Model for the Translational Vestibuloocular Reflex (VOR)

1999 ◽  
Vol 82 (4) ◽  
pp. 2010-2014 ◽  
Author(s):  
Wissam S. Musallam ◽  
R. D. Tomlinson
Keyword(s):  
Translational Motion ◽  
Primary Afferents ◽  
Vestibuloocular Reflex ◽  
Neural Integrator ◽  
Primary Afferent ◽  
Velocity Signal ◽  
Afferent Signal ◽  
Central Processing ◽  
Position Signal ◽  
Oculomotor Nuclei

The function of the translational vestibuloocular reflex (tVOR) and the angular vestibuloocular reflex (aVOR) is to stabilize images on the retina during translational and rotational motion, respectively. It has generally been assumed that these two reflexes differ in their central processing because they differ significantly in their primary afferent behavior and characteristics at the motor level. So far, models of the tVOR have focused on the type of processing that the primary afferent signal must undergo before reaching the neural integrator. Here, we propose a model that does not require any prefiltering. It is known that the eye plant requires signals in phase with velocity and position. We propose that the velocity signal is obtained directly from the neural integrator, whereas the position signal is obtained directly from the primary afferents synapsing onto the oculomotor nuclei. This design proved sufficient to simulate eye movements in response to translational motion.

Hypothesis for Shared Central Processing of Canal and Otolith Signals

1998 ◽  
Vol 80 (4) ◽  
pp. 2222-2228 ◽  
Author(s):  
Andrea M. Green ◽  
Henrietta L. Galiana
Keyword(s):  
Dynamic Characteristics ◽  
Alternative Hypothesis ◽  
Sensory Information ◽  
Vestibuloocular Reflex ◽  
Neural Integrator ◽  
Head Acceleration ◽  
Central Processing ◽  
Low Pass ◽  
Dynamic Processing ◽  
Low Pass Filters

Green, Andrea M. and Henrietta L. Galiana. Hypothesis for shared central processing of canal and otolith signals. J. Neurophysiol. 80: 2222–2228, 1998. A common goal of the translational vestibuloocular reflex (TVOR) and the rotational vestibuloocular reflex (RVOR) is to stabilize visual targets on the retinae during head movement. However, these reflexes differ significantly in their dynamic characteristics at both sensory and motor levels, implying a requirement for different central processing of canal and otolith signals. Semicircular canal afferents carry a signal proportional to angular head velocity, whereas primary otolith afferents modulate approximately in phase with linear head acceleration. Behaviorally, the RVOR exhibits a robust response down to ∼0.01 Hz, yet the TVOR is only significant above ∼0.5 Hz. Several hypotheses were proposed to address central processing in the TVOR pathways. All rely on a central filtering process that precedes a “neural integrator” shared with the RVOR. We propose an alternative hypothesis for the convergence of canal and otolith signals that does not impose the requirement for additional low-pass filters for the TVOR. The approach is demonstrated using an anatomically based, simple model structure that reproduces the general dynamic characteristics of the RVOR and TVOR at both ocular and central levels. Differential dynamic processing of otolith and canal signals is achieved by virtue of the location at which sensory information enters a shared but distributed neural integrator. As a result, only the RVOR is provided with compensation for the eye plant. Hence canal and otolith signals share a common central integrator, as in previous hypotheses. However, we propose that the required additional filtering of otolith signals is provided by the eye plant.

Excitability of primary afferents in feline spinal cord: taurine, homotaurine, and γ-aminobutyric acid compared

1982 ◽  
Vol 60 (6) ◽  
pp. 850-855 ◽  
Author(s):  
Radan Čapek ◽  
Barbara Esplin
Keyword(s):  
Primary Afferents ◽  
Aminobutyric Acid ◽  
Primary Afferent Depolarization ◽  
Conditioning Stimulation ◽  
Primary Afferent ◽  
Antagonistic Muscle ◽  
Consistent Change ◽  
Muscle Nerve ◽  
Gaba Synthesis ◽  
Stimulation Of

