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Notes: Abstract Autonomic effects of vestibular stimulation are important components of phenomena as diverse as acute vestibular dysfunction and motion sickness. How ever, the organization of neural circuits mediating these responses is poorly understood. This study presents evidence for direct vestibular nucleus projections to brain stem regions that mediate autonomic function. One group of albino rabbits received injections of Phaseolus vulgaris leucoagglutinin into the vestibular nuclei. The tracer was visualized immunocytochemically with standard techniques. Anterogradely labeled axons from the caudal medial vestibular nucleus (cMVN) and inferior vestibular nucleus (IVN) could be traced bilaterally to nucleus tractus solitarius (NTS). Fewer axons ended near the somata of neurons in the dorsal motor nucleus of the vagus nerve (DMX). A second group of rabbits received pressure or iontophoretic injections of cholera toxin B-HRP or Fluoro-Gold into a region including NTS and DMX. Retrogradely labeled neurons were observed bilaterally in the caudal half of cMVN and ipsilaterally in IVN. The labeled somata were small and they tended to occupy the center of cMVN in transverse sections. These previously unreported vestibular nucleus projections to NTS and DMX are a potential substrate for vestibular influences on autonomic function. In particular, they may contribute to both cardiovascular control during head movements (e.g., orthostatic reflexes) and autonomic manifestions of vestibular dysfunction, motion sickness and exposure to altered gravitational environments.

Notes: Abstract Acute vestibular dysfunction and motion sickness are characterized by autonomic effects such as pallor, nausea, and vomiting. Previous anatomic and physiologic studies suggest that one potential mediator of these effects may be light, direct vestibular nuclear projections to the nucleus tractus solitarius and the dorsal motor nucleus of the vagus nerve. This study presents evidence for relatively dense, direct projections from the vestibular nuclei to the parabrachial nucleus. Male albino rabbits received injections of Phaseolus vulgaris leucoagglutinin into the vestibular nuclei. The tracer was visualized immunocytochemically with standard techniques. Anterogradely labeled axons were traced bilaterally from the vestibular nuclei to the parabrachial nuclear complex, where they terminated around somata in the Kölliker-Fuse nucleus, external medial parabrachial nucleus, medial parabrachial nucleus, and lateral parabrachial nucleus. Less dense terminations were observed in the ventrolateral aspect of the medullary reticular formation, the subtrigeminal nucleus, lateral tegmental field, and nucleus ambiguus. These findings have several important implications. First, they suggest that vestibular input converges directly at brain stem levels with visceral sensory input in both nucleus of the solitary tract and the parabrachial complex. Second, they suggest that vestibular input influences brain stem autonomic outflow via two parallel pathways: (1) direct, light projections to the nucleus of the solitary tract, dorsal motor nucleus of the vagus nerve, and ventrolateral medullary reticular formation; and (2) denser projection to regions of the parabrachial nucleus that project to these brain stem regions. Finally, since the parabrachial nucleus regions that receive vestibular input also project to the hypothalamus and the insular and infralimbic prefrontal cortex, the parabrachial nucleus may serve as an important relay and integrative structure for the cognitive impairment and vegetative symptoms associated with motion sickness, vestibular dysfunction, and responses to altered gravitational environments.

