presence or absence of a latency shift in some subjects may be open to interpretation, our findings do not support the hypothesis that the latency of the major positive waves is an index of the time involved in memory scanning.

Adult↗
PubMed1986

Median and tibial somatosensory evoked potentials. Changes in short- and long-latency components in patients with lesions of the thalamus and thalamo-cortical radiations.

Alterations in short- and long-latency components of median and tibial somatosensory evoked potentials (SEPs) were studied in patients with lesions in the thalamus and thalamo-cortical radiations. When the lesions were located primarily in the ventro-posterior thalamus, the SEP changes consisted of the following combination: absence of response; decrease in response amplitude; delay in peak latency; and attenuation of median N20-P25 and tibial P40. The laterally situated ventro-posterior lesions tended to preferentially affect tibial SEPs whereas the medially situated lesions tended to preferentially affect median SEPs. The lateral thalamic lesions affected primarily the long-latency SEP components, whereas the medial thalamic lesions affected primarily the mid-latency or the mid- and long-latency SEP components. Corona radiata infarcts produced SEP changes similar to those with the ventro-posterior thalamic lesions except that absence of evoked responses was not observed. Subcortical infarcts tended to affect the mid- and long-latency SEP components with relative preservation of the short-latency components. The present data indicate that only the lesions involving the primary thalamic relay area affected all SEP components, particularly the short-latency components, and that the lesions in other thalamic areas can also influence the SEPs, particularly the mid- and long-latency components. The present study further demonstrates that a combined use of median and tibial SEPs is useful in delineating the topographic organization of the somatosensory system in the thalamus.

Adult↗
PubMed1986

Latency variability and temporal interrelationships of the auditory event-related potentials (N1, P2, N2, and P3) in normal subjects.

Peak latency variation and the temporal interrelationships of the auditory event-related potential were investigated in 12 normal adults (ages 28-42). Measures of variation were based on both conventional averages and single trials. Estimates of N1, P2, N2 and P3 latencies were made on a trial-by-trial basis to target stimuli recorded from Fz, Cz and Pz scalp locations. Results showed that single-trial latency variability of the auditory ERP differed both among the various components and between subjects. Larger standard deviations were measured for the later N2 and P3 components than the earlier N1 and P2 components. Regression analyses between various component latencies indicated a strong covarying relationship between N2 and P3, with N2 accounting for up to 61% of the variance of P3 latency at Pz. Earlier N1 and P2 components added little to the overall prediction of either P3 or N2. For the other components, P2 accounted for 9-16% of the variance of N2, while N1 accounted for approximately 1% of the variance of N2; N1 accounted for 8-10% of the latency variation of P2. The correlations between single-trial peak latencies and RTs were positive but of low magnitude. The highest correlations between peak latency and RT were found for N2 (r = 0.33) and P3 (r = 0.24). The low correlations between the single-trial latencies of N1 and P3 suggest that the processes reflected by these components are independent and support a distinction between the earlier and the later components of the ERP. The close temporal coupling between N2 and P3 suggests that N2 may reflect cognitive properties in common to P3 in stimulus evaluation processes.

Adult↗
PubMed1985

Origin of latency shift of cochlear nerve potentials with sound intensity.

Compound action potentials were recorded from the round window in anesthetized rats in response to tonebursts and to continuous tones. The responses to tonebursts were compared to cross-correlograms of the responses to continuous tones that were amplitude modulated by pseudorandom noise. The cross-correlograms were similar in shape to the responses to tonebursts, but the latencies of the two cross-correlogram peaks decreased less when the sound intensity was increased from near threshold values than did the latencies of the peaks in the responses to tonebursts. When an unmodulated tone was added to these stimuli, the latencies of peaks in the response to tonebursts increased as the intensity of the unmodulated tone was increased. However, the effect of an unmodulated tone on the latencies of the peaks in the cross-correlograms was more complex: when the frequency of the unmodulated tone was below that of the modulated tone, there was a decrease in the latency of the peaks in cross-correlograms. This decrease in latency was a function of the intensity of the unmodulated tone, and was similar to the decrease in latency seen when the intensity of a single modulated tone is increased. These results are interpreted as supporting the findings of earlier research, which showed that the cross-correlogram of the unit response to amplitude-modulated tones has a latency that is nearly independent of the stimulus intensity. In addition, the data indicate that the decrease in the latency of the peaks in the cross-correlograms of the gross response from the round window is a result of nonlinearity of the cochlear frequency analyzer and is not directly related to neural excitation in the cochlea.

