Peripheral organization of the vestibular efferent system in the frog: an electrophysiological study

The distribution and the properties of efferent fibers in vestibular nerve were studied in the isolated frog labyrinth. Electrical stimulation of the central stump of any vestibular nerve branchlet elicited compound action potentials in all the other eighth nerve branchlets, indicating the existence of neural links between the various vestibular organs. The same experimental paradigm, when repeated in frogs with chronic section of the eighth nerve roots, demonstrated that these pathways are efferent collaterals extending to all vestibular organs. There are more collaterals linking the 3 semicircular canals than the otolith organs and the otoliths with the canal organs. Efferent connections in the eighth nerve were preserved in full after ablation of the ipsilateral hemi-cerebellum, suggesting that the efferent pathways probably originate in the brainstem. Intracellular recordings from single afferent fibers of both canal and otolith organs revealed that efferent fiber activation could elicit either inhibition or facilitation of the receptor discharge. It was concluded that the frog efferent vestibular system is endowed with non-selective control channels which allow single neurons to influence the receptor activity of different labyrinthine organs.     

Influence of stimulation of auditory and somatosensory systems on the activity of vestibular nuclear neurons in the frog

In the frog, we have recorded extracellularly the activity of vestibular nuclear neurons driven by the horizontal semicircular canals. About 28% of the neurons recorded (n = 300) responded to auditory stimulation (clicks 150/s and pure tones 300-2,000 Hz, about 80 dB above threshold) or to somatosensory stimulation (electrical stimulation of the ipsilateral or contralateral sciatic nerve and vibratory stimulation of the ipsilateral gastrocnemius). Whatever the stimulus, the response was always an increase of the discharge frequency. Such a frequency increase was much more important for somatosensory stimulation (62-145%) than for auditory (20%) and sciatic nerve input was about twice as efficient as gastrocnemius input. Except for type IV units which were only exceptionally recorded, all the other neuronal types (according to Duensing and Schaefer 's classification, 1959) responded to auditory or somatosensory volleys. In particular, activation of type III units, which are partly efferent vestibular neurons ending at the base of the sensory hair cells, may result in a modulation of the peripheral vestibular discharges. The latencies of the responses varied over a wide range (5-40 ms); long latency responses are probably mediated by polysynaptic pathways including the reticular formation and/or the cerebellum, and short latency ones by oligosynaptic pathways. These pathways and the functional meaning of convergence of auditory and somatosensory input onto vestibular nuclei are discussed.     

Efferent vestibular system in the toadfish: action upon horizontal semicircular canal afferents

The influence of the efferent vestibular system (EVS) upon the background discharge and response dynamics of horizontal semicircular canal afferents was examined in the toadfish. In one set of experiments the EVS was activated using a behavioral paradigm; in the second, electrical shocks were applied to the efferent vestibular nucleus in the brain stem. The afferent's background discharge and responses to rotation were recorded before and during efferent stimulation. Both EVS activation paradigms gave qualitatively similar results: a facilitation of the afferent's rate, while the animal was at rest or in motion, and a reduction in response sensitivity. Afferents were not affected uniformly: low-gain, velocity-sensitive afferents were weakly influenced, while high-gain and acceleration afferents having low rates were the most excited. The afferents' phase of response was unmodified by electrical EVS stimulation. In many afferents a prominent form of response nonlinearity is discharge silencing over large portions of the stimulus cycle. Efferent-evoked rate increase was often sufficient to produce a full-cycle bidirectional response. Caloric facilitation of afferent rate confirmed that the EVS-induced sensitivity decrease was rate independent. These results show a dual action of the efferent system: (1) facilitating the afferent's rate and (2) reducing its sensitivity to adequate stimulation that may be correlated with the dual EVS synaptic innervation of the labyrinth, namely postsynaptic efferent-afferent synapses and presynaptic efferent-hair cell synapses.     

