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Biomedical subjects

F R Robinson

Publications and source records attributed to F R Robinson.

At least 19 recordsLinked to original sources
PubMed1999

Comparison of hepatic lesions in veal calves with concentrations of copper, iron and zinc in liver and kidney.

Veal calf producers in Indiana have reported condemnation of carcasses due to icterus as well as condemnation of livers because of yellow discoloration, hepatomegaly and fibrosis. This study assessed the degree of hepatic injury in affected veal calves and correlated it with copper, iron and zinc concentrations in the liver and kidney. Tissues examined histopathologically were from slaughtered and necropsied veal calves. Hepatic lesions were divided into histopathologic categories of severity (minimal, moderate, marked or severe) based upon the degree of fibrosis, biliary epithelial hyperplasia, and inflammation. Hepatic copper levels decreased as the severity of lesions increased. The clinical observations and morphologic changes suggested initial hepatic damage before 9 w-of-age. The affected calves either died of acute copper toxicosis or survived to develop hepatomegaly, hepatic discoloration and/or fibrosis at the time of slaughter.

Age Factors↗
PubMed1998

Distribution of effective synaptic currents in cat triceps surae motoneurons. VI. Contralateral pyramidal tract.

We measured the effective synaptic currents (IN) produced by stimulating the contralateral pyramidal tract (PT) in triceps surae motoneurons of the cat. This is an oligosynaptic pathway in the cat that generates both excitation and inhibition in hindlimb motoneurons. We also determined the effect of the PT synaptic input on the discharge rate of some of the motoneurons by inducing repetitive firing with long, injected current pulses during which the PT stimulation was repeated. At resting potential, all but one triceps motoneuron received a net depolarizing effective synaptic current from the PT stimulation. The effective synaptic currents (IN) were much larger in putative type F motoneurons than in putative type S motoneurons [+4.6 +/- 2.9 (SD) nA for type F vs. 0.9 +/- 2.4 nA for putative type S]. When the values of IN at the threshold for repetitive firing were estimated, the distribution was markedly altered. More than 60% of the putative type S motoneurons received a net hyperpolarizing effective synaptic current from the pyramidal tract stimulation as did 33% of the putative type F motoneurons. This distribution pattern is very similar to that observed previously for the effective synaptic currents produced by stimulating the contralateral red nucleus. As would be expected from the wide range of IN values at threshold (-4.8 to +8.7 nA), the PT stimulation produced dramatically different effects on the discharge of different triceps motoneurons. The discharge rates of those motoneurons that received depolarizing effective synaptic currents at threshold were accelerated by PT stimulation (+1 to +8 imp/s), whereas the discharge rates of cells that received hyperpolarizing currents were retarded by the PT input (-2 to -7 imp/s). The change in firing rates produced by the PT stimulation was generally approximated by the product of the effective synaptic currents and the slopes of the motoneurons' frequency-current relations. Our findings indicate that the contralateral pyramidal tract may provide a powerful source of synaptic drive to some high-threshold motoneurons while concurrently inhibiting low-threshold cells. Thus this input system, like that from the contralateral red nucleus, can potentially alter the gain of the input-output function of the motoneuron pool as well as disrupt the normal hierarchy of recruitment thresholds.

Animals↗
PubMed1997

Characteristics of saccadic gain adaptation in rhesus macaques.