Animals↗
PubMed2005

Auditory brain-stem, middle- and long-latency evoked potentials in mild cognitive impairment.

OBJECTIVE: Mild cognitive impairment (MCI) is a selective episodic memory deficit in the elderly with a high risk of Alzheimer's disease. The amplitudes of a long-latency auditory evoked potential (P50) are larger in MCI compared to age-matched controls. We tested whether increased P50 amplitudes in MCI were accompanied by changes of middle-latency potentials occurring around 50 ms and/or auditory brain-stem potentials. METHODS: Auditory evoked potentials were recorded from age-matched controls (n = 16) and MCI (n = 17) in a passive listening paradigm at two stimulus presentation rates (2/s, 1/1.5 s). A subset of subjects also received stimuli at a rate of 1/3 s. RESULTS: Relative to controls, MCI subjects had larger long-latency P50 amplitudes at all stimulus rates. Significant group differences in N100 amplitude were dependent on stimulus rate. Amplitudes of the middle-latency components (Pa, Nb, P1 peaking at approximately 30, 40, and 50 ms, respectively) did not differ between groups, but a slow wave between 30 and 49 ms on which the middle-latency components arose was significantly increased in MCI. ABR Wave V latency and amplitude did not differ significantly between groups. CONCLUSIONS: The increase of long-latency P50 amplitudes in MCI reflects changes of a middle-latency slow wave, but not of transient middle-latency components. There was no evidence of group difference at the brain-stem level. SIGNIFICANCE: Increased slow wave occurring as early as 50 ms may reflect neurophysiological consequences of neuropathology in MCI.

Aged↗
PubMed2006

Effect of latency period after premature rupture of membranes on 2 years infant mortality (DOMINOS study).

OBJECTIVE: To assess the impact of a short latency period after preterm premature rupture of the membranes (PPROM) on infant mortality. STUDY DESIGN: A prospective cohort study of women with PPROM between 24(0/7) and 33(6/7) weeks' in singleton gestation was performed in all maternity wards of the Rhône-Alpes Region. Neonatal and infant outcomes were compared according to the latency period (<48 h and > or =48 h). The primary outcome was the mortality rate and the secondary outcome was a composite variable of significant neurological disorders at 2 years of age. Outcomes was stratified according to gestational age at rupture. Univariate and multiple logistic regression analyses were used with SAS statistical software. RESULTS: Out of 471 women recruited in the study at a mean gestational age of 30.5+/-0.2 weeks, 170 (37%) presented with a <48-h latency period, and 301 (63%), a > or =48-h latency period. While prior to 30 weeks' gestation, the mortality rate was higher in neonates with a short latency period (16.3% versus 7.3%, p < 0.01) with pulmonary disease being the major cause of death, a short latency period was associated with a lower mortality rate after 30 weeks' gestation (0% versus 3.7%, p=0.02). After adjusting for confounding factors, a <48-h latency period remained an independent factor associated with infant mortality prior to 30 week's gestation (odds ratio 3.8, 95% confidence interval 1.3-11.7). Significant neurological disorders were not modified by the length of the latency period. CONCLUSION: For PPROM that occur before 30 weeks' gestation, a short latency period was associated with a higher infant mortality rate. Inversely, it was associated with a lower mortality rate after 30 weeks'. There is an urgent need for a thorough evaluation of expectant management of PPROM after 30 weeks' gestation.

Adult↗
PubMed2004

Latency to onset of status epilepticus determines molecular mechanisms of seizure-induced cell death.

