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S M Highstein

Publications and source records attributed to S M Highstein.

At least 91 records · Page 5Linked to original sources
PubMed1982

Comparison of the morphology of physiologically identified abducens motor and internuclear neurons in the cat: a light microscopic study employing the intracellular injection of horseradish peroxidase.

Abducens motoneurons and internuclear neurons were identified electrophysiologically in anesthesized, paralyzed cats and stained by intracellular injection of horseradish peroxidase. Neurons were reconstructed and surface area of selected cells measured by light microscopy. Surface area of motoneurons and internuclear neuron with similar soma size and shape were roughly comparable. Dendrites of motoneurons were highly tapered and highly branched. By contrast, dendrites of internuclear neurons were less tapered and less branched. Axons of motoneurons had no collaterals within the brainstem. Internuclear axons crossed the midline at the level of their parent somata and ascended in the medial longitudinal fasciculus toward the oculomotor nucleus. Approximately 30% of the internuclear axons branched in the contralateral medial longitudinal fasciculus sending a fine collateral caudal toward the prepositus hypoglossi nucleus. The results suggest that, on the average, structural correlates of injected neurons (i.e., soma-dendritic morphology) can account at least in part for the earlier firing and higher intraburst frequencies of internuclear neurons versus motoneurons during on-direction rapid eye movements in alert cats.

Abducens Nerve↗
PubMed1978

Vestibular nucleus neurons relaying excitation from the anterior canal to the oculomotor nucleus.

A morphological approach was undertaken to determine which vestibular nucleus neurons relay excitation from the anterior canal to the IIIrd nucleus. In anesthetized rabbits HRP was iontophoresed into the IIIrd nucleus and cells filled with HRP reaction product (positive cells) searched for within the vestibular nuclear complex. By lesioning the MLF or brachium conjunctivum immediately after iontophoresis it was demonstrated that positive cells in the dorsum of the superior vestibular nucleus are backfilled via their axons which ascend in the brachium conjunctivum. By contrast positive cells in the center of the superior nucleus are backfilled via their axons in the MLF. In electrophysiological experiments in the presence of a severed MLF the anterior canal was selectively stimulated for orthodromic, and the 3rd nucleus stimulated for antidromic, activation of vestibular nucleus neurons. Recording extracellularly with glass microelectrodes filled with fast green FCF the only cells both ortho- and antidromically activated were localized to the dorsum of the superior vestibular nucleus. It is concluded that cells dorsally located in the superior nucleus relay the disynaptic excitatory vestibulo-ocular reflex from the anterior canal to the contralateral 3rd nucleus via their axons which ascend in the brachium conjunctivum.

Animals↗
PubMed1978

Excitatory termination of abducens internuclear neurons on medial rectus motoneurons: relationship to syndrome of internuclear ophthalmoplegia.

1. Field potentials and intracellular records were obtained from the medial rectus subdivision of the IIIrd nucleus in anesthetized cats following electrical stimulation of the abducens nuclei, vestibular nerves, pontomedullary brain stem, and the medial longitudinal fasciculi (MLF). 2. Stimulation of the contralateral abducens nucleus produced unique field potentials in the medial rectus subdivision. They consisted of an early sharp transient volley followed by a slower postsynaptic negativity. 3. Monosynaptic EPSPs were evoked in medial rectus motoneurons following contralateral abducens nucleus stimulation. The EPSP amplitudes were graded when the stimulus intensity was increased from threshold to supramaximal. EPSPs produced by contralateral abducens nucleus stimulation were larger in amplitude than those produced by ipsilateral vestibular nerve stimulation. The current-voltage relationship and reversal potentials for Vi- and abducens-evoked EPSPs were similar and indicated an overlapping location of excitatory synaptic terminals on medial rectus motoneurons. 4. Secondary vestibular axons activated monosynaptically by ipsilateral vestibular nerve stimulation were not recruited by abducens nucleus stimulation. 5. Ipsilateral MLF stimulation produced EPSPs with similar profiles as those observed following abducens nucleus stimulation; however, stimulation of the contralateral MLF at comparable stimulus intensities did not produce any changes in transmembrane potential. 6. When higher intensity stimuli were applied to the contralateral MLF, the synaptic potentials recorded in the medial rectus were occluded by those produced by weaker stimulation applied to the ipsilateral MLF. This suggests that the potentials resulting from stronger contralateral stimulation were due to current spread to the ipsilateral MLF. 7. While recording in the medial rectus subdivision, various sites in the ponto-medullary brain stem were explored with a stimulating electrode. Analysis of evoked field potentials suggested that the ascending internuclear axons were contained only in the MLF ipsilateral to the medial rectus. Acute brain stem lesions confirmed this suggestion. 8. Chronic lesions were placed in the brain stem to isolate the abducens nucleus from either extrinsic fibers of passage or axon collaterals. Acute electrophysiological experiments in these chronic animals corroborated the suggestion that the medial rectus pathway originated from within the abducens nucleus. 9. We conclude that axons from the internuclear neurons of the abducens nucleus exit from the nucleus medially, cross the midline, ascend in the opposite MLF, and terminate monosynaptically on medial rectus motoneurons. 10. we believe that the syndrome of internuclear ophthalmoplegia associated clinically with lesions of the medial longitudinal fasciculus could be due to the absence of ascending physiological activity from internuclear neurons of the abducens nucleus.

Abducens Nerve↗
PubMed1977

Vestibular and medullary brain stem afferents to the abducens nucleus in the cat.

