Peripheral Sensory Organs Research Articles

Sensing hypoxia in the carotid body: from stimulus to response

The carotid body is a peripheral sensory organ that can transduce modest falls in the arterial PO(2) (partial pressure of oxygen) into a neural signal that provides the afferent limb of a set of stereotypic cardiorespiratory reflexes that are graded according to the intensity of the stimulus. The stimulus sensed is tissue PO(2) and this can be estimated to be around 50 mmHg during arterial normoxia, falling to between 10-40 mmHg during hypoxia. The chemoafferent hypoxia stimulus-response curve is exponential, rising in discharge frequency with falling PO(2), and with no absolute threshold apparent in hyperoxia. Although the oxygen sensor has not been definitely identified, it is believed to reside within type I cells of the carotid body, and presently two major hypotheses have been put forward to account for the sensing mechanism. The first relies upon alterations in the cell energy status that is sensed by the cytosolic enzyme AMPK (AMP-activated protein kinase) subsequent to hypoxia-induced increases in the cellular AMP/ATP ratio during hypoxia. AMPK is localized close to the plasma membrane and its activation can inhibit both large conductance, calcium-activated potassium (BK) and background, TASK-like potassium channels, inducing membrane depolarization, voltage-gated calcium entry and neurosecretion of a range of transmitter and modulator substances, including catecholamines, ATP and acetylcholine. The alternative hypothesis considers a role for haemoxygenase-2, which uses oxygen as a substrate and may act to gate an associated BK channel through the action of its products, carbon monoxide and possibly haem. It is likely however, that these and other hypotheses of oxygen transduction are not mutually exclusive and that each plays a role, via its own particular sensitivity, in shaping the full response of this organ between hyperoxia and anoxia.

Recurrent neuronal circuits in the neocortex

We thank our colleagues John Anderson and Tom Binzegger for their collaboration; and EU grant DAISY (FP6-2005-015803) for financial support.

Quantitative study on cell types in adult mouse taste buds

Taste buds are peripheral sensory organs that respond to a wide variety of sapid chemicals. Recent studies showed that taste bud cells (TBCs), constituent cells of taste buds, may form cell-to-cell communication to transmit taste information to taste nerves. In this study, I showed two types of TBCs in a single taste bud: type II, expressing taste receptors, and type III cells, forming synapses with taste nerves. The ratio of type II to type III cells was 5 to 1. This ratio may be important for signal transduction within taste buds.

The topographic brain: from neural connectivity to cognition

A hallmark feature of vertebrate brain organization is ordered topography, wherein sets of neuronal connections preserve the relative organization of cells between two regions. Although topography is often found in projections from peripheral sense organs to the brain, it also seems to participate in the anatomical and functional organization of higher brain centers, for reasons that are poorly understood. We propose that a key function of topography might be to provide computational underpinnings for precise one-to-one correspondences between abstract cognitive representations. This perspective offers a novel conceptualization of how the brain approaches difficult problems, such as reasoning and analogy making, and suggests that a broader understanding of topographic maps could be pivotal in fostering strong links between genetics, neurophysiology and cognition.

Functional and morphological effects of repeated sodium arsenite exposure on rat peripheral sensory nerves

Exposure to inorganic arsenic (iAs) is known to result in peripheral neuropathy. To better understand the functional and morphological consequences of iAs exposure, we examined the electrophysiological and histological characteristics of the sensory sural nerves in adult Male Wistar rats following 30 days of sodium arsenite administration by gavage (10 mg/kg body weight/day). Arsenic (As) levels in the peripheral nerves of exposed animals were about 150 times greater than those in controls. Lipid peroxidation was also increased in iAs-exposed animals. Compound action potentials (CAPs) evoked in iAs-exposed nerves were characterized by a slower conduction velocity (∼ 26%). iAs-exposed nerves also showed a trend towards a decreased CAP area (∼ 35%). These electrophysiological changes were consistent with histological alterations such as a ∼ 56% decrease in myelin thickness. In addition, the perimeter and transverse area of axons were reduced to 29% and 45% of control, respectively. Our results suggest that accumulation of As produced by iAs exposure induces oxidative damage, severe demyelination, and other morphological alterations in axons of peripheral nerves. These changes may, in turn, induce changes in the generation and propagation of action potentials in peripheral nerves, leading to decreased transmission of information from peripheral sensory organs to the central nervous system.