Notes: Abstract An analysis of optokinetic responses was used to derive an iterative model that reproduces the duration of nystagmus slow phases and eye position control during optokinetic nystagmus. Optokinetic nystagmus was recorded with magnetic search coils from red-eared turtles (Pseudemys scripta elegans) during monocular, random dot pattern stimulation at constant velocities ranging from 0.25–63%. The beat-to-beat behavior of slow phase durations was consistent with the existence of an underlying neural clock, termed the basic interval generator, that is based on an integrate-to-fire neuron model. This hypothetical basic interval generator produces an interval that is the product of the duration of the previous interval and a mean 1 truncated normal variate with variance σ2. Data analyses indicated that the initial value of the interval generator during a period of nystamus, termed τ0, is proportional to the inverse square root of slow phase eye velocity. Further, if the eye was deviated in the slow phase direction (re mean eye position) when the slow phase began, the slow phase duration was consistent with a single cycle of the basic interval generator. However, if the eye was deviated in the fast phase direction, the distribution of the durations of the ensuing slow phases indicated that a proportion of the slow phases were produced by more than one cycle of the basic interval generator. This phenomenon is termed “skipping a beat” and occurs with probability p s . Finally, the amplitude of fast phases behaved as a linear function of eye position at the fast phase onset and the product of τ0 and slow phase eye velocity. A computer simulation reproduced the observed distribution of slow phase durations, the proportion of fast phases in the fast phase and slow phase directions and the distribution of eye positions at the onset and end of fast phases. This novel model suggests that both timing and eye position information contribute to the alternation of nystagmus fast and slow phases.

Notes: The dorsal ventricular ridge (DVR) is a subcortical, telencephalic structure in reptiles and birds that protrudes into the lateral ventricle. The structure of DVR has been studied in the red-eared turtle (Pseudemys scripta elegans) in Nissl and Golgi preparations. The DVR in Pseudemys is divided into the anterior dorsal ventricular ridge (ADVR) and the basal dorsal ventricular ridge (BDVR) by the dorsal branch of the middle ventricular sulcus. The structure of ADVR has been examined in detail.The ADVR is divided into four regions with distinct boundaries termed dorsal area, medial area, ventral area and central area. Dorsal area, medial area and ventral area border on the lateral ventricle; central area lies deep to the other areas. Three classes of neurons are found in Golgi preparations of ADVR. Juxtaependymal cells have somata near the perikarya of ependymal cells; their dendrites are found primarily in a periventricular fiber zone. Aspiny neurons were observed only in the dorsal half of ADVR and appear to be restricted to deep regions of the ridge. These multipolar neurons are rarely encountered in Golgi preparations, and the observed distribution may not represent their actual distribution in ADVR. The majority of the cells observed in ADVR are spiny neurons with dendritic fields that range from stellate to double-pyramidal. Cells in this class may be subdivided on the basis of axonal morphology into at least two groups, but further studies are needed to determine the range of axonal morphology exhibited by these neurons.An analysis of the distribution of these cell types in Golgi material shows that dorsal area, medial area and ventral area are organized in four zones concentric with the ventricular surface. Central area apparently lacks a concentric pattern of organization. Zone 1 is a periventricular fiber band that contains juxtaependymal neurons and ascending dendrites of zone 2 spiny neurons, and it may serve as a structural substrate for segregated input onto these cell populations. Zone 2 contains clusters of spiny neurons with apposed somata, which vary in size and distribution between areas. Dendrites of zone 4 neurons are also found in the deep half of zone 2. Zone 3 is a cell-poor region which lies at the center of a region of overlapping dendritic fields of zone 2 and zone 4 neurons. Zone 4 contains predominantly spiny neurons (aspiny neurons are found only in the dorsal half of ADVR) which are either isolated or in small clusters with apposed somata. Dendrites of zone 2 cells extend superficially into zone 4, so that the deep portions of zone 4 may be a substrate for segregated input to zone 4 neurons. These zones are differentially elaborated in each area. Central area, by contrast, consists of scattered spiny and aspiny neurons among fibers connecting ADVR and the lateral forebrain bundle.A comparison of these findings with the ADVR of snakes (Ulinski, '78a,b) shows both similarities and differences in DVR organization in the two taxa. Although snakes lack areal divisions, ADVR is organized in four concentric zones (zones A-D). Zones A and B resemble zones 1 and 2 in turtles, consisting of a superficial fiber zone and a subjacent cell cluster zone. The clusters are smaller in snakes than in turtles. However, snakes lack a cell-poor band deep to zone B, and dendrites of cells in zone C enter zone A. Thus, there are differences in both areal and zonal dimensions of ADVR organization in turtles and snakes.