The molecular mechanisms mediating degeneration in response to neuronal insults, including damage evoked by prolonged seizure activity, show substantial variability across laboratories and injury models. Here we investigate the extent to which the proportion of cell death occurring by apoptotic vs. necrotic mechanisms may be shifted by changing the temporal parameters of the insult. In initial studies with continuous seizures (status epilepticus, SE), signs of apoptotic degeneration were most clearly observed when SE occurred following a long latency (>86 min) after injection of kainic acid as compared with a short-latency SE (<76 min). Therefore, in this study we directly compared short- with long-latency SE for the expression of molecular markers for apoptosis and necrosis in an especially vulnerable brain region (rhinal cortex). Molecular markers of apoptosis (DNA fragmentation, cleavage of ICAD, an inhibitor of "caspase-activated DNase" (CAD), and prevalence of a caspase-generated fragment of alpha-spectrin) were detected following long-latency SE. Short-latency SE resulted in expression of predominantly necrotic features of cell death, such as "non-ladder" pattern of genomic DNA degradation, prevalence of a calpain-generated alpha-spectrin fragment, and absence of ICAD cleavage. Silver staining revealed no significant difference in the extent and spatial distribution of degeneration between long- or short-latency SE. These data indicate that the latency to onset of SE determines the extent to which apoptotic or necrotic mechanisms contribute to the degeneration following SE. The presence of a long latency period, during which multiple brief seizure episodes may occur, favors the occurrence of apoptotic cell death. It is possible that the absence of such "preconditioning" period in short-latency SE favors predominantly necrotic profile.

Animals↗
PubMed2003

Response latencies of neurons in visual areas MT and MST of monkeys with striate cortex lesions.

Cortical area, MT (middle temporal area) is specialized for the visual analysis of stimulus motion in the brain. It has been suggested [Brain 118 (1995) 1375] that motion signals reach area MT via two dissociable routes, namely a 'direct' route which bypasses primary visual cortex (area, striate cortex (V1)) and is specialized for processing 'fast' motion (defined as faster than 6 degrees/s) with a relatively short latency, and an 'indirect' route via area V1 for processing 'slow' motion (slower than 6 degrees/s) with a relatively long latency. We tested this proposal by measuring the effects of unilateral V1 lesions on the magnitudes and latencies of responses to fast- and slow-motion (depicted by random dot kinematograms (RDK) ) of single neurons in areas MT and medial superior temporal area (MST) of anaesthetized macaque monkeys. In the unlesioned hemisphere contralateral to a V1 lesion, response magnitudes and latencies of MT neurons were similar to those previously reported from MT neurons in normal monkeys, and there was no significant association between slow movement and long response latency (>100 ms), or between fast movement and short latency (< or =100 ms). V1 lesions led to diminished response magnitudes and increased latencies in area MT of the lesioned hemisphere, but did not selectively abolish MT responses to slow moving stimuli, or abolish long-latency responses to either slow- or fast-moving stimuli. Response magnitudes and latencies in area MST, which receives visual inputs directly from area MT and is also specialized for visual analysis of motion, were unaffected by V1 lesions (though we have shown elsewhere that directionally-selective responses in both areas were impaired by V1 lesions). Overall, the results are incompatible with the hypothesis that there are dissociable routes to MT specialized for processing separately fast and slow motion.

Action Potentials↗
PubMed1976

Decision theory analysis of response latencies in vigilance.

In two separate experiments, the latencies associated with all four categories of response (correct detections, false alarms, correct rejections, and omissions) were recorded during the performance of a 45-min. visual monitoring task. In the first experiment, concerned primarily with criterion changes in vigilance, signal probability was manipulated. The second experiment was concerned with sensitivity changes resulting from changes in event rate. In the first experiment, latencies associated with correct detections and false alarms increased, whereas those associated with correct rejections and omission errors decreased, with an increase in criterion. In the second experiment, a reduction in sensitivity associated with an increased event rate exerted significant and opposing effects on latencies of responses to signals (correct detections and omissions) while leaving the latencies of responses to nonsignals (correct rejections and false alarms) unchanged. In both experiments, it was observed that while the latencies associated with positive responses increased with time on task, the latencies of negative responses decreased with time. These results are consistent with the predictions of a decision theory model for response latency extended from signal detection theory, which assumes an inverse relation between response latency and distance from the criterion; A decision theory analysis thus enables the interpretation of both detectability and latency measures of vigilance performance within the same theoretical framework.

