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Biomedical subjects

W Precht

Publications and source records attributed to W Precht.

At least 19 recordsLinked to original sources
PubMed1989

Effects of kainic acid lesions of the nucleus reticularis tegmenti pontis on fast and slow phases of vestibulo-ocular and optokinetic reflexes in the pigmented rat.

The nucleus reticularis tegmenti pontis (NRTP) and adjacent pontine reticular formation were lesioned chemically using the neurotoxic agent kainic acid, and the effects of these lesions on horizontal ocular optokinetic and vestibular nystagmus were examined. Eye position was measured in the alert, NRTP-lesioned animals with the electromagnetic search coil technique. Optokinetic and vestibular stimuli consisted of steps of rotations or sinusoidal oscillations of a fullfield visual pattern surrounding the animal or of the animal in total darkness, respectively. In a first group of animals, small unilateral NRTP lesions were produced by placing a single kainic acid injection in the area of the left NRTP. In one third of the animals, ipsilateral quick phases of optokinetic and vestibular nystagmus were abolished. In the remaining animals, quick phases were deficient to various degrees or not affected at all. There were no changes in the characteristics of optokinetic step responses to ipsilateral pattern rotations which activate predominantly optokinetic pathways on the side of the brainstem lesion. In animals with ipsiversive quick phase deficits, contralateral pattern rotations elicited tonic eye deviations. In a second group of animals, large uni- or bilateral lesions were produced by injecting kainic acid into three separate rostral, middle and caudal levels of the right NRTP. These animals had uni- or bilateral quick phase deficits during optokinetic and vestibular nystagmus. Optokinetic nystagmus in response to velocity steps of pattern rotation towards the lesion side was strongly reduced in gain even in those animals that had no apparent deficits in the fast contraversive reset phases. In four out of six animals, responses to sinusoidal optokinetic pattern oscillations were reduced in gain and showed increased phase lags compared to controls. Vestibulo-ocular responses to velocity steps of head rotations were of normal gain but reduced in duration (measured from onset of stimulation to reversal of nystagmus). Sinusoidal vestibulo-ocular responses evoked by head oscillations exhibited reduced gain values and strongly increased phase leads in the frequency range below 0.5 Hz. The vestibular time constant was found to be around 4.5 s in animals with NRTP lesions compared to about 7.5 s in control animals. The present results show that large kainic acid lesions of the NRTP (and adjacent area) do not abolish optokinetic eye movements in the rat, in contrast to what has been reported after electrolytic lesions.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1987

Pharmacological aspects of excitatory synaptic transmission to second-order vestibular neurons in the frog.

Synaptic excitation of second-order vestibular neurons is mediated by two principal afferents: vestibular afferents projecting into the brain via the VIIIth cranial nerve and commissural afferents from the contralateral vestibular nuclear complex. The shape of the excitatory postsynaptic potentials (EPSPs) generated by selectively activating these two inputs differs qualitatively, such that ipsilateral VIIIth nerve afferents generate a faster-rising EPSP than do the commissural afferents. We have investigated the synaptic pharmacology of these two inputs in the isolated, intact medulla of the frog in order to determine the nature of the transmitter substances released by the afferents and the nature of the subsynaptic receptors with which these transmitters interact. Electrical stimulation of the ipsilateral VIIIth cranial nerve evokes in the region of the vestibular nuclear complex a field potential that exhibits a presynaptic (afferent volley) and a postsynaptic (slow negativity) component. Bath application of glutamate receptor antagonists, such as kynurenic acid (KENYA), blocks the postsynaptic component of this field potential in a dose-dependent manner, without affecting the presynaptic volley, suggesting that the VIIIth nerve afferent releases glutamate and/or similar substances as its neurotransmitter. A comparison of the actions of various glutamate receptor antagonists to block this postsynaptic negativity gives a rank order of effectiveness such that KENYA greater than gamma-D-glutamylglycine (gamma DGG) = gamma-D-glutamylaminomethylsulfonic acid (GAMS) greater than gamma-D-glutamyltaurine (gamma DGT) much greater than gamma-D-glutamylaminomethylphosphonic acid (GAMP) greater than D-2-amino-5-phosphonovaleric acid (D-APV) greater than D,L-APV greater than D-2-amino-7-phosphonoheptanoic acid (APH). This rank order of effectiveness suggests that the VIIIth nerve transmitter activates second-order neurons through kainate (KA)/quisqualate (QUIS) synaptic receptors. Intracellular studies support these conclusions. Chemically mediated EPSPs evoked from ipsilateral VIIIth nerve stimulation are completely blocked by high concentrations of KENYA (greater than or equal to 1 mM). Occasionally an extremely short-latency, probably electrically mediated, component to these EPSPs persists in the presence of KENYA. The slower-rising EPSPs evoked from contralateral VIIIth nerve or contralateral vestibular nuclear complex stimulation are also completely blocked by KENYA, suggesting that the transmitter released by the commissural afferents is also glutamate and/or related compounds.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1987