Sex steroid hormones and sexual dimorphism of chemosensory structures in a terrestrial salamander ( Plethodon shermani)

The volume of the vomeronasal organ (VNO) in the terrestrial salamander Plethodon shermani was approximately 1.7 times larger in adult males compared to adult females, even though male body size was, on average, slightly smaller than female body size. VNO cell density, however, was the same in adult males and females. The sex difference in VNO volume was found in sexually immature animals as well, indicating that the increase of plasma androgens that occurs at sexual maturity does not produce the sex difference in VNO volume. There was no difference in VNO volume between reproductive and nonreproductive adult females, despite differences in plasma estradiol (E2) levels. The volumes of the main olfactory epithelium and muscles regulating diameter of the external nares were similar between males and females, indicating that the VNO per se, and not other aspects of the nasal cavity, was sexually dimorphic. To conclude, the sex difference in VNO volume appears to be a permanent sex difference that develops before sexual maturity. Future studies will examine the functional consequences of this structural sexual dimorphism in a peripheral sensory organ, the VNO.

The Evolution of Sensory Placodes

The vertebrate cranial sensory placodes are ectodermal embryonic patches that give rise to sensory receptor cells of the peripheral paired sense organs and to neurons in the cranial sensory ganglia. Their differentiation and the genetic pathways that underlay their development are now well understood. Their evolutionary history, however, has remained obscure. Recent molecular work, performed on close relatives of the vertebrates, demonstrated that some sensory placodes (namely the adenohypophysis, the olfactory, and accoustico-lateralis placodes) first evolved at the base of the chordate lineage, while others might be specific to vertebrates. Combined with morphological and cellular fate data, these results also suggest that the sensory placodes of the ancestor of all chordates differentiated into a wide range of structures, most likely to fit the lifestyle and environment of each species.

Mouse Taste Buds Release Serotonin in Response to Taste Stimuli

Cell-to-cell interactions and synaptic integration may occur within taste buds prior to signals being exported from these peripheral sensory organs to the CNS (Roper, 1992; Kaya et al., 2004). In principle, these interactions could include chemical and electrical synapses between taste cells and synapses from taste cells to sensory afferent fibers. Knowing which transmitters are released at synapses in taste buds would help clarify how signals are processed in taste buds but to date this information is lacking. A number of neurotransmitter candidates have been proposed for taste bud synapses, including serotonin (5 hydroxytryptamine, 5HT), glutamate, acetylcholine, ATP, peptides and others, but none has been unambiguously identified (reviewed by Nagai et al., 1996). On balance, the preponderance of evidence suggests that 5HT is one of the transmitters. For example, 5HT is found in a subset of taste cells in a wide variety of species (Kim and Roper, 1995). Taste bud cells that possess synapses with nerve fibers take up the 5HT precursor (Takeda, 1977; Yee et al., 2001), and tryptophan hydroxylase, the enzyme that converts tryptophan to 5 hydroxytryptophan (5HTP), is found in taste buds (Cao et al., 2004). There is indirect evidence from autoradiographic studies that amphibian taste cells release 5HT when they are depolarized (Nagai et al., 1998). Pharmacological and molecular biological studies suggest that taste cells express 5HT1A-like receptors and primary afferent fibers possess 5HT3 receptors (Delay et al., 1997; Herness and Chen, 1997; Kaya et al., 2004). Yet despite all the above evidence, one of the canonical criteria for identifying synaptic neurotransmitters, namely detecting its release from stimulated synapses, has yet to be established for 5HT in taste buds. We have addressed this question by using biosensor cells that are sensitive to 5HT to reveal transmitter release from mouse taste buds during sensory stimulation. The results indicate that depolarizing mouse taste cells with KCl or stimulating them with sweet and bitter tastants elicits 5HT release. Collectively, these data firmly identify 5HT as a taste cell neurotransmitter.