Influence of standing on vestibular neuronal activity in awake cats

Single-unit activity of vestibular nuclear neurons was recorded in chronically prepared, awake cats. To examine the influence of tonic activation of limb proprioception on vestibular function, the vestibular modulation by horizontal rotation (0.2 Hz, 17 deg) and head-tilt (0.1 Hz, 7 deg) was recorded in animals with freely hanging limbs and was compared with the modulation in standing cats. Of 29 examined cells responding to horizontal rotation, only about 30% were affected during standing, with most exhibiting a decrease of the mean discharge rate and gain. In contrast, about 70% of the 28 tilt-modulated cells showed pronounced effects during standing with a decrease of the gain and an increase of the mean discharge rate. The increase of the mean discharge rate in tilt cells may be caused by the excitatory spinovestibular afferent fibers or by the efferent vestibular system. For the observed inhibitory effects on the gain different mechanisms may be responsible: cerebellar inhibition and/or efferent vestibular receptor control. This control of labyrinthine information by somatosensory afferent fibers may serve for the stability of equilibrium in the moving animal.     

Responses of afferent and efferent neurons to visual inputs in the vestibular nerve of the frog

In the frog immobilized by intralymphatic injection of D-tubocurarine, stimulation of the visual apparatus with either electrical shocks applied to the optic chiasma or light pulses elicited, in many cases, an increase and a decrease of firing of efferent and afferent vestibular neurons, respectively, recorded from the horizontal semicircular canal nerve. Optokinetic stimulation was completely inefficient in modulating the efferent and afferent discharge. These results show that stimulation of the visual system can modify vestibular apparatus fuctioning at the most peripheral level. However, it is likely that the effects observed were due to an arousal phenomenon or/and to a motor corollary discharge.     

Functional organization of the peripheral efferent vestibular system in the frog

The functional organization of the efferent vestibular system (EVS) was studied in the isolated frog labyrinth. To ascertain whether, besides the efferent branching fibres that innervate several end-organs, the EVS is also endowed with efferent non-branching axons which might control a given population of sensory units in each end-organ, the 8th nerve and one of its branchlets were electrically stimulated while recordings of the spontaneous activity arising from the different sensors were made by impaling single afferent axons in all the 8th nerve branchlets. The results demonstrated that the vast majority of the sensory units whose activity was modified by stimulating the whole 8th nerve was also affected by stimulating an 8th nerve branchlet. These findings therefore rule out the possibility that the EVS is endowed with projective fibres and strengthen the view that the EVS is a highly divergent system with collaterals arising from single parent axons that innervate several end-organs. These experiments have also shown that the percentage of sensory units which are actually controlled by the EVS varies amongst the different labyrinthine organs. It is maximal in the sacculus (ca. 90%), somewhat lower in canal organs (ca. 80%) and the utriculus (ca. 70%) and considerably lower in the lagena (ca. 50%). This EVS arrangement therefore might allow information arising from some organs to be modified more extensively than that from others.     

Electro-acupuncture stimulation to a hindpaw and a hind leg produces different reflex responses in sympathoadrenal medullary function in anesthetized rats

The effects of electro-acupuncture stimulation (EAS) of two different areas of a hindlimb with different stimulus intensities on sympathoadrenal medullary functions were examined in anesthetized artificially ventilated rats. Two needles of 160 microm diameter and about 5 mm apart were inserted about 5 mm deep into a hindpaw (Chungyang, S42) or a hind leg (Tsusanli, S36) and current of various intensities passed to excite various afferent nerve fiber groups at a repetition rate of 20 Hz and pulse duration of 0.5 ms for 30-60 s. Fiber groups of afferent nerves stimulated in a hindlimb were monitored by recording evoked action potentials from the afferents innervating the areas stimulated. The sympathoadrenal medullary functions were monitored by recording adrenal sympathetic efferent nerve activity and secretion rates of catecholamines from the adrenal medulla. EAS of a hindpaw at a stimulus strength sufficient to excite the group III and IV somatic afferent fibers produced reflex increases in both adrenal sympathetic efferent nerve activity and the secretion rate of catecholamines. EAS of a hind leg at a stimulus strength sufficient to excite the group III and IV afferent fibers produced reflex responses of either increases or decreases in sympathoadrenal medullary functions. All responses of adrenal sympathetic efferent nerve activity were lost after cutting the afferent nerves ipsilateral to the stimulated areas, indicating that the responses are the reflexes whose afferents nerve pathway is composed of hindlimb somatic nerves. It is concluded that electro-acupuncture stimulation of a hindpaw causes an excitatory reflex, while that of a hind leg causes either excitatory or inhibitory reflex of sympathoadrenal medullary functions, even if both group III and IV somatic afferent fibers are stimulated.     