Vestibular nerve and nuclei unit responses and eye movement responses to repetitive galvanic stimulation of the labyrinth in the rat.

Two-second cathodal current pulses were applied at one-minute intervals at a point external to the round window in the ear of each albino rat subject. Responses were recorded in the vestibular nerve ganglion, the vestibular nuclei (single units), or in the eye movements (search coil recording method) of anaesthetized, decerebrated, or alert rats. The unit responses to the galvanic stimuli were characterized and compared with responses to galvanic and rotational stimuli reported in the literature. The main focus of the study, however, was effects of stimulus repetition. In both the vestibular nerve and vestibular nuclei recordings, the responses of many units were substantially larger or smaller at the end of a 13-pulse stimulus train than at the beginning. In the vestibular nuclei, but not in the nerve, there was a slight bias towards a decrease in response magnitude, with 10/88 units showing decreases great enough to be considered as reflecting an habituation process. In contrast, the eye movement responses showed more consistent response decrements, especially in the alert condition, but also in the other conditions (none of the unit recordings were done in alert rats). It is concluded that some of the modifications underlying habituation of the vestibuloocular reflex probably occur in portions of the neuronal reflex pathways that are downstream from the vestibular nuclei.

Animals↗
PubMed1986

Evidence for an alteration in brainstem cholinergic pathways following unilateral labyrinthectomy in the frog.

Following VIIIth nerve stimulation, field potentials recorded in the contralateral vestibular nuclei of isolated medullae are larger in amplitude and more sensitive to atropine in chronically hemilabyrinthectomized frogs than those of controls. The atropine-sensitive component occurs at a latency which precludes involvement of the monosynaptic commissural projection between second order vestibular neurons. Therefore, in addition to this commissural projection, the contributions of more indirect pathways have to be considered in an attempt to understand the neuronal basis of behavioral improvement following vestibular lesions.

Animals↗
PubMed1986

Anatomical studies on the nucleus reticularis tegmenti pontis in the pigmented rat. I. Cytoarchitecture, topography, and cerebral cortical afferents.