The genetics of ray pattern variation in Caenorhabditis briggsae

BackgroundHow does intraspecific variation relate to macroevolutionary change in morphology? This question can be addressed in species in which derived characters are present but not fixed. In rhabditid nematodes, the arrangement of the nine bilateral pairs of peripheral sense organs (rays) in tails of males is often the most highly divergent character between species. The development of ray pattern involves inputs from hometic gene expression patterns, TGFβ signalling, Wnt signalling, and other genetic pathways. In Caenorhabditis briggsae, strain-specific variation in ray pattern has provided an entrée into the evolution of ray pattern. Some strains were fixed for a derived pattern. Other strains were more plastic and exhibited derived and ancestral patterns at equal frequencies.ResultsRecombinant inbred lines (RILs) constructed from crosses between the variant C. briggsae AF16 and HK104 strains exhibited a wide range of phenotypes including some that were more extreme than either parental strain. Transgressive segregation was significantly associated with allelic variation in the C. briggsae homolog of abdominal B, Cb-egl-5. At least two genes that affected different elements of ray pattern, ray position and ray fusion, were linked to a second gene, mip-1. Consistent with this, the segregation of ray position and ray fusion phenotypes were only partially correlated in the RILs.ConclusionsThe evolution of ray pattern has involved allelic variation at multiple loci. Some of these loci impact the specification of ray identities and simultaneously affect multiple ray pattern elements. Others impact individual characters and are not constrained by covariance with other ray pattern elements. Among the genetic pathways that may be involved in ray pattern evolution is specification of anteroposterior positional information by homeotic genes.

Integrating Growth with Developmental Timing

During development, temporal and spatial cues control cell fate and tissue organization. Using a screen for mutations that cause patterning defects in the Drosophila eye, Bateman and McNeill identified the gene encoding tuberous sclerosis complex 1 (TSC1). Further analysis of the patterning defect indicated that the organization was disrupted by premature differentiation of the photoreceptor cells, leading to overrotation of the ommatidia. The secretion of the epidermal growth factor ligand spitz, which activates a known pathway involved in photoreceptor differentiation, was apparently normal in tsc –/– cells, because they and wild-type cells had similar amounts of phosphorylated extracellular signal-regulated kinase (ERK) and of various downstream components. Premature acquisition of differentiation markers was also observed with a mutation that inactivated the phosphatase PTEN, which like TSC1 is a negative regulator of the pathways controlled by TOR and the insulin receptor. Analysis of the ommatidial differentiation timing in cells carrying mutations that disrupted signaling through the insulin receptor pathway revealed delayed photoreceptor differentiation, whereas excessive activation of the pathway produced precocious differentiation. Similar alterations in developmental timing were noted for the peripheral sensory organ, the chorodontal organ, but not for hair formation in the pupal wing. The change in timing did not appear to be a consequence of a change in the size of the cells, because overexpression of Myc or cyclin D and cyclin-dependent kinase 4 (CDK4) did not produce the same patterning defects. Thus, the pathways that regulate growth also appear to contribute to developmental timing, providing a mechanism for coordination of development with nutritional status. J. M. Bateman, H. McNeill, Temporal control of differentiation by the insulin receptor/Tor pathway in Drosophila . Cell 119 , 87-96 (2004). [Online Journal]

Decreased arousals among healthy infants after short-term sleep deprivation.

