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Daniel Cattaert - One of the best experts on this subject based on the ideXlab platform.
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In vivo analysis of proprioceptive coding and its Antidromic modulation in the freely behaving crayfish.
Journal of Neurophysiology, 2005Co-Authors: Didier Le Ray, Denis Combes, Cyril Déjean, Daniel CattaertAbstract:Although sensory nerves in vitro are known to convey both orthodromic (sensory) and Antidromic (putatively modulating) action potentials, in most cases very little is known about their bidirectional characteristics in intact animals. Here, we have investigated both the sensory coding properties and Antidromic discharges that occur during real walking in the freely behaving crayfish. The activity of the sensory nerve innervating the proprioceptor CBCO, a chordotonal organ that monitors both angular movement and position of the coxo-basipodite (CB) joint, which is implicated in vertical leg movements, was recorded chronically along with the electromyographic activity of the muscles that control CB joint movements. Two wire electrodes placed on the sensory nerve were used to discriminate orthodromic from Antidromic action potentials and thus allowed for analysis of both sensory coding and Antidromic discharges. A distinction is proposed between 3 main classes of sensory neuron, according to their firing in relation to levator muscle activity during free walking. In parallel, we describe 2 types of Antidromic activity: one produced exclusively during motor activity and a second produced both during and in the absence of motor activity. A negative correlation was found between the activity of sensory neurons in each of the 3 classes and identified Antidromic discharges during walking. Finally, a state-dependent plasticity of CBCO nerve activity has been found by which the distribution of sensory orthodromic and Antidromic activity changes with the physiological state of the biomechanical apparatus.
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Effects of Antidromic discharges in crayfish primary afferents.
Journal of Neurophysiology, 2002Co-Authors: Daniel Cattaert, Michelle BévengutAbstract: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.
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Antidromic Modulation of a Proprioceptor Sensory Discharge in Crayfish
Journal of neurophysiology, 1997Co-Authors: Michelle Bévengut, François Clarac, Daniel CattaertAbstract:Bevengut, Michelle