We adapted the saccadic gain (saccadic amplitude/target step amplitude) by requiring monkeys to track a small spot that stepped to one side by 5, 10, or 15 degrees and then, during the initial targeting saccade, jumped either forward or backward by a fixed percentage of the initial step. Saccadic gain increased or decreased, respectively, as a function of the number of adapting saccades made in that direction. The relation between gain and the number of adapting saccades was fit with an exponential function, yielding an asymptotic gain and a rate constant (the number of saccades to achieve 63% of the total change in gain). Backward intrasaccadic target jumps of 15, 30, and 50% of the initial target step reduced the asymptotic gain by an average of 12.2, 23.1, and 36.4%, respectively, with average rate constants of 163, 368, and 827 saccades, respectively. During 50% backward jumps, some saccades, especially those to larger target steps, became slower and lasted longer. Forward intrasaccadic jumps of 30% increased the asymptotic gain by 23.3% (average rate constant of 1,178 saccades). After we had caused adaptation, we induced recovery of gain toward normal by requiring the animal to track target steps without intrasaccadic jumps. Recovery following forward adaptation required about one third fewer saccades than the preceding gain increase. Recovery following backward adaptation required about the same average number of saccades as the preceding gain decrease. The first saccades of recovery were slightly less adapted than the last saccades of adaptation, suggesting that a small part of adaptation might have been strategic. After 50% backward jumps had reduced saccadic gain, the hypometric primary saccades during recovery were followed by hypometric corrective saccades, suggesting that they too had been adapted. When saccades of only one size underwent gain reduction, saccades to target steps of other amplitudes showed much less adaptation. Also, saccades in the direction opposite to that adapted were not adapted. Gain reductions endured if an adapted animal was placed in complete darkness for 20 h. These data indicate that saccadic gain adaptation is relatively specific to the adapted step and does not produce parametric changes of all saccades. Furthermore, adaptation is not a strategy, but involves enduring neuronal reorganization in the brain. We suggest that this paradigm engages mechanisms that determine saccadic gain in real life and therefore offers a reversible means to study their neuronal substrate.

Adaptation, Physiological↗
PubMed1997

Participation of caudal fastigial nucleus in smooth pursuit eye movements. II. Effects of muscimol inactivation.

We studied the effect of temporarily inactivating the caudal fastigial nucleus (CFN) in three rhesus macaques trained to make smooth pursuit eye movements. We injected the gamma-aminobutyric acid A agonist muscimol into one or both CFNs where we had recorded pursuit-related neurons a few minutes earlier. Inactivating the CFN on one side impaired pursuit in one monkey so severely that it could not follow step-ramp targets moving at 20 degrees/s, the target velocity that we used to test the other two monkeys. We tested this monkey with targets moving at 10 degrees/s. In all three monkeys, unilateral CFN inactivation either increased the acceleration of ipsilateral step-ramp pursuit (in 2 monkeys, to 144 and 220% of normal) or decreased the acceleration of contralateral pursuit (in 1 monkey, to 71% of normal). Muscimol injected into both CFNs in two of the monkeys left both ipsilateral and contralateral acceleration nearly normal in both monkeys (101% of normal). Unilateral CFN inactivation also impaired the velocity of maintained pursuit as the monkeys tracked a target moving at a constant velocity or oscillating sinusoidally. Averaged across both types of movements in all three monkeys, gains for ipsilateral, contralateral, upward, and downward pursuit were 94, 67, 84, and 73% of normal, respectively. Unilateral CFN inactivation also impaired the monkeys' ability to suppress their vestibuloocular reflex (VOR). Averaged across the two monkeys VOR gain during suppression increased from 0.06 to 0.25 during yaw rotation and from 0.21 to 0.59 during pitch rotation. Bilateral CFN inactivation reduced pursuit gains in all directions more than unilateral injection did. In the two monkeys tested, ipsilateral, contralateral, upward, and downward gains went from 94, 86, 85, and 74% of normal, respectively, after we inactivated one CFN to 88, 73, 80, and 64% of normal after we also inactivated the second CFN. We can explain many, but not all, of the effects of CFN activation on smooth pursuit with the behavior of CFN neurons, and the assumption that the activity of each CFN neuron helps drive pursuit movements in the direction that best activates that neuron. We conclude that the CFN, like the flocculus-ventral paraflocculus, is a cerebellar region involved in control of smooth pursuit.

Animals↗
PubMed1997

Decrease in saccadic performance after many visually guided saccadic eye movements in monkeys.

PURPOSE: To investigate the influence of repeated saccades and of background illumination on the metrics and dynamics of visually guided targeting saccades. METHODS: Eye movements were measured by magnetic search coil technique in seven trained monkeys (Macaca mulatta) while they performed many visually guided saccades in the dark or in dim background light. RESULTS: After 2000 to 7000 saccades in the dark, peak eye velocity on the average decreased by 20%, saccadic gain decreased slightly by 4.5%, and saccadic latency increased by 15%. All parameters also showed increased variability. In contrast, when testing was done in dim light, there was little to no change in average saccadic metrics and latency. CONCLUSIONS: The changes in saccadic metrics and dynamics in the dark do not reflect a change of the ocular plant but may reflect a change in the cortical or cerebellar influences on the brain stem burst generator linked to the monkeys attentional state. Background light mostly prevents this change.

