Vestibular nucleus units in alert monkeys are also influenced by moving visual fields

Navigation gets us from place to place, creating a path to arrive at a goal. We trained a monkey to steer a motorized cart in a large room, beginning at its trial-by-trial start location and ending at a trial-by-trial cued goal location. While the monkey steered its autonomously chosen path to its goal, we recorded neural activity simultaneously in both the hippocampus (HPC) and medial superior temporal (MST) cortex.

Local field potentials (LFPs) in these sites show similar patterns of activity with the 15–30 Hz band highlighting specific room locations. In contrast, 30–100 Hz LFPs support a unified map of the behaviorally relevant start and goal locations. The single neuron responses (SNRs) do not substantially contribute to room or start-goal maps. Rather, the SNRs form a continuum from neurons that are most active when the monkey is moving on a path toward the goal, versus other neurons that are most active when the monkey deviates from paths toward the goal.

Granger analyses suggest that HPC firing precedes MST firing during cueing at the trial start location, mainly mediated by off-path neurons. In contrast, MST precedes HPC firing during steering, mainly mediated by on-path neurons. Interactions between MST and HPC are mediated by the parallel activation of on-path and off-path neurons, selectively activated across stages of this wayfinding task.

This chapter provides a review of early studies into the neural substrate for optokinetic-vestibular responses. Properties and connections of retinal and brainstem neurons contributing to optokinetic responses in the afoveate rabbit are summarized. Electrophysiological and lesion studies provide support for confluence of optokinetic and vestibular signals in the vestibular nucleus to provide the brain's estimate of self-rotation. Evidence for optokinetic-vestibular symbiosis in humans comes from the observation that individuals who have lost vestibular function show no optokinetic after-nystagmus in darkness, following full-field stimulus motion. An anatomical scheme for brainstem elaboration of optokinetic responses is proposed and cerebellar contributions are reviewed.

Our perception of verticality relies on combining sensory information from multiple sources. Neuronal recordings in animals implicate the cerebellum in the process, yet disease of the human cerebellum was not found to affect this perception. Here we show that a perceptual disturbance of verticality is indeed present in people with a genetically determined and pure form of cerebellar degeneration (spinocerebellar ataxia type 6; SCA 6), but is only revealed under dynamic visual conditions. Participants were required to continuously orient a visually displayed bar to vertical while the bar angle was perturbed by a low-frequency random signal and a random dot pattern rotated in their visual periphery. The random dot pattern was rotated at one of two velocities (4°/s and 16°/s), traveling with either coherent or noisy motion. Perceived vertical was biased by visual rotation in healthy participants, particularly in a more elderly group, but SCA 6 participants were biased more than both groups. The bias was reduced by visual noise, but more so for SCA 6 participants than young controls. Distortion of verticality by visual rotation stems from the stimulus creating an illusion of self-rotation. We modeled this process using a maximum-likelihood sensory cue-combination model operating on noisy visual- and vestibular-rotation signals. The observed effects of visual rotation and visual noise could be compellingly explained by cerebellar degeneration, and to a lesser extent aging, causing an increase in central vestibular noise. This is consistent with the human cerebellum operating on dynamic vestibular signals to inform the process that estimates which way is up.

The roles of histaminergic and cholinergic neuron systems in the regulation of body temperature have been studied almost exclusively in animals. Recently, we have found that motion sickness, i.e. a condition where hippocampal cholinergic mismatch signals induce a release of histamine in the vomiting centre, accelerates the decline in body temperature in men during exposure to cold. In the present study we measured the thermoregulatory effects of two substances commonly used against motion sickness, i.e. the histamine (H1) receptor blocker dimenhydrinate (DMH) and the muscarine receptor blocker scopolamine (SCOP). In three trials, control (CN), DMH and SCOP, 10 male subjects were immersed in 15 °C water for a maximum of 90 min. The trials were separated by a minimum of three days and their order was alternated between subjects. In all trials the subject received, in a double blind fashion, a transdermal patch (SCOP or placebo) 12–14 h before immersion and a tablet (DMH or placebo) 1 h before immersion. Mean skin temperature, rectal temperature (T_rec), the difference in temperature between the non-immersed right forearm and 3rd finger of the right hand (T_ff), and oxygen uptake (VO₂) were recorded. The fall in T_rec was smaller in the DMH than in the CN and SCOP conditions. The recordings of T_ff and VO₂ suggest that SCOP attenuates peripheral vasoconstriction while DMH increases shivering thermogenesis. Notably, thermal discomfort was reduced in the SCOP condition. Findings are thoroughly discussed in the context of animal studies on the neuropharmacology and neurophysiology of thermoregulation and motion sickness.