Sleep deprivation is a risk factor for sudden infant death syndrome (SIDS). Recent changes in normal life routines were more common among SIDS victims, compared with control infants. Sleep deprivation can result from handling conditions or from sleep fragmentation attributable to respiratory or digestive conditions, fever, or airway obstructions during sleep. Compared with matched control infants, future SIDS victims exhibited fewer complete arousals by the end of the night, when most SIDS cases occur. Arousal from sleep could be an important defense against potentially dangerous situations during sleep. Because the arousal thresholds of healthy infants were increased significantly under conditions known to favor SIDS, we evaluated the effects of a brief period of sleep deprivation on sleep and arousal characteristics of healthy infants. Fourteen healthy infants, with a median age of 8 weeks (range: 6-18 weeks), underwent polygraphic recording during a morning nap and an afternoon nap, in a sleep laboratory. The infants were sleep-deprived for 2 hours before being allowed to fall asleep. Sleep deprivation was achieved by keeping the infants awake, with playing, handling, and mild tactile or auditory stimulations, for as long as possible beyond their habitual bedtimes. To avoid any confounding effect attributable to differences in sleep tendencies throughout the day, sleep deprivation was induced before either the morning nap or the afternoon nap. Seven infants were sleep-deprived before the morning nap and 7 before the afternoon nap. The sleep and arousal characteristics of each infant were compared for the non-sleep-deprived condition (normal condition) and the sleep-deprived condition. During each nap, the infants were exposed, during rapid eye movement (REM) sleep, to white noise of increasing intensity, from 50 dB(A) to 100 dB(A), to determine their arousal thresholds. Arousal thresholds were defined on the basis of the lowest auditory stimuli needed to induce arousal. After the induced arousal, the infants were allowed to return to sleep to complete their naps. Sleep deprivation lasted a median of 120 minutes (range: 90-272 min). Most sleep characteristics were similar for the normal and sleep-deprived conditions, including sleep efficiency, time awake, percentages of REM sleep and non-REM sleep, frequency and duration of central apnea and of periodic breathing, duration of obstructive apnea, mean heart rate and variability, and mean breathing rates during REM sleep and non-REM sleep. After sleep deprivation, the duration of the naps increased, whereas there were decreases in the latency of REM sleep and in the density of body movements. More-intense auditory stimuli were needed for arousal when the infants were sleep-deprived, compared with normal nap sleep. Sleep deprivation was associated with a significant increase in the frequency of obstructive sleep apnea episodes, especially during REM sleep. No significant differences were noted when the effects of morning and afternoon sleep deprivation were compared. No correlation was found between the duration of sleep deprivation and either the frequency of obstructive apnea or the changes in arousal thresholds, although the infants who were more sleep-deprived exhibited tendencies toward higher auditory arousal thresholds and shorter REM sleep latencies, compared with less sleep-deprived infants. There were tendencies for a negative correlation between the auditory arousal thresholds and REM sleep latencies and for a positive correlation between the auditory arousal thresholds and the frequencies of obstructive apnea during REM sleep. Short-term sleep deprivation among infants is associated with the development of obstructive sleep apnea and significant increases in arousal thresholds. As already reported, sleep deprivation may induce effects on respiratory control mechanisms, leading to impairment of ventilatory and arousal responses to chemical stimulation and decreases in genioglossal electromyographic activity during REM sleep. These changes in respiratory control mechanisms could contribute to the development of obstructive apnea. The relationship between the development of obstructive apnea and increases in arousal thresholds remains to be evaluated. Adult subjects with obstructive sleep apnea exhibited both sleep fragmentation and increases in arousal thresholds. Conversely, sleep deprivation increased the frequency and severity of obstructive sleep apnea. In this study, the increases in arousal thresholds and the development of obstructive apnea seemed to result from the preceding sleep deprivation. The depressed arousals that follow sleep deprivation have been attributed to central mechanisms, rather than decreases in peripheral sensory organ function. Such mechanisms could include disturbances within the reticular formation of the brainstem, which integrates specific facilitory inputs, such as ascending pathways from auditory receptors, and inhibitory inputs from the cortex. It remains to be determined whether the combination of upper airway obstruction and depressed arousability from sleep contributes to the increased risk of sudden death reported for sleep-deprived infants.

Hyperalgésie et allodynie : les mécanismes périphériques

Nociceptive signals are generated by peripheral sensory organs called nociceptors, which are endings of small-diameter nerve fibers responsive to the tissue environment. The myriad chemical mediators capable of activating, sensitizing, or arousing nociceptors include kinins, proinflammatory and anti-inflammatory cytokines, prostanoids, lipooxygenases, the “central immune response mediator” NF-κB, neurotrophins and other growth factors, neuropeptides, nitric oxide, histamine, serotonin, proteases, excitatory amino acids, adrenergic amines, and opioids. These mediators may act in combination or at a given time in the inflammatory process, producing subtle changes that result in hyperalgesia or allodynia. We will review the most extensively studied molecular and cellular mechanisms underlying these two clinical abnormalities. The role of the peripheral nervous system in progression of inflammatory joint disease to chronicity is discussed.

Hyperalgesia and allodynia: peripheral mechanisms

Nociceptive signals are generated by peripheral sensory organs called nociceptors, which are endings of small-diameter nerve fibers responsive to the tissue environment. The myriad chemical mediators capable of activating, sensitizing, or arousing nociceptors include kinins, proinflammatory and anti-inflammatory cytokines, prostanoids, lipooxygenases, the “central immune response mediator” NF-κB, neurotrophins and other growth factors, neuropeptides, nitric oxide, histamine, serotonin, proteases, excitatory amino acids, adrenergic amines, and opioids. These mediators may act in combination or at a given time in the inflammatory process, producing subtle changes that result in hyperalgesia or allodynia. We will review the most extensively studied molecular and cellular mechanisms underlying these two clinical abnormalities. The role of the peripheral nervous system in progression of inflammatory joint disease to chronicity is discussed.