Activation of the efferent system in the isolated frog labyrinth: Effects on the afferent EPSPs and spike discharge recorded from single fibers of the posterior nerve

Intra-axonal recordings were obtained from single afferent fibres of the posterior nerve in the isolated labyrinth of the frog (Rana esculenta). EPSPs spike discharge were recorded both at rest and during rotary stimulation of the canal. Electrical stimulation of either the distal end of the cut posterior nerve or of the central stumps of the anterior-horizontal nerves elicited a frequency-dependent inhibitory effect on the afferent discharge arising from the posterior canal. Denervation experiments revealed that inhibition is mediated by efferent fibres exhibiting a high degree of branching in the proximal part of the eight nerve. The inhibitory effect was selectively cancelled by (1)d-tubocurarine 10-⁶ M; (2) atropine 5 x 10-⁵ M;(3) acetylcholine or carbachol 10⁻⁴ M; (4) eserine 10⁻⁵ M. Inhibition is thus most likely to be sustained by the release of acetylcholine from the efferent nerve terminals. Experiments in which the ionic composition of the external medium was modified suggest that the transmitter acts mainly by opening the chloride ion channels of the hair cell membrane. In some units the same stimulation pattern evoked a consistent increase in both EPSP and spike discharge, instead of inhibition. Such facilitation was unaffected by drugs or ionic modifications which block the efferent synapse, but disappeared after denervation. Inhibition and facilitation, therefore, act as two control mechanisms which are able to modify substantially, at the first stage of processing, the sensory information which is sent to the vestibular second order neurones.     

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.     

Characteristics of regenerating horizontal semicircular canal afferent and efferent fibers in the toadfish, Opsanus tau.

The horizontal semicircular canal nerve of the toadfish, Opsanus tau, was transected and allowed to regenerate. The time course, morphometrics, and projection patterns of regenerating afferent and efferent vestibular fibers were determined. Nerve transections were performed both pre- and postganglionically, and regeneration was assessed in afferent and efferent fibers by bulk labeling the peripheral axons of the horizontal semicircular canal nerve with biocytin after nerve regrowth. Afferent fibers regrew through the transection site within 14 days and projected to all vestibular nuclei within 3 weeks. Bouton and branch number, axon length, surface area, volume, fiber diameter, and internodal distance were quantified for afferent fibers from eight sites within the vestibular nuclei, and axon number and soma size was quantified for the efferent fibers. Extensive regeneration was seen within 5 weeks of transection in all nuclei, and most morphometric parameters approached or exceeded control levels within 10 weeks. Regeneration appeared to recapitulate morphogenesis with an initial overproduction of boutons and branch points followed by elimination of presumably superfluous structures. Internodal distance remained significantly shorter in regenerating afferent axons than in control fish throughout the 15-week observation period. Efferent fibers also were observed to regenerate. Efferent axon number, diameter, and soma size were indistinguishable from those in controls from 3 weeks posttransection through week 15. Electrophysiological recordings from the horizontal canal nerve during mechanical stimuli of the canal confirmed that the regenerated axons transmitted normal signals. The return of normal equilibrium and behavior coincided with the projection of afferent fibers into the central vestibular nuclei, indicating that functional connections had been reestablished.     

Central vestibular system: vestibular nuclei and posterior cerebellum

The vestibular nuclei and posterior cerebellum are the destination of vestibular primary afferents and the subject of this review. The vestibular nuclei include four major nuclei (medial, descending, superior and lateral). In addition, smaller vestibular nuclei include: Y-group, parasolitary nucleus, and nucleus intercalatus. Each of the major nuclei can be subdivided further based primarily on cytological and immunohistochemical histological criteria or differences in afferent and/or efferent projections. The primary afferent projections of vestibular end organs are distributed to several ipsilateral vestibular nuclei. Vestibular nuclei communicate bilaterally through a commissural system that is predominantly inhibitory. Secondary vestibular neurons also receive convergent sensory information from optokinetic circuitry, central visual system and neck proprioceptive systems. Secondary vestibular neurons cannot distinguish between sources of afferent activity. However, the discharge of secondary vestibular neurons can distinguish between “active” and “passive” movements.