Adaptation, Ocular↗
PubMed1995

Distribution of vestibulospinal synaptic input to cat triceps surae motoneurons.

We applied supramaximal, repetitive stimulation to the lateral vestibular nucleus (Deiters' nucleus, DN) at 200 Hz to evoke stead-state synaptic potentials in ipsilateral triceps surae motoneurons of the cat. The effective synaptic currents underlying these potentials were measured using a modified voltage-clamp technique. The steady-state effective synaptic currents evoked by activating DN were generally small and depolarizing (mean 2.5 +/- 2.6 nA). DN stimulation generated hyperpolarizing synaptic currents in 2 of the 34 triceps motoneurons studied. The effective synaptic currents from DN tended to be larger in putative type F motoneurons than in putative type S cells (type F mean 3.0 +/- 3.1 nA; type S mean 1.8 +/- 1.0 nA). There was a statistically significant difference between the inputs to putative type FF and putative type S motoneurons (mean difference 2.8 nA, t = 2.87, P < 0.01). The synaptic input from DN to medial gastrocnemius motoneurons had approximately the same amplitude as that from homonymous Ia afferent fibers. However, the distribution of DN input with respect to putative motor unit type was the opposite of that previously reported for Ia afferent input. Thus, the synaptic input from DN might act to compress the range of recruitment thresholds within the motoneuron pool and thereby increase the gain of its input-output function.

Animals↗
PubMed1995

Role of the cerebellum in movement control and adaptation.

Three recent discoveries have substantially improved our knowledge of cerebellar function. First, the forelimb regions of the interpositus nuclei specialize in control of one particular limb movement, reach to grasp. Second, a new model indicates that vestibulo-ocular reflex adaptation requires neural changes in both the cerebellum and the brainstem. Finally, the caudal fastigial nucleus uses both short- and long-term influences to maintain saccade accuracy.

Adaptation, Physiological↗
PubMed1995

Effect of dietary retinyl palmitate on the promotion of altered hepatic foci by 3,3',4,4'-tetrachlorobiphenyl and 2,2',4,4',5,5'-hexachlorobiphenyl in rats initiated with diethylnitrosamine.

The purpose of this study was to determine the effects of dietary vitamin A on the tumor promoting effect of 3,3',4,4'-TCB and 2,2',4,4',5,5'-HCB in a two-stage rat hepatocarcinogenesis model with diethylnitrosamine (DEN, 150 mg/kg) as the initiator. Two weeks after DEN injection rats were fed a purified diet containing either 2000 or 100,000 IU of vitamin A in the form of retinyl palmitate. Rats received four biweekly injections of 3,3',4,4'-TCB, 2,2',4,4',5,5'-HCB (300 mumol/kg), or both (150 mumol/kg each) in corn oil (10 ml/kg) for 8 weeks. Control animals received vehicle only. Six rats in each group that received no DEN treatment were used as additional control animals. Ten days after the last injection the rats were killed. In rats fed the low retinyl palmitate diet, treatment with 3,3',4,4'-TCB, 2,2',4,4',5,5'-HCB or both compounds lowered hepatic retinyl palmitate content. This effect was prevented by high dietary retinyl palmitate supplementation in rats treated with 2,2',4,4',5,5'-HCB, but not 3,3',4,4'-TCB or both compounds together. Histopathological examination of the liver showed that high dietary retinyl palmitate lessened the severity of hepatocellular necrosis and fatty changes induced by 3,3',4,4'-TCB alone or in combination with 2,2',4,4',5,5'-HCB. The latter did not cause significant pathological lesions to the liver. However, high dietary retinyl palmitate was not able to prevent thymic involution caused by 3,3',4,4'-TCB. The number and volume of altered hepatic foci were increased by 2,2',4,4',5,5'-HCB and particularly 3,3',4,4'-TCB; no synergistic effect was seen. Supplementation with high dietary retinyl palmitate diminished the number and volume of foci. These results show that supplementation with high dietary retinyl palmitate protects against hepatocellular necrosis, fatty changes, and preneoplastic changes induced by 3,3',4,4'-TCB as well as against preneoplastic changes induced by 2,2',4,4',5,5'-HCB. In addition, these two agents did not synergistically induce preneoplastic changes in DEN-induced rats.