Cellular expression of src-suppressed C kinase substrate (SSeCKS) in the peripheral nervous system and sensory organs

Src-suppressed C kinase substrate (SSeCKS) is expressed in a variety of cells and plays an important role in cell differentiation, migration and shaping via remodeling of the actin-based cytoskeleton. In the present study, the cellular distribution of SSeCKS was studied in the peripheral nervous system and sensory organs of mice by in situ hybridization and immunohistochemistry. In the dorsal root ganglia and trigeminal ganglia, small- and medium-sized neurons expressed SSeCKS, whereas large-sized neurons showed negative or faintly positive reactions. Definite positive signals of SSeCKS mRNA and protein in the sensory ganglia were also found in some satellite cells which frequently enveloped ganglion cells without SSeCKS expression. In autonomic ganglia (celiac ganglia, pelvic ganglia, and intestinal myenteric nerve plexus), SSeCKS immunoreactivity was confined to satellite cells, and not detectable in neuronal somata. No significant immunoreactivity for SSeCKS appeared in most sensory organs, including the retina, organ of Corti, taste buds, and olfactory mucosa. In contrast, the vomeronasal organ displayed intense and selective expression of SSeCKS in the sensory epithelium, where only supporting cells were immunolabeled. SSeCKS-immunoreactive Schwann cells were widely distributed in nerve bundles including the vomeronasal nerve, olfactory nerve, and dorsal root. These findings suggest that SSeCKS might be involved in regulation and homeostasis of the peripheral nervous system and of the vomeronasal organ among sensory organs.

Cortical spatial aspects of optical intrinsic signals in response to sucrose and NaCl stimuli.

To examine whether cortical taste neurons use spatial codes for discriminating taste information, we investigated the spatial aspects of optical intrinsic signal (OIS) responses in the gustatory insular cortex (GC) elicited by the administration of two essential tastants, sucrose and NaCl, on the tongue. OIS responses to sucrose appeared in the rostral part of the GC, whereas those to NaCl appeared in the central part of the GC. Local anesthetization of the tongue abolished OIS responses, and the administration of distilled water elicited no OIS response. Thus, taste information elicited by sucrose and NaCl from the peripheral sensory organs is segregated in the GC, suggesting that the information from two essential tastants is assembled as spatial codes in the primary cortical taste area through the process of taste quality perception.

Restoration of morphological and functional integrity in the regenerating eye of the giant African land snail Achatina fulica

AbstractTo determine whether vision returns to its original state following eye removal in Achatina fulica, light and electron microscope examinations, electrophysiological recordings and behavioural tests were carried out on the regenerating snails. Reparative morphogenesis can result in the restoration of the peripheral sense organ even in the absence of complete regrowth of the tentacle, but it can also lead to the formation of aberrant regenerates. We found that anatomically and ultrastructurally the eyes of the ‘most normal’ regenerates were basically the same as the original eyes. Under normal conditions each eye is composed of a principal and an accessory eye, both sharing a common cornea. The only difference between regenerated and native eyes is the smaller size of the former, as a result of a reduced number of retinal cells. Electroretinographic responses revealed that the molecular mechanism of phototransduction is restored, in principle, but that flicker fusion frequency in the regenerated eye is significantly lower than in the normal eye. The directional movement to a visual stimulus (a black stripe of 45° width) had not completely recovered even 6 months after amputation. This suggests that the central projections of the optic nerve had not become fully re‐established at the time of testing.

Central projections of the saccular and utricular nerves in macaques.

The central projections of the utricular and saccular nerve in macaques were examined using transganglionic labeling of vestibular afferent neurons. In these experiments, biotinylated dextran amine was injected directly into the saccular or utricular neuroepithelium of fascicularis (Macaca fascicularis) or rhesus (Macaca mulatta) monkeys. Two to 5 weeks later, the animals were killed and the peripheral vestibular sensory organs, brainstem, and cerebellum were collected for analysis. The principal brainstem areas of saccular nerve termination were lateral, particularly the spinal vestibular nucleus, the lateral portion of the superior vestibular nucleus, ventral nucleus y, the external cuneate nucleus, and cell group l. The principal cerebellar projection was to the uvula with a less dense projection to the nodulus. Principle brainstem areas of termination of the utricular nerve were the lateral/dorsal medial vestibular nucleus, ventral and lateral portions of the superior vestibular nucleus, and rostral portion of the spinal vestibular nucleus. In the cerebellum, a strong projection was observed to the nodulus and weak projections were present in the flocculus, ventral paraflocculus, bilateral fastigial nuclei, and uvula. Although there is extensive overlap of saccular and utricular projections, saccular inputs to the lateral portions of the vestibular nuclear complex suggest that saccular afferents contribute to the vestibulospinal system. In contrast, the utricular nerve projects more rostrally into areas of known concentration of vestibulo-ocular related cells. Although sparse, the projections of the utricle to the flocculus/ventral paraflocculus suggest a potential convergence with floccular projection inputs from the vestibular brainstem that have been implicated in vestibulo-ocular motor learning.