Effects of taurine and homotaurine (3-aminopropancsuIfonic acid), on excitability of primary afferents were compared with effects of γ-aminobutyric acid (GABA) in spinal unanaesthesized cats. Homotaurine and GABA, administered intravenously or topically, produced a marked increase in afferent excitability. Homotaurine was about 10 times more potent than GABA. Taurine (up to 2 mmol/kg i.v., or 10 mM topically) did not produce a consistent change in afferent excitability. The effect of homotaurine was antagonized by bicuculline or picrotoxin in doses which suppressed the primary afferent depolarization, as indicated by an increase of afferent excitability, evoked by conditioning stimulation of an antagonistic muscle nerve. Semicarbazidc, an inhibitor of GABA synthesis, did not attenuate the homotaurine-induced excitability changes of afferents while suppressing entirely the primary afferent depolarization. These findings suggest that homotaurine exerts a direct GABA-like action on feline primary afferents.

scholarly journals Contribution of intravestibular sensory conflict to motion sickness and dizziness in migraine disorders

2016 ◽  
Vol 116 (4) ◽  
pp. 1586-1591 ◽  
Author(s):  
Joanne Wang ◽  
Richard F. Lewis
Keyword(s):  
Motion Sickness ◽  
Semicircular Canals ◽  
Inverse Correlation ◽  
Normal Subjects ◽  
Otolith Organs ◽  
Rotational Axis ◽  
Vestibuloocular Reflex ◽  
Sensory Conflict ◽  
Velocity Signal ◽  
Episodic Vertigo

Migraine is associated with enhanced motion sickness susceptibility and can cause episodic vertigo [vestibular migraine (VM)], but the mechanisms relating migraine to these vestibular symptoms remain uncertain. We tested the hypothesis that the central integration of rotational cues (from the semicircular canals) and gravitational cues (from the otolith organs) is abnormal in migraine patients. A postrotational tilt paradigm generated a conflict between canal cues (which indicate the head is rotating) and otolith cues (which indicate the head is tilted and stationary), and eye movements were measured to quantify two behaviors that are thought to minimize this conflict: suppression and reorientation of the central angular velocity signal, evidenced by attenuation (“dumping”) of the vestibuloocular reflex and shifting of the rotational axis of the vestibuloocular reflex toward the earth vertical. We found that normal and migraine subjects, but not VM patients, displayed an inverse correlation between the extent of dumping and the size of the axis shift such that the net “conflict resolution” mediated through these two mechanisms approached an optimal value and that the residual sensory conflict in VM patients (but not migraine or normal subjects) correlated with motion sickness susceptibility. Our findings suggest that the brain normally controls the dynamic and spatial characteristics of central vestibular signals to minimize intravestibular sensory conflict and that this process is disrupted in VM, which may be responsible for the enhance motion intolerance and episodic vertigo that characterize this disorder.

scholarly journals Prior perineural or neonatal treatment with capsaicin does not alter the development of spinal microgliosis induced by peripheral nerve injury

2020 ◽  
Author(s):  
Ivett Dorina Szeredi ◽  
Gábor Jancsó ◽  
Orsolya Oszlács ◽  
Péter Sántha
Keyword(s):  
Peripheral Nerve ◽  
Dorsal Horn ◽  
Nerve Injury ◽  
Peripheral Nerve Injury ◽  
Spinal Dorsal Horn ◽  
Primary Afferents ◽  
Primary Afferent ◽  
Spinal Dorsal ◽  
C Fiber ◽  
Spinal Afferents

Abstract Peripheral nerve injury is associated with spinal microgliosis which plays a pivotal role in the development of neuropathic pain behavior. Several agents of primary afferent origin causing the microglial reaction have been identified, but the type(s) of primary afferents that release these mediators are still unclear. In this study, specific labeling of C-fiber spinal afferents by lectin histochemistry and selective chemodenervation by capsaicin were applied to identify the type(s) of primary afferents involved in the microglial response. Comparative quantitative morphometric evaluation of the microglial reaction in central projection territories of intact and injured peripheral nerves in the superficial (laminae I and II) and deep (laminae III and IV) spinal dorsal horn revealed a significant, about three-fold increase in microglial density after transection of the sciatic or the saphenous nerve. Prior perineural treatment of these nerves with capsaicin, resulting in a selective defunctionalization of C-fiber afferent fibers failed to affect spinal microgliosis. Similarly, peripheral nerve injury-induced increase in microglial density was unaffected in rats treated neonatally with capsaicin known to result in a near-total loss of C-fiber dorsal root fibers. Perineural treatment with capsaicin per se did not evoke a significant increase in microglial density. These observations indicate that injury-induced spinal microgliosis may be attributed to phenotypic changes in injured myelinated primary afferent neurons, whereas the contribution of C-fiber primary sensory neurons to this neuroimmune response is negligible. Spinal myelinated primary afferents may play a hitherto unrecognized role in regulation of neuroimmune and perisynaptic microenvironments of the spinal dorsal horn.