Animals↗
PubMed1994

Anatomical connections of the primate pretectal nucleus of the optic tract.

The pretectal nucleus of the optic tract (NOT) plays an essential role in optokinetic nystagmus, the reflexive movements of the eyes to motion of the entire visual scene. To determine how the NOT can influence structures that move the eyes, we injected it with lectin-conjugated horseradish peroxidase and characterized its afferent and efferent connections. The NOT sent its heaviest projection to the caudal half of the ipsilateral dorsal cap of Kooy in the inferior olive. The rostral dorsal cap was free of labeling. The NOT sent lighter, but consistent, projections to other visual and oculomotor-related areas including, from rostral to caudal, the ipsilateral pregeniculate nucleus, the contralateral NOT, the lateral and medial terminal nuclei of the accessory optic system bilaterally, the ipsilateral dorsolateral pontine nucleus, the ipsilateral nucleus prepositus hypoglossi, and the ipsilateral medial vestibular nucleus. The NOT received input from the contralateral NOT, the lateral terminal nuclei bilaterally, and the ipsilateral pregeniculate nucleus. Although our injections involved the pretectal olivary nucleus (PON), there was neither orthograde nor retrograde labeling in the contralateral PON. Our results indicate that the NOT can influence brainstem preoculomotor pathways both directly through the medial vestibular nucleus and nucleus prepositus hypoglossi and indirectly through both climbing and mossy fiber pathways to the cerebellar flocculus. In addition, the NOT communicates strongly with other retino-recipient zones, whose neurons are driven by either horizontal (contralateral NOT) or vertical (medial and lateral terminal nuclei) fullfield image motion.

Animals↗
PubMed1994

Coordination of gaze shifts in primates: brainstem inputs to neck and extraocular motoneuron pools.

To determine whether there are brainstem regions that provide common input to the motoneurons that move both the head and the eyes, we injected wheat germ agglutinin-horseradish peroxidase complex (WGA-HRP) into neck motoneuron pools at spinal level C2 (N = 3) and extraocular motoneuron pools in the abducens (N = 1) and oculomotor/trochlear (N = 1) nuclei of rhesus and fascicularis macaques. We also injected WGA-HRP into spinal level C5-7 (N = 1) of a fascicularis macaque for comparison. After injections into C2, we observed retrogradely labeled cells in the ventral reticular formation (NRV), the gigantocellular reticular formation (NRG), and both the oral (NRPO) and the caudal (NRPC) divisions of the paramedian pontine reticular formation (PPRF). There was also a column of labeled cells in the cuneate reticular nucleus (NCUN) just lateral to the ipsilateral periaqueductal gray (PAG). This column extended rostrally into the central mesencephalic reticular formation (CMRF). In addition, there were labeled cells in the region ventral and caudal to the rostral interstitial nucleus of the MLF (riMLF), the area lateral to the interstitial nucleus of Cajal (INC), and the ventral part of the lateral vestibular nucleus (LVN) and lateral part of the medial vestibular nucleus (MVN). There were also a few labeled cells in the fastigial (FN) and interposed (IN) nuclei of the cerebellum but very few in the superior colliculus (SC). In contrast, the injection into C5-7 labeled many cells in the lateral vestibular nucleus (LVN) and very few in FN or IN. Injecting WGA-HRP into the abducens nucleus and the surrounding tissue labeled many cells in SC, PPRF, MVN, FN, and nucleus prepositus hypoglossi (NPH). Injecting into the oculomotor/trochlear nuclei and nearby tissue labeled cells in SC, INC, riMLF, FN, IN, MVN, and superior vestibular nucleus (SVN). Structures that project to both neck and eye motoneuron pools, and therefore probably participate in both head and eye movements, include the lateral part of the MVN and both NRPO and NRPC in the PPRF. Those that project primarily to neck motoneurons in C2 include the NRV, the NRG, and the NCUN-CMRF column. Those projecting exclusively to extraocular nuclei include the NPH, INC, riMLF, NRPD, and SC. We use these data to propose a scheme for control of combined eye-head movements in monkeys.