Adolescent↗
PubMed2000

Median nerve latency measurement agreement between portable and conventional methods.

A portable nerve conduction testing device was compared with a conventional method of measuring median nerve distal latencies. In a population-based study, a health questionnaire was mailed to a random sample of 3000 participants (aged 25 to 74 years). Two hundred and sixty-two responders with numbness and/or tingling in the median nerve distribution, and 125 asymptomatic responders underwent clinical examination as well as portable and conventional median nerve distal latency measurements. Motor latency measured with the portable device was on average 0.1 millisecond (ms) lower than motor latency measured with the conventional method (95% limits of agreement, -0.8-0.5 ms). Sensory latency (wrist-to-index finger) measured with the portable device was on average 0.3 ms lower than sensory latency (long finger-to-wrist) measured with the conventional method (95% limits of agreement, -0.7-0.1 ms). Strong correlations were found between the latencies measured by the portable and conventional methods (Pearson correlation coefficient, 0.90-0.93). The agreement between the portable and conventional methods in measuring median nerve distal latencies appears to be acceptable. The cut-off value for abnormal sensory latency needs to be lower for the portable than the conventional method if the present measurement techniques are used.

Adult↗
PubMed1996

Overestimation of sleep latency by patients with suspected hypersomnolence.

The latency to sleep onset has been reported to be overestimated by chronic insomniacs. Observing that some patients evaluated for suspected hypersomnolence complain of insomnia and others fail to report that they are sleepy, we wondered whether overestimation of sleep latency could be occurring in these subjects as well. Since polysomnography (PSG) only provides one sleep onset with which to assess a patient's estimation, we investigated the use of the multiple sleep latency test (MSLT) for this purpose. Among 147 patients who had an MSLT, 137 of whom had a preceding PSG, overestimation of sleep latency occurred on 78% and 74% of the respective tests. The magnitude of overestimation averaged 3 minutes and 27 minutes, respectively, and was not dependent on diagnosis. Subjects who had reported a history of difficulty falling asleep, compared to those who did not, tended to show equivalent objective sleep latencies, longer subjective nocturnal sleep latencies and less overall accuracy in their estimates. Those who denied having a problem with excessive daytime sleepiness (EDS) showed objective sleep latencies nearly identical to those who complained of EDS but had only a trend toward higher overestimation on the MSLT. Overestimation of sleep latency is therefore more readily part of an explanation for why hypersomnolent patients sometimes complain of insomnia than it is for failure to recognize EDS. The MSLT as well as nocturnal recordings can provide data with which to assess overestimation of sleep latency.

Adult↗
PubMed1996

The effects of early and late preterm birth on brainstem and middle-latency auditory evoked responses in children with normal neurodevelopment.

In preterm and term infants, brainstem and middle latency auditory evoked responses (ABR and MLR) were obtained at 40 and 52 weeks conceptional age (CA) and at 5 years of age. A neurological and neuropsychological evaluation was performed at 5 years of age. To study the effect of preterm birth on the maturation of the ABR and MLR, the preterm infants were divided into early and late preterm groups. Only children with a normal neurodevelopmental outcome at 5 years of age were entered into the study. For ABR, the late preterm group showed significantly longer mean latencies IIc, III, V, and Vc when compared with the term group at 52 weeks CA. There was a trend to longer ABR latencies I in the early preterm group compared with the term group. At 52 weeks CA, the late preterm group showed longer mean interpeak latencies III-I and V-I when compared with the term as well as the early preterm group. At 5 years, the late preterm group showed significantly longer mean ABR latencies IIc and III when compared to the early preterm group. For MLR, the early preterm group showed significantly longer mean latencies of MLR component PO when compared with the term group at 40 weeks CA. At 52 weeks, the late preterm group also had longer mean MLR latencies P0 than the term group. At 5 years of age, the term group showed higher mean peak-to-peak amplitudes Na-P0 than the early as well as the late preterm group. To a large extent, the ABR results support the hypothesis that middle ear effusions in combination with retarded myelination of the central auditory pathway are responsible for the ABR differences found between term and preterm infants with a normal neurodevelopmental outcome at 5 years of age. The longer latencies and interpeak latencies found in late preterm infants when compared with early preterm infants might be explained by an augmented vulnerability of the auditory pathway between 30 and 34 weeks CA. The MLR differences found between term and preterm infants might be explained by a difference in the maturation of primary and nonprimary MLR components.