The nucleus reticularis tegmenti pontis (NRTP) is a precerebellar reticular nucleus that has been found to be related to cerebropontocerebellar pathways and, more recently, to eye movements. The present study investigates the cytoarchitecture, the topography, and the cerebral cortical projections to the NRTP in the pigmented rat. The cytoarchitecture and topography of the NRTP was determined by examination of Nissl-stained material sectioned in the transverse and sagittal planes. Two cytoarchitectonically distinct portions of the NRTP are apparent; a central subdivision (NRTPc) composed of large multipolar, small spherical, and fusiform neurons, and a pericentral subdivision (NRTPp) composed of loosely packed small fusiform and spherical neurons. The NRTPc is located dorsal to the medial lemniscus and pyramidal tracts over the caudal two-thirds of the pons. It extends caudodorsally to the region just rostral and ventral to the abducens nucleus. The NRTPp is adjacent to the lateral margins of the NRTPc, rostrally, and lies ventral to the caudal portions of the NRTPc. Large injections of horseradish peroxidase (HRP) were made into the cerebellum in order to determine the degree to which each subdivision of the NRTP contributes to the cerebellar projection. A high percentage of NRTPc neurons and a lower percentage of NRTPp neurons were labeled. These differences in labeling density and neuronal morphology noted above confirm the appropriateness of subdividing the NRTP into central and pericentral subdivisions. The cerebral cortical afferents to the NRTP were examined by placing small iontophoretic injections of HRP into the NRTPc and NRTPp. A systematic examination of all cortical areas revealed that the HRP-labeled neurons are entirely localized within pyramidal layer V of three major cortical areas: the ipsilateral prefrontal cortex (Brodmann areas 8, 8a, 11, and 32); the ipsilateral motor and somatosensory cortices (Brodmann areas 2, 4, 6, and 10), and the bilateral cingular cortex (Brodmann areas 24a, 24b, 29c, and 29d). By far, the heaviest cortical labeling with HRP injections into the medial NRTPc is within the cingular cortex that may, in the rat, be homologous to the frontal eye field of the cat and monkey. In contrast, injections involving the lateral NRTPc or the NRTPp produced labeling within wide regions of the cortex with the greatest number in the somatomotor cortex.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1986

Anatomical studies on the nucleus reticularis tegmenti pontis in the pigmented rat. II. Subcortical afferents demonstrated by the retrograde transport of horseradish peroxidase.

The subcortical nuclear groups projecting to the nucleus reticularis tegmenti pontis (NRTP) were studied in pigmented rats with the aid of the retrograde horseradish peroxidase (HRP) technique. Small iontophoretic injections of HRP were placed in the medial regions of the NRTP, an area that has been shown in several species to be involved in eye movements. Other large injections in the NRTP or small injections placed just outside the nucleus were used to clarify the projections to the NRTP. Results indicate that the NRTP receives afferents from visual relay nuclei, including the nucleus of optic tract, the superior colliculus, and the ventral lateral geniculate nucleus; oculomotor-associated structures including the zona incerta, the H1 and H2 fields of Forel, the nucleus subparafasciculus, the interstitial nucleus of Cajal, the visual tegmental relay zone of the ventral tegmental area of Tsai, the mesencephalic, pontine, and medullary reticular formations, the nucleus of the posterior commissure, and a portion of the periaqueductal gray termed the supra-oculomotor periaqueductal gray; cerebellar and pontomedullary nuclei, including the superior, lateral, and medial vestibular nuclei, the deep cerebellar nuclei, and NRTP interneurons, and nuclei related to limbic functions including the lateral habenula, the mammillary nuclei, the hypothalamic nuclei, the preoptic nuclei, and the nucleus of diagonal band of Broca. A surprisingly large number of afferents to the medial regions of the NRTP arise from visual- or eye-movement-related nuclei. The projection from the nucleus of the optic tract (NOT) confirms previous anatomical and physiological studies on the pathways involved in horizontal optokinetic nystagmus, but the number of NOT afferents is small in relation to other areas potentially related to visuomotor pathways such as the zona incerta, ventral lateral geniculate nucleus, fields of Forel, perirubral area, and subparafasciculus. The NRTP may also relay information related to vertical visuomotor reflexes (e.g., vertical optokinetic nystagmus) given the strong projections from the medial terminal nucleus of the accessory optic system, visual tegmental relay zone, supra-oculomotor periaqueductal gray, interstitial n. of Cajal, and midbrain reticular formation. The presence of significant NRTP projections from the superior colliculus and the mesencephalic and pontine reticular formations suggests that these nuclei may provide the pathways for the noted saccade-related activity of NRTP neurons. In addition, projections from the vestibular nuclei were found that provide the anatomical basis for head velocity signals recorded in NRTP neurons.(ABSTRACT TRUNCATED AT 400 WORDS)

Afferent Pathways↗
PubMed1986

Partial restitution of lesion-induced deficits in the horizontal vestibulo-ocular reflex performance measured from the bilateral abducens motor output in frogs.