Afferent Pathways↗
PubMed1994

Participation of the caudal fastigial nucleus in smooth-pursuit eye movements. I. Neuronal activity.

1. We recorded single-unit activity from neurons of an output of the cerebellum, the fastigial nucleus, in two rhesus macaques while the monkeys tracked small moving targets with their eyes. Many neurons in the caudal part of the fastigial nucleus exhibited a modulation in their discharge rates when smooth-pursuit eye movements were elicited by either sinusoidal or step-ramp motions of a small target. 2. The pursuit direction that elicited the most vigorous modulation in unit firing to sinusoidal target motion could be horizontal, vertical, or oblique. Most often, the preferred direction was in the contralateral and/or downward direction (50 of 69 neurons) or in the ipsilateral and/or upward direction (13 of 69). 3. For units whose preferred smooth-pursuit directions were either contralateral/downward or ipsilateral/upward during sinusoidal pursuit, peak firing as measured by the phase shift of periodic modulation at 0.5-0.8 Hz occurred near the time of peak velocity. The discharge of 80% of the neurons with contralateral/downward preferred directions preceded eye velocity by an average of -27 degrees; thus these neurons discharged maximally during eye acceleration. In contrast, neurons with ipsilateral/upward preferred directions lagged peak velocity by an average of +10.5 degrees and therefore discharged during eye deceleration. 4. The average eye velocity sensitivity for sinusoidal pursuit between 0.5 and 0.8 Hz was 0.83 +/- 0.57 (SD) spikes/s per degrees/s. We also tested 36 units during pursuit at a variety of frequencies in their preferred directions and found that firing rates increased monotonically with peak eye velocity. However, the firing rate saturated at velocities ranging from 20 to 60 degrees/s for different units. 5. When a monkey tracked a step-ramp target motion, three discharge patterns emerged in the 27 units tested. Just over half of the units discharged a burst of spikes that preceded (average lead of 27.4 +/- 17 ms) and lasted throughout the initial third of the eye acceleration; the burst was followed by a subsequent steady firing that continued after the eye had accelerated to its steady velocity. Fewer neurons discharged a burst that began late in the acceleration and was followed by steady firing. Occasional neurons showed only a gradual increase in firing rate during acceleration followed by a steady discharge. 6. Thirty of the 31 fastigial smooth-pursuit units tested also were modulated during sinusoidal yaw and/or pitch oscillations while the animals fixated a spot that rotated with them.(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗
PubMed1993

Distribution of rubrospinal synaptic input to cat triceps surae motoneurons.

1. We evoked steady-state synaptic potentials in triceps surae motoneurons of the cat by stimulating the hindlimb projection area of the contralateral magnocellular red nucleus at 200 Hz. We measured the effective synaptic currents (IN) underlying the synaptic potentials using a modified voltage-clamp technique. We also determined the effect of the rubrospinal input on the discharge rate of some of the motoneurons by inducing repetitive discharge with long injected current pulses during which the red nucleus stimulation was repeated. 2. At motoneuron resting potential, the distribution of IN from the red nucleus within the triceps surae pools was qualitatively similar to the distribution of synaptic potentials: 86% of the putative type F motoneurons received a net depolarizing IN from the red nucleus stimulation, whereas only 38% of the putative type S units did so. The mean values of IN were significantly different in the two groups [+4.1 +/- 5.0 nA (SD) for putative type F and -1.6 +/- 3.1 nA for putative type S]. 3. However, when the values of IN at threshold for repetitive firing were estimated, the distribution of IN from the red nucleus was quite different. At threshold, all of the putative type S units received hyperpolarizing IN but so did nearly half of the putative type F units. 4. As would be expected from the wide range of IN at threshold (-20 to +12 nA), the red nucleus input produced dramatically different effects on the discharge of different motoneurons.(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗
PubMed1993

Role of the caudal fastigial nucleus in saccade generation. I. Neuronal discharge pattern.