The posterior cerebellum has extensive afferent and efferent connections with vestibular nuclei. Vestibular primary afferents are distributed to the ipsilateral uvula-nodulus as mossy fibers. Vestibular secondary afferents are distributed bilaterally. Climbing fibers to the cerebellum originate from two subnuclei of the contralateral inferior olive; the dorsomedial cell column and β-nucleus. Vestibular climbing fibers carry information only from the vertical semicircular canals and otoliths. They establish a coordinate map, arrayed in sagittal zones on the surface of the uvula-nodulus. Purkinje cells respond to vestibular stimulation with antiphasic modulation of climbing fiber responses (CFRs) and simple spikes (SSs). The modulation of SSs is out of phase with the modulation of vestibular primary afferents. Modulation of SSs persists, even after vestibular primary afferents are destroyed by a unilateral labyrinthectomy, suggesting that an interneuronal network, triggered by CFRs is responsible for SS modulation. The vestibulo-cerebellum, imposes a vestibular coordinate system on postural responses and permits adaptive guidance of movement.     

Reflex activation of the lower oesophageal sphincter in the cat induced by stimulation of the splanchnic afferent fibres

Reflex responses of the lower oesophageal sphincter (l.o.s.) to electrical stimulation of the splanchnic afferent fibres were recorded by electromyographic and manometric techniques. Repetitive stimulation of the central end of a splanchnic nerve induced a long latency excitation of the l.o.s., i.e. bursts of spike potentials concomitant with repetitive phasic contractions. Experiments involving nerve sections showed that the efferent pathways of this reflex were served either by stellate sympathetic and/or splanchnic fibres, or by vagal fibres. These responses were abolished following the administration of atropine. These results show that the splanchnic afferent fibres are involved in l.o.s. reflex motor responses through the activation of the sympathetic and parasympathetic efferent supply to the sphincter.     

Investigation of the vagally induced changes in transmural potential difference in the ferret jejunum in vivo

This study was designed to determine whether the non-cholinergic, non-adrenergic rise in transmural potential difference (PD), induced by vagal nerve stimulation is an efferent effect or one caused by the antidromic stimulation of afferent fibers. Unilateral left supranodose vagotomy was performed, which caused degeneration of efferent fibers within the vagus nerve, leaving the nodose ganglion, and consequently afferent cell bodies, undamaged. After stimulating the unoperated nerve there was an increase in jejunal motility, a rise in transmural PD and a fall in systemic blood pressure. Although cholinergic blockade with atropine and adrenergic blockade with or a combination of phentolamine and propranolol abolished this vagally induced motor activity and fall in systemic blood pressure, the transmural PD response induced by stimulation of the unoperated nerve was only partially inhibited. However, the subsequent administration of the nicotinic ganglionic blocker, hexamethonium, abolished this transmural PD response. In contrast, stimulation of the operated vagus nerve failed to produce these effects. Therefore, cholinergic and non-cholinergic efferent fibers are responsible for the vagally induced rise in transmural PD and thus fluid secretion in the ferret jejunum.     

The effect of supranodose vagotomy on the hexamethonium-resistant bradycardia in the anaesthetized rabbit

Previous studies from this laboratory have established that electrical stimulation of non-myelinated axons in the rabbit vagus nerve produces a bradycardia which is unaffected by the nicotinic ganglion blocker hexamethonium. The present study was undertaken to determine whether this effect is mediated by afferent or efferent axons. A unilateral supranodose vagotomy was performed on four New Zealand White rabbits, one further animal served as a sham-operated control. Fourteen days later the effects of vagal nerve stimulation (10 Hz, 20 s) were assessed. On the operated side, where the supranodose vagotomy would have led to the degeneration of efferent axons, vagal stimulation had no effect on heart rate. The integrity of afferent axons was demonstrated by recording both electrically evoked volleys and characteristically normal patterns of afferent activity from the nerve. On the unoperated side the bradycardia produced by vagal stimulation was consistent with previous studies. It is concluded that the hexamethonium-resistant bradycardia evoked by stimulation of the rabbit vagus is mediated by non-myelinated preganglionic efferent axons.     