Brain stem neurons that project to the abducens nucleus (nVI) were labeled by the technique of retrograde transport of horseradish peroxidase (HRP). Following iontophoresis of HRP into nVI a large number of labeled cells are found in the ipsilateral vestibular nuclear complex, extending from the rostral medial vestibular nucleus into the ventral lateral vestibular nucleus. A smaller number of HRP-positive cells are also found in the contralateral medial vestibular nucleus. In addition, labeled cells are localized to the contralateral dorsomedial gigantocellular tegmental field as well as the nucleus praepositus hypoglossi of both sides, evidence that these neuronal groups may also be involved in eye movement control.

Abducens Nerve↗
PubMed1976

Stimulation-induced depletion of vesicles, fatigue of transmission and recovery processes at a vertebrate central synapse.

The Mauthner fiber giant fiber synapses of the hatchetfish are chemically transmitting axo-axionic synapses in the medulla. Tetanic stimulation at room temperature depletes the presynaptic Mauthner terminal of vesicles and leads to the appearance of large numbers of irregular membraneous compartments in the terminal. Stimulation during cooling to 12 degrees C depletes the terminal of vesicles and greatly increases the external surface, which forms large whorls of invaginating double membranes. Many coated vesicles are attached to the surface and the invaginating whorls. It is concluded that vesicles are discharged by exocytosis and fusion of their membrane with the external surface, and that at room temperature, membrane is reinternalized by coated vesicles and formed into irregular compartments. In completion of the cycle, these compartments disappear, and the vesicle population recovers over an hour or two of rest. When the Mauthner fibers are stimulated at low rates, the p.s.p.'s in the giant fibers are large and suprathreshold. Minature p.s.p.'s are generated spontaneously or can be evoked by subthreshold depolarization or tetanic stimulation of the Mauthner fiber. Stimulation of the Mauthner fibers at gradually increasing frequencies depresses p.s.p. amplitude to or below the level of miniature p.s.p.'s, but no failures are observed. Small p.s.p.'s without failures suggest that the quantum number remains high but that quantal size is greatly reduced, either by partial filling, as is supported by the morphological observation of vesicle depletion, or by desensitization. When stimulation is stopped, recovery of p.s.p. amplitude occurs in 1 or 2 seconds, but if tetanic stimulation is resumed immediately, p.s.p. amplitude decreases again and much more rapidly than in the initial rundown. This result suggests that depression of p.s.p. amplitude is not due to desensitization and leaves partial filling as the most likely explanation of small quanta. Calculated quantal size following a tetanus recovers in 200-500 ms, which probably largely reflects the time for filling since enough vesicles can be supplied to prevent failures with much shorter intervals between stimuli. Because quantal size appears to decrease gradually as stimulation frequency increases, it appears that release of vesicles can interrupt filling, leading to the conclusion that filling and release sites are very close together. This conlusion is consistent with other data in the literature obtained by different techniques.

Animals↗
PubMed1975

Depletion of vesicles and fatigue of transmission at a vertebrate central synapse.

Synapses from Mauthner to giant fibers in the hatchetfish are chemically transmitting excitatory axo-axonic synapses located in the medulla. The synapses are 4--10 mum in diameter and easily identified for electron microscopy. Presynaptic vesicles are clustered near the contact regions and are round, clear and 40-60 nm in diameter. Stimulation of the Mauthner fiber at 10/sec for 10 min greatly reduces PSP amplitude and causes profound changes in presynaptic structures. Synaptic vesicles become few in number and there is a marked accumulation of irregular membranous structures. These changes are reversible. During the recovery period, the number of synaptic vesicles progressively increases to control values, and the number of irregular membranous structures declines. Further, stimulation during cooling induces depletion of vesicles together with a great increase in the surface area of the presynaptic membrane and in the number of coated vesicles. Internal irregular membranous structures are few. Our data provide evidence for the vesicular release of transmitter and are consistent with there being a mechanism of membrane recycling in which vesicle membrane fuses with the presynaptic membrane and is reclaimed from it by coated vesicles that then coalesce to form irregular membranous structures from which new synaptic vesicles are formed.

Animals↗
PubMed1975

Fatigue and recovery of transmission at the Mauthner fiber-giant fiber synapse of the hatchetfish.

When the Mauthner fiber-giant fiber synapse of the hatchetfish is activated at gradually increasing frequencies, postsynaptic potentials (PSPs) in the giant fiber become progressively smaller, but complete failures of transmission are not observed even when PSP size is as small or smaller than miniature PSPs (mPSPs) simultaneously recorded. On the assumption of a Poisson distribution of amplitudes, calculations from the absence of failures and from variance suggest that guantum number remains at least as high as 5--10 and that quantal size is greatly reduced. During tetanic stimulation the frequency of mPSPs first increases and then decreases again, sometimes to a very low frequency. However, mPSP amplitude is reduced by no more than about 50%, which indicates that quanta giving rise to mPSPs come from a different population of vesicles than those comprising evoked PSPs. During rest following a tetanus, calculated quantal size in evoked PSPs recovers within several hundred milliseconds to mPSP size simultaneouly recorded. Most of this recovery time represents time for filling, since vesicles can be supplied at much higher rates during tetanic stimulation. After one second rest PSP amplitude exceeds threshold but recovery for later PSPs in a short train requires many minutes. The slowness of this recovery is consistent with the morphological demonstration of slow recovery of the vesicle population after depletion. These data are interpreted in terms of vesicle release, depletion and membrane recycling. Following depletion new vesicles are released after only partial filling which accounts for small quanta. Very small mPSPs are not seen because filling time is short compared to time for release as mPSPs. Since quantal size can be gradually reduced, release can interrupt filling, and filling and release sites are likely to be the same. The data in combination with the morphological observations support the hypothesis of vesicular release of transmitter and provide new evidence as to rates and sites for filling of vesicles.

Animals↗