1. The effects of lesions in both human and nonhuman primates have implicated the cerebellum in the control of rapid eye movements, i.e., saccades. To examine the neural substrate of this control, we recorded the discharge patterns of cerebellar output cells in the fastigial nucleus while monkeys tracked a small, jumping spot of light. 2. In the caudal fastigial nucleus, neurons discharged for saccades in one or several directions. All exhibited a burst. Some also exhibited a saccade-related pause in firing either before or after saccades greater than approximately 3-5 degrees. Thirty-seven percent discharged only a burst, 44% also exhibited a pause before bursts in certain directions, and 19% also paused after the saccade-related burst in certain directions. Although many cells discharged steadily during intersaccadic intervals, few exhibited a robust relation between firing rate and eye position. 3. As a measure of directional selectivity, we plotted the burst lead time as a function of saccade direction for saccades of similar (10 degrees) radial amplitudes. Of 20 neurons tested, 17 burst earliest for contralateral saccades and 1 for upward saccades; 2 others showed little dependence on direction. Of 19 additional units tested only in the horizontal direction, 18 burst earlier for contralateral saccades. 4. For contralateral saccades the burst preceded saccades of all sizes by at least 7.7 ms on average. For ipsilateral saccades, the burst preceded small saccades by an average of 10.3 ms. However, as ipsilateral saccade size increased, the burst began later and later relative to saccade onset so that, on average, it always occurred after the onset of 20 degrees saccades but well before the saccade ended. 5. Many fastigial saccade-related units showed increases in the number of spikes with saccade size and in burst duration with saccade duration in one or more directions. For either relation the highest average correlation coefficients ranged from 0.6 to 0.65. In general, the average correlation coefficients and slopes for either relation were slightly larger for contralateral saccades. Pure burst neurons did not display better average correlations than neurons that also paused. For neurons that also paused either before or after saccades, there was a weak tendency for pause duration to increase with the duration of larger saccades. 6. We tested the effect of eye position on unit discharge in 13 cells by requiring the monkey to make 10 degrees ipsilateral and contralateral saccades from a variety of starting positions.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1993

Role of the caudal fastigial nucleus in saccade generation. II. Effects of muscimol inactivation.

1. We studied the effect of temporarily inhibiting neurons in the caudal fastigial nucleus in two rhesus macaques trained to make saccades to jumping targets. We placed injections of the gamma-aminobutyric acid (GABA) agonist muscimol unilaterally or bilaterally at sites in the caudal fastigial nucleus where we had recorded saccade-related neurons a few minutes earlier. 2. Unilateral injections (n = 9) made horizontal saccades to the injected side hypermetric and those to the other side hypometric (mean gain of 1.37 and 0.61, respectively, for 10 degrees target steps, and 1.26 and 0.81 for 20 degrees target steps; normal saccade gain was 0.96). Saccades to vertical targets showed a small but significant hypermetria and curved strongly toward the side of the injection. The trajectories and end points of all targeted saccades were more variable than normal. 3. After unilateral injections, centripetal saccades were slightly larger than centrifugal saccades (mean gains for ipsilateral saccades were 1.42 and 1.31, respectively, for 10 degrees target steps, and 1.37 and 1.15 for 20 degrees target steps). 4. Unilateral injections increased the average acceleration of ipsilateral saccades and decreased the acceleration of contralateral saccades. Injections decreased both the acceleration and deceleration of vertical saccades. 5. After dysmetric saccades, monkeys acquired the target with an abnormally high number of hypometric corrective saccades. Injection increased the average number of corrective saccades from 0.6 to 2.1 after 10 degrees horizontal target steps and from 0.8 to 2.1 after 20 degrees steps. The size of each successive corrective saccade in a series decreased, and the latency from the previous corrective saccade increased. 6. Bilateral injections (n = 2) of muscimol, in which we injected first into the left caudal fastigial nucleus and then, within 30 min, into the right, made all saccades hypermetric (mean gain for 10 degrees right, left, up, and down saccades was 1.18, 1.49, 1.43, and 1.10, respectively). Paradoxically, bilateral injection decreased both saccade acceleration and deceleration. Saccade trajectories and end points were more variable than normal. 7. To account for the effects of our injections, we propose that the activity of caudal fastigial neurons on one side normally helps to decelerate ipsilateral saccades and helps to accelerate contralateral saccades by influencing the feedback loop of the saccade burst generator in the brain stem. Without caudal fastigial activity the brain stem burst generator produces hypermetric, variable saccades. We therefore also propose that the influence of caudal fastigial neurons on the burst generator makes saccades more consistent and accurate.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