The responses of the bilateral abducens nerves to small table velocity steps in the dark were measured in four groups of animals: One group was intact prior to recording (controls), one group was hemi-labyrinthectomized the day before the recordings (acute HL), the horizontal canal nerve was sectioned the day before the recordings (acute HCN) in another and the last group was hemi-labyrinthectomized between 60 and 90 days prior to recording (chronic HL). In controls (N = 6) the slopes of the change in discharge rate to increasingly larger velocity steps increased maximally with about 200 imp/s per 1 degree/s and decreased maximally with about -60 imp/s per 1 degree/s. This difference is explained by low resting rates and by recruitment of spontaneously inactive vestibular afferent, central vestibular and abducens neurons. Results obtained from acute HL (N = 4) and acute HCN (N = 4) animals were practically identical. In neither case was a spontaneous nystagmic activity pattern observed. Results differed from those obtained in controls due to an asymmetric reduction in responsiveness. Comparison of the slopes of the evoked increases and decreases in discharge rates of abducens nerves to increasingly larger velocity steps with those in controls show that normal abducens responses are predominantly controlled by crossed excitation and by uncrossed inhibition. Disinhibition and disfacilitation play minor roles. In chronic HL animals (N = 6) that had posturally recovered to a similar degree, responses evoked by steps towards the intact side at larger velocity steps were slightly reduced with respect to those in acute HL or HCN animals. Responses evoked by steps towards the lesioned side differed between individuals. They were either similar to those in controls (N = 1), to those in acute animals (N = 2) or lay between these two extremes (N = 3). The improvement in response to velocity steps towards the lesioned side in 4 of 6 animals is explained by an increase in activity released by disinhibition. This inhibition in turn is controlled by horizontal canal-dependent input from the intact side. Plugging of this canal abolished all direction-specific responses in this plane in the dark, suggesting that the partial restitution of function of horizontal reflex performance depends exclusively on signals derived from receptors of this canal.

Abducens Nerve↗
PubMed1985

Presynaptic actions of cholinergic agents upon the hair cell-afferent fiber synapse in the vestibular labyrinth of the frog.

Spontaneous activity of semicircular canal afferents in the isolated labyrinth of the frog is altered by bath application of cholinergic agonists. Muscarinic agonists can produce an increase in action potential frequency of individual afferents. This increase develops slowly and is prolonged in the time course of its action. Nicotinic agonists can either increase (most cases) or decrease afferent activity. These effects occur rapidly and decay during the period of activation, suggesting desensitization. Muscarinic effects are blocked by prior administration of atropine and nicotinic effects (both increases and decreases in action potential frequency) by curare. Intracellular recordings reveal that the nicotinic effects on afferent action potential frequency are the result of alterations in the frequency of spontaneous synaptic potentials, indicating a presynaptic site of action on the hair cells for these compounds. This conclusion is supported by the fact that in the presence of high Mg2+/low Ca2+, which blocks hair cell release of transmitter, cholinergic agonists do not affect the resting membrane potential of the vestibular afferent. Electrical stimulation of the VIIIth cranial nerve can result in either an increase or a decrease in spontaneous synaptic potential and action potential frequency of an afferent. These effects are blocked by prior administration of curare or of nicotinic agonists. Repetitive or continuous stimulation of the VIIIth nerve results in a reversible reduction of the evoked response, suggesting desensitization. Transection of the VIIIth cranial nerve two weeks prior to recording eliminates these actions of electrical stimulation, but not the responses to cholinergic agonists, indicating that the effects of electrical stimulation are mediated by centrally arising efferents. These findings confirm that acetylcholine is probably the transmitter released from centrally arising vestibular efferents, and, in addition, demonstrate that efferent-mediated effects are predominantly expressed through nicotinic receptors. Studies comparing the effects of isolation of the semicircular canal alone versus the intact labyrinth suggest that the method of isolation may be an important factor in determining whether efferent activity results in a predominant increase or decrease in afferent activity.