scholarly journals Transmitters Involved in Central Processing of Nociceptive Information

1982 ◽  
Vol 10 (2) ◽  
pp. 133-138 ◽  
Author(s):  
Arthur W. Duggan
Keyword(s):  
Amino Acids ◽  
Substance P ◽  
Primary Afferents ◽  
Aminobutyric Acid ◽  
Membrane Properties ◽  
Central Processing ◽  
Nociceptive Information ◽  
Nociceptive Afferents ◽  
Distribution Studies ◽  
Dorsal Horn Neurones

Distribution studies suggest that substance P is a transmitter released by nociceptive primary afferent fibres. Acceptance of this role, however, needs more electro-physiological comparisons of the effects of substance P and the transmitter released by primary afferents on the membrane properties of dorsal horn neurones. The transmission of impulses from nociceptive afferents to supraspinal areas is subject to inhibition of both segmental and supraspinal origin. Segmental inhibition probably involves glycine and γ-aminobutyric acid as transmitters. Of supraspinal inhibitions investigated in the cat none have been shown to involve amino acids, enkephalins or 5-hydroxytryptamine but there is evidence to suggest a role for noradrenaline.

Inhibition Evoked From Primary Afferents in the Electrosensory Lateral Line Lobe of the Weakly Electric Fish (Apteronotus leptorhynchus)

1998 ◽  
Vol 80 (6) ◽  
pp. 3173-3196 ◽  
Author(s):  
Neil J. Berman ◽  
Leonard Maler
Keyword(s):  
Lateral Line ◽  
Granule Cell ◽  
Electric Fish ◽  
Inhibitory Response ◽  
Primary Afferents ◽  
Weakly Electric Fish ◽  
Apteronotus Leptorhynchus ◽  
Primary Afferent ◽  
Weakly Electric ◽  
Stimulation Of

Berman, Neil J. and Leonard Maler. Inhibition evoked from primary afferents in the electrosensory lateral line lobe of the weakly electric fish ( Apteronotus leptorhynchus). J. Neurophysiol. 80: 3173–3196, 1998. The responses of two types of projection neurons of the electrosensory lateral line lobe, basilar (BP) and nonbasilar (NBP) pyramidal cells, to stimulation of primary electrosensory afferents were determined in the weakly electric fish, Apteronotus leptorhynchus. Using dyes to identify cell type, the response of NBP cells to stimulation of primary afferents was inhibitory, whereas the response of BP cells was excitation followed by inhibition. γ-Aminobutyric acid (GABA) applications produced biphasic (depolarization then hyperpolarization) responses in most cells. GABAA antagonists blocked the depolarizing effect of GABA and reduced the hyperpolarizing effect. The GABAB antagonists weakly antagonized the hyperpolarizing effect. The early depolarization had a larger increase in cell conductance than the late hyperpolarization. The conductance changes were voltage dependent, increasing with depolarization. In both cell types, baclofen produced a slow small hyperpolarization and reduced the inhibitory postsynaptic potentials (IPSPs) evoked by primary afferent stimulation. Tetanic stimulation of primary afferents at physiological rates (100–200 Hz) produced strongly summating compound IPSPs (∼500-ms duration) in NBP cells, which were usually sensitive to GABAA but not GABAB antagonists; in some cells there remained a slow IPSP that was unaffected by GABAB antagonists. BP cells responded with excitatory or mixed excitatory + inhibitory responses. The inhibitory response had both a fast (∼30 ms, GABAA) and long-lasting slow phase (∼800 ms, mostly blocked by GABAA antagonists). In some cells there was a GABAA antagonist-insensitive slow IPSP (∼500 ms) that was sensitive to GABAB antagonists. Application of glutamate ionotropic receptor antagonists blocked the inhibitory response of NBP cells to primary afferent stimulation and the excitatory response of BP cells but enhanced the BP cell slow IPSP; this remaining slow IPSP was reduced by GABAB antagonists. Unit recordings in the granule cell layer and computer simulations of pyramidal cell inhibition suggested that the duration of the slow GABAA inhibition reflects the prolonged firing of GABAergic granule cell interneurons to primary afferent input. Correlation of the results with known GABAergic circuitry in the electrosensory lobe suggests that the GABAergic type 2 granule cell input to both pyramidal cell types is via GABAA receptors. The properties of the GC2 GABAA input are well suited to their putative role in gain control, regulation of phasicness, and coincidence detection. The slow GABAB IPSP evoked in BP cells is likely due to ovoid cell input to their basal dendrites.