Location of dye-coupled second order and of efferent vestibular neurons labeled from individual semicircular canal or otolith organs in the frog

Vestibular nerve branches innervating the sensory epithelia of the three semicircular canals or of the three otolith organs of frogs were selectively labeled in-vitro with biocytin. Labeled afferent fibers from the semicircular canals, utricle, and lagena were encountered in each of the four vestibular nuclei and their projections overlapped considerably. Saccular afferent fibers projected to the dorsal (acoustic) nuclei and smaller projections to the vestibular nuclei were regionally restricted. Per semicircular canal or otolith organ about equal numbers (11-14) of medium sized vestibular neurons (between 7.5 and 17 microm in diameter) were dye-coupled to afferent fibers. Most of these dye-coupled vestibular neurons were located in the lateral and descending vestibular nuclei between the VIIIth and IXth nerves. The superior vestibular nucleus was relatively free of dye-coupled vestibular neurons. The location of this subpopulation of central vestibular neurons supports the notion that these neurons are part of a particular vestibulospinal pathway. In addition, from each of the canal and/or otolith organs about 3-4 efferent vestibular neurons were labeled retrogradely. These neurons (between 15 and 26 microm in diameter) were located ventral to the vestibular nuclear complex. The branching of efferent vestibular neurons was shown by the presence of neurons that were double labeled by two different fluorescent dyes applied in the same experiment to the anterior and posterior ramus of the same VIIIth nerve, respectively. The branching of these efferent neuron axons explained the presence of collaterals and terminals in the sensory epithelia of a number of untreated ipsilateral endorgans.     

Evidence for NMDA receptor in the afferent synaptic transmission of the vestibular system

This study aimed to define the pharmacology and physiological role of the N-methyl-d-aspartate (NMDA) receptor in the synapse between the hair cells and primary afferent neurons in the vestibular system. The spontaneous and mechanically evoked spike discharges of vestibular nerve fibers were extracellularly recorded in isolated inner ear from the axolotl (Ambystoma tigrinum). Pressure ejection of NMDA (10⁻⁶ to 10⁻³ M) elicited a dose-dependent increase of the basal spike discharge from the vestibular nerve fibers. Extracellular magnesium antagonized the NMDA effect in a dose-dependent manner.d(-)-2-amino-5-phosphonovaleric acid (AP5, 10⁻⁵ to 10⁻³ M) and 7-chloro-kynurenic acid (7ClKyn, 10⁻⁶ to 10⁻³ M) inhibited the basal activity of the vestibular nerve fibers. 7ClKyn also diminished the responses elicited by the mechanical stimulation of the preparation. Glycine (10⁻⁹ to 10⁻⁶ M) applied by bath substitution enhanced the NMDA responses, and the glycine agonistd-serine partially reversed the 7ClKyn inhibitory action. These results suggest that NMDA receptors participate in the generation of the basal spike discharge of vestibular system primary afferent neurons, but its activation is not critical for the response to brief mechanical stimuli.     

Influences of neck afferents on sympathetic and respiratory nerve activity

It is well established that the vestibular system influences the sympathetic nervous system and the respiratory system; presumably, vestibulosympathetic and vestibulorespiratory responses participate in maintaining stable blood pressure and blood oxygenation during movement and changes in posture. Many brainstem neurons that generate vestibulospinal reflexes integrate signals from the labyrinth and neck muscles to distinguish between head movements on a stable body and whole body movements. In the present study, responses were recorded from the splanchnic (sympathetic), hypoglossal (inspiratory) and abdominal (expiratory) nerves during stimulation of the C2 dorsal root ganglion or C2 or C3 nerve branches innervating dorsal neck muscles. Stimulation of neck afferents using low current intensities, in many cases less than twice the threshold for producing an afferent volley recordable from the cord dorsum, elicited changes in sympathetic and respiratory nerve activity. These data suggest that head rotation on a stable body would elicit both cervical and vestibular inputs to respiratory motoneurons and sympathetic preganglionic neurons. The effects of cervical afferent stimulation on abdominal, splanchnic and hypoglossal nerve activity were not abolished by transection of the brainstem caudal to the vestibular nuclei; thus, pathways in addition to those involving the vestibular nuclei are involved in relaying cervical inputs to sympathetic preganglionic neurons and respiratory motoneurons. Transection of the C1-3 dorsal roots enhanced responses of the splanchnic and abdominal nerves to pitch head rotations on a fixed body but diminished responses of the hypoglossal nerve. Thus, neck and vestibular afferent influences on activity of respiratory pump muscles and sympathetic outflow appear to be antagonistic, so that responses will occur during whole body movements but not head movements on a stationary trunk. In contrast, neck and vestibular influences on tongue musculature are complementary, presumably to produce tongue protrusion either during movements of the head alone or of the whole body.     