Acetylcholine↗
PubMed1985

On the role of vestibulo-ocular reflex plasticity in recovery after unilateral peripheral vestibular lesions.

Although adaptive plasticity is a well-known feature of the vestibulo-ocular reflex (VOR), deficits in VOR performance after unilateral labyrinthectomy are poorly compensated in a large percentage of cats. To assess whether VOR plastic capabilities are affected by labyrinthectomy, forced oscillation in front of a patterned surround was imposed in unilaterally labyrinthectomized cats. This experimental paradigm has been shown to be very effective in inducing adaptive VOR gain changes in intact animals. We demonstrate that plasticity of VOR gain is still present both in acute and chronic stages following vestibular lesions. By contrast, forced oscillation did not significantly alter the lesion-induced asymmetry of responses. We conclude that VOR gain control mechanisms are not used to their fullest possible extent in a large percentage of animals suffering unilateral vestibular damage.

Acoustic Stimulation↗
PubMed1985

Optokinetic nystagmus in albino rats depends on stimulus pattern.

Ocular responses to optokinetic stimulation were reexamined in adult albino rats of two different strains. Eye movements were measured in head-restrained animals using the search coil method. In contrast to some previous results, the albino rats showed optokinetic nystagmus, and some of them made responses comparable to those previously recorded from pigmented rats. However, the type of stimulus pattern used to elicit optokinetic nystagmus proved to be crucial for albino rats. The deficit is attributed to abnormalities in the albino rat's visual sensory apparatus. Inverted optokinetic nystagmus was elicited in albino rats by restricting the optokinetic stimulation to the anterior visual field of both eyes. The same phenomenon has been observed previously in albino rabbits and mice, and has been suggested to be due to the abnormally small number of uncrossed optic nerve fibers in albinos.

Albinism↗
PubMed1985

Horizontal optokinetic ocular nystagmus in the pigmented rat.

Horizontal optokinetic nystagmus was elicited in rats by rotation of a pattern of bright dots projected onto a cylinder surrounding the animal. Eye position was measured with the electromagnetic search coil technique. Optokinetic stimuli consisted either of velocity steps of pattern rotation or sinusoidal oscillations. Closed-loop gain (slow phase eye velocity/pattern velocity) of steady-stage step responses in binocular vision ranged between 0.8 and 1.0 for pattern velocities up to 20-40 degrees/s and decreased thereafter. Open-loop gain (steady-state slow phase velocity/retinal slip velocity) was dependent on retinal slip velocity and decreased linearly in double logarithmic plot from about 30 (at 0.5 degree/s) to about 9 (at 5 degrees/s). For retinal slip velocities larger than 5 degrees/s open-loop gain decayed faster and reached about 1 at 30 degrees/s. Step response profiles showed a gradual increase in slow phase eye velocity reaching steady-state after a time period roughly proportional to stimulus velocity. Initial slow phase velocity measured within 500 ms after stimulus onset reached between 2 and 4 degrees/s and was largely independent of stimulus amplitudes above 10 degrees/s. Occasionally rats showed fast rises in slow phase eye velocity at the onset of the step response profiles. Primary and secondary optokinetic afternystagmus were present. Duration of primary afternystagmus was largely independent of stimulus amplitude and lasted 8.0 +/- 4 s. Closed-loop gain of steady-state step responses in monocular vision was, for temporonasal stimuli, similar to that measured in binocular condition while for nasotemporal stimulation gain was much smaller even at low stimulus velocities. Sinusoidal modulation of slow phase velocity was linearly dependent on stimulus velocity; the linear range decreased as frequency of stimulation increased. Slow phase velocity gain was relatively constant (ca 0.8) between 0.05 and 0.3 Hz and showed only a small tendency to decrease at larger stimulus frequencies. Phase-lag increased strongly with stimulus frequency and could be fitted by assuming a response time delay of 100 ms. The results show that the rat's optokinetic system is qualitatively similar to that found in another lateral-eyed species, namely the rabbit. At a quantitative level, however, both fast and slow optokinetic response dynamics appear to be better developed in the rat than in the rabbit.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1979

The postnatal development of functional properties of central vestibular neurons in the rat.