Lesion of the nodulus and ventral uvula abolish steady-state off-vertical axis otolith response

1995 ◽  
Vol 73 (4) ◽  
pp. 1716-1720 ◽  
Author(s):  
D. E. Angelaki ◽  
B. J. Hess
Keyword(s):  
Steady State ◽  
Constant Velocity ◽  
Rhesus Monkeys ◽  
Low Frequency ◽  
Vertical Axis ◽  
Primary Afferents ◽  
Vestibuloocular Reflex ◽  
Neural Substrate ◽  
Sinusoidal Oscillations ◽  
Otolith System

1. During rotations that dynamically activate utricular and saccular primary afferents, the otolith system centrally detects the velocity and direction of rotation of the head in space. This property is experimentally manifested as a steady-state compensatory nystagmus during constant velocity off-vertical axis rotations. The computational, physiological, and anatomic details of this response remain presently unknown. Here we report that surgical inactivation of the cerebellar nodulus and ventral uvula abolished the ability of the otolith system to generate steady-state nystagmus during constant velocity rotation and to improve the dynamics of the vestibuloocular reflex (VOR) during low-frequency sinusoidal oscillations about off-vertical axes in rhesus monkeys. These results suggest that the cerebellar nodulus and/or ventral uvula comprise part of the neural substrate that is involved in these computations.

α5GABAA receptors mediate primary afferent fiber tonic excitability in the turtle spinal cord

2013 ◽  
Vol 110 (9) ◽  
pp. 2175-2184 ◽  
Author(s):  
Emanuel Loeza-Alcocer ◽  
Martha Canto-Bustos ◽  
Justo Aguilar ◽  
Ricardo González-Ramírez ◽  
Ricardo Felix ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Dorsal Root Ganglia ◽  
Dorsal Root ◽  
Afferent Fiber ◽  
Primary Afferents ◽  
Equilibrium Potential ◽  
Primary Afferent Depolarization ◽  
Primary Afferent ◽  
Dorsal Root Reflex

γ-Amino butyric acid (GABA) plays a key role in the regulation of central nervous system by activating synaptic and extrasynaptic GABAA receptors. It is acknowledged that extrasynaptic GABAA receptors located in the soma, dendrites, and axons may be activated tonically by low extracellular GABA concentrations. The activation of these receptors produces a persistent conductance that can hyperpolarize or depolarize nerve cells depending on the Cl− equilibrium potential. In an in vitro preparation of the turtle spinal cord we show that extrasynaptic α5GABAA receptors mediate the tonic state of excitability of primary afferents independently of the phasic primary afferent depolarization mediated by synaptic GABAA receptors. Blockade of α5GABAA receptors with the inverse agonist L-655,708 depressed the dorsal root reflex (DRR) without affecting the phasic increase in excitability of primary afferents. Using RT-PCR and Western blotting, we corroborated the presence of the mRNA and the α5GABAA protein in the dorsal root ganglia of the turtle spinal cord. The receptors were localized in primary afferents in dorsal root, dorsal root ganglia, and peripheral nerve terminals using immunoconfocal microscopy. Considering the implications of the DRR in neurogenic inflammation, α5GABAA receptors may serve as potential pharmacological targets for the treatment of pain.

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