Differential effects of benzodiazepines on cochlear and auditory nerve responses

The influence exerted by chlordiazepoxide or midazolam upon auditory nerve compound action potential (cAP) and cochlear microphonic (CM) has been analyzed in chronic as well as in acutely prepared guinea pigs. Pre-receptorial variables were carefully controlled. The benzodiazepines dissociated the cochlear recorded potentials, increasing the cAP amplitude, in response to clicks, and decreasing the CM area, produced by a coherent pure tone pip. Both responses were dose related. A direct effect upon the cochlea was eliminated by local infusion of the drugs. It was also demonstrated to be a specific benzodiazepinic action because the use of an antagonist, Ro 15-1788, abolished the effect. Benzodiazepines could have increased the GABAergic activity at the pontine origins of the olivo-cochlear bundle or in the reticulo-cochlear fibers. These are the only central pathways that could be responsible for the effects obtained at the cochlea or auditory nerve levels. We suggest that this is the cause of the withdrawal of inhibitory tonus from the primary afferent fibers mediated by the efferent system (lateral superior olive), as may occur during dishabituation. It may also be the cause of the CM decrement, but the effect in this case would be exerted mainly through another set of efferent fibers (trapezoid body nucleus).     

Involvement of gastrointestinal mechano- and intestinal chemoreceptors in vagal reflexes: an electrophysiological study

The role of gastrointestinal mechanoreceptors and intestinal chemoreceptors in the genesis of vago-vagal reflexes was assessed by recording single vagal efferent fibre discharge in the urethane-anaesthetized ferret during procedures known to activate discrete populations of gastrointestinal afferent fibres. Distension of the stomach, duodenum and jejunum was used to activate mechanoreceptors while perfusion of the intestinal loops with various chemical solutions was used to activate mucosal chemoreceptors. Mechanical stimulation of the stomach and/or intestine was effective in modulating vagal efferent discharge in 90% of units tested. The response (either excitation or inhibition of efferent firing) was characterized by its short-latency (less than 1 s), slow-adaptation, and rapid return on removal of the stimulus. In contrast, chemical stimulation was much less potent evoking clear-cut responses in only 26 of the 109 efferent units. Luminal HCl was the most effective stimulus accounting for 81% of the efferent responses although these were of long-latency (greater than 1 min), gradual in onset and poorly maintained. Other efferent responses to HCl and hypertonic saline were characterized by a long-latency, sudden increase in discharge associated with the prodrome of vomiting. We conclude that while the mechanosensitive afferent input is well represented in terms of the genesis of vagal reflexes, the chemosensitive afferent input may be more important in behavioural aspects of visceral stimuli like vomiting.     

Responses of semicircular canal and otolith afferents to small angle static head tilts in the Gerbil

The discharge activity of first-order vestibular neurons was recorded in anesthetized or decerebrated gerbils from the post-ganglionic fibers of the vestibular nerve. Semicircular canal afferents were distinguished from otolith afferents on the basis of their responses to linear and angular head acceleration. In decerebrated preparations, canal afferents exhibited significantly faster discharge activity (average= 87.8impulses/s) than that of canal afferents in anesthetized preparations (average= 66.2impulses/s), when the head was held to position the lateral semicircular canals coplanar with the earth horizontal plane (standard position).

The effects of changes in linear forces on vestibular afferent activity were determined by statically tilting the head ± 10° about either the fore-aft and/or left-right head axes. A change in activity, from that recorded in the standard position, of 10% or greater was considered significant. Using this criterion, significant changes in the tilt response in anesthetized animals were observed in both anterior (23 of 48 neurons, 48%) and lateral (22 of 31, 71%) canal afferents as well as otolith (18 of 25, 72%) afferents. In decerebrated preparations for tilts around the pitch (left-right) axis, comparable effects were measured in (19 of 36, 53%) anterior and (17 of 30, 57%) lateral canal afferents. Neurons with irregular firing activity were more likely than regularly firing canal afferents to change their average discharge rate during static tilt. No significant differences in response magnitude to ± 10° head tilt were found between canal and otolith afferents in anesthetized animals. Mechanisms to account for the responses to linear acceleration of canal afferents are discussed.