Auditory Cortex↗
PubMed1972

The dependence of the latency relaxation on sarcomere length and other characteristics of isolated muscle fibres.

1. The latency relaxation has been examined in single fibres from frog striated muscle with particular attention given to its possible relation to Ca(2+) release during excitation-contraction coupling.2. Latency relaxations were recorded at 19-23 degrees C from massively stimulated (0.2 msec pulses) single fibres using two selected RCA 5734 transducer tubes in a bridge circuit.3. The depth of the latency relaxation has its full value when stimulus strength is between 40 and 400% above twitch threshold. Stronger stimuli reversibly diminish the latency relaxation.4. The variation in depth of latency relaxation with sarcomere length was found similar to that reported previously for multifibre preparations but in single fibres the peak of the curve consists of a plateau between sarcomere lengths of 2.8 mu and 3.2 mu.5. Sucrose hypertonicity increases the depth of the latency relaxation at sarcomere lengths below 2.8 mu but above this length it has either no effect or a depressant effect depending on the degree of hypertonicity.6. The maximal depth of the latency relaxation (measured at 3 mu) averaged 0.23% of the maximal tetanus tension (measured at 2.2 mu) and was strongly correlated (r = 0.87) with the latter in forty-five single fibres.7. The maximal depth of the latency relaxation is not correlated with the number of sarcomeres in series in a fibre.8. The results of this study are shown to fully support and extend Sandow's (1966) hypothesis that the latency relaxation is caused by release of activator Ca(2+) from the sarcoplasmic reticulum.

Animals↗
PubMed1976

Calcium and the control of discrete wave latency in the ventral photoreceptor of Limulus.

1. Discrete, transient depolarization (discrete waves) of the ventral photoreceptor of the horseshoe crab, Limulus, occur spontaneously in the dark adapted photoreceptor and are also evoked by light. They form the basic events which comprise the receptor potential. A brief, low energy flash of light evokes variable numbers of discrete waves which have variable latencies. Evidence suggesting that discrete wave latency reflects the kinetics of the chemical reactions of phototransduction is reviewed. 2. The concentration of extracellular Ca influences both the average discrete wave latency and its variability. Lowering extracellular Ca prolongs the latency and increases its variability. Increasing extracellular Ca has the opposite effect. 3. Changes in discrete wave latency caused by changes in extracellular Ca require 10--15 min to become fully manifest, whereas when the concentration of extracellular K is increased the photoreceptor achieves a steady-state depolarization in 10-15 sec. 4. Iontophoresis of the Ca-chelating agent EGTA into the photoreceptor increases both the average discrete wave latency and its variability. Iontophoresis of Ca-EGTA mixtures may either increase or decrease discrete wave latency and its variability depending upon the proportion of Ca mixed with EGTA. 5. It is suggested that the concentration of intracellular rather than extracellular ionized Ca is the prime factor indicating discrete wave latency. The effects of changing extracellular Ca can be explained if the photoreceptor is permeable to Ca in the dark and if it maintains a low intracellular Ca concentration by virtue of active metabolic processes (a pump-leak system). 6. Lowering the temperature of the photoreceptor also has the dual effect of increasing discrete wave latency and its variability. However, effects of lowering temperature and Ca simultaneously are greater than the sum of the two effects in individually. This suggests that Ca may be a reactant in the chemical process of phototransduction. 7. Changing the concentration of extracellular Ca does not change the quantum efficiency of discrete wave production. A previous study showed that quantum efficiency is not changed by temperature. Thus, once initiated by the absorption of light, the reactions that subserve phototransduction may be forced to completion. Ca probably exerts its influence by changing one or more rate constants in the reaction sequence.

Action Potentials↗