Differential activities of Sonic hedgehog mediated by Gli transcription factors define distinct neuronal subtypes in the dorsal thalamus

The dorsal thalamus (DT) is a pivotal region in the vertebrate brain that relays inputs from the peripheral sensory organs to higher cognitive centers. It consists of clusters of neurons with relevant functions, called brain nuclei. However, the mechanisms underlying development of the DT, including specification of the neuronal subtypes and morphogenesis of the nuclear structures, remain largely unknown. As a first step to this end, we focused on two transcription factors Sox14 and Gbx2 that are expressed in the specific brain nuclei in the chick DT. The onset of their expression was found in distinct populations of the postmitotic cells in the prosomere 2, which was regulated by the differential activities of Sonic hedgehog (Shh) in a manner consistent with the action as a morphogen. Furthermore, both gain- and loss-of-function results strongly suggest that such distinct inductive activities are mediated selectively by different Gli factors. These results suggest that cooperation of the differential expression of Gli factors and the activity gradient of Shh signaling generates the distinct thalamic neurons at the specific locations.

Individual mouse taste cells respond to multiple chemical stimuli.

Sensory organs are specialized to detect and decode stimuli in terms of intensity and quality. In the gustatory system, the process of identifying and distinguishing taste qualities (e.g. bitter versus sweet) begins in taste buds. A central question in gustatory research is how information about taste quality is extracted by taste receptor cells. For instance, whether and how individual taste cells respond to multiple chemical stimuli is still a matter for debate. A recent study showed that taste cells expressing bitter-responsive taste receptors do not also express sweet-responsive taste receptors and vice versa. These results suggest that the gustatory system may use separate cellular pathways to process bitter and sweet signals independently. Results from electrophysiological studies, however, reveal that individual taste receptor cells respond to stimuli representing multiple taste qualities. Here we used non-invasive Ca(2+) imaging in slices of lingual tissue containing taste buds to address the issue of quality detection in murine taste receptor cells. We recorded calcium transients elicited by chemical stimuli representing different taste qualities (sweet, salty, sour and bitter). Many receptor cells (38 %) responded to multiple taste qualities, with some taste cells responding to both appetitive ("sweet") and aversive ("bitter") stimuli. Thus, there appears to be no strict and separate detection of taste qualities by distinct subpopulations of taste cells in peripheral gustatory sensory organs in mice.

Effects of antidromic discharges in crayfish primary afferents.

Contrary to orthodromic spikes that are generated in sensory organs and conveyed to CNS, antidromic spikes are generated in the axon terminals of the sensory neurons within the CNS and are conveyed to the peripheral sensory organ. Antidromic discharges are observed in primary afferent neurons of both vertebrates and invertebrates and seem to be related to the rhythmic activity of central neural networks. In this study, we analyzed the effect of antidromic discharges on the sensory activity of a leg proprioceptor in in vitro preparations of the crayfish CNS. Intracellular microelectrodes were used both to record the orthodromic spikes and to elicit antidromic spikes by injecting squares pulses of depolarizing current at various frequencies. Experiments were performed on the three types of identified sensory afferents (tonic, phasotonic, and phasic). The main results showed a reduction of the firing frequency of the orthodromic activity in 82% of the tested afferents. In tonic afferents, during their occurrences and according to their frequency, antidromic spikes or bursts reduced or suppressed the orthodromic activity. Following their terminations, they also induced a silent period and a gradual recovery of the orthodromic activity, both of which increased as the duration and the frequency of the antidromic bursts increased. In phasotonic and phasic afferents, antidromic bursts reduced or suppressed the phasic responses as their frequency and durations increased. In phasotonic afferents, if elicited prior to the movements, long-duration bursts with increasing frequency reduced more rapidly the tonic background activity than the phasic one whereas short-duration bursts at high frequency produced strong decreases of both. The effect of antidromic bursts accumulated when they are repetitively elicited. Antidromic bursts induced a much larger decrease of the sensory activity than adaptation alone. The occurrences of antidromic spikes or bursts may have a functional role in modulating the incoming sensory messages during locomotion. The mechanisms by which antidromic spikes modulate the firing sensitivity of the primary afferents may well lie in modifications of the properties of either mecanotransduction and/or spike initiation.