The postnatal development of the responses of rat central vestibular neurons to horizontal angular acceleration was studied in the time and frequency domain. The resting discharge was very low and irregular during the first postnatal days, increased gradually and became more regular throughout the first month and reached adult values approximately by the end of the first month. The relative distribution of type I and type II units was the same in all age groups. Threshold for frequency increase to angular acceleration and sensitivity of unit responses became lower and higher, respectively, as time elapsed after birth. Adult values were reached approximately by the end of the first month. There was a slight tendency towards shorter time constants and smaller phase lags in one-month-old animals when compared with the younger animals. The results are discussed in conjunction with similar work performed in vestibular afferents and correlated with known morphological and behavioral studies.

Acceleration↗
PubMed1979

Mechanisms of compensation for vestibular deficits in the frog. I. Modification of the excitatory commissural system.

In hemilabyrinthectomized frogs excitatory responses of central vestibular neurons to electrical stimulation of the remaining vestibular nerve were recorded extra- and intracellulary at different stages (0, 3, and 60 days) after the operation. The output pattern of ipsilateral vestibular neurons sending an axon across the midline via the vestibular commissure to the deafferented nucleus did not change postoperatively. The synaptic efficacy of these commissural axons ending on partially deafferented vestibular neurons on the lesioned side increased with time. This enhanced synaptic potency was associated with a shortening in time to peak and duration and an increase in amplitude of the evoked EPSPs. As a result most vestibular neurons were readily excited by single shock stimulation of the contralateral vestibular nerve, a finding which was rarely observed in control animals. These plastic changes are explained by the assumption of reactive synaptogenesis. The consequences of this modification for the readjustment of static and dynamic vestibular reflexes are discussed.

Afferent Pathways↗
PubMed1979

Mechanisms of compensation for vestibular deficits in the frog. II. Modification of the inhibitory Pathways.

In hemilabyrinthectomized frogs inhibitory responses of central vestibular neurons to electrical stimulation of the remaining vestibular nerve were recorded extra- and intracellularly at different stages (0, 3, and 60 days) after the operation. In acute animals inhibition of vestibular neurons following stimulation of the VIIIth nerve is rarely observed. In chronic animals about 30% of the vestibular neurons on the partially deafferented side and about 15% of the vestibular neurons on the intact side are inhibited. The distribution of the latencies of these inhibitory responses is bimodal with ranges from 4 to 14 ms and 18 to 24 ms. Removal of the cerebellum reduced the number of inhibited vistibular neurons and picrotoxin abolished all inhibitory responses. The vestibular input to the cerebellar dorsal rim is bilateral. In chornic animals excitation of Purkinje cells was similar as in acute preparations but many more cells were disfacilitated. Inhibition of partially deafferented vestibular neurons by cerebellar and brain stem neurons increases in parallel with their excitatory commissural input. The balance between these plastic changes may be crucial for the functional recovery of appropriate compensatory reflexes.

Afferent Pathways↗
PubMed1979

Timing of bilateral cerebellar output evoked by unilateral vestibular stimulation in the frog.

Electrical stimulation of one VIIIth nerve evoked simple spike activity in Purkinje cells located on either side of the cerebellum. This cellebullar output was delayed by ca. 10 ms with respect to its mossy fiber-parallel fiber input. The onset of the cerebellar output occurs on the average simultaneously on either side of the corpus cerebelli. The delay is explained by slowly rising EPSPs in PC induced by primary afferent and by second and higher order vestibular fibers. The latter inputs are stronger and terminate ipsi- and contralaterally in the granular layer.

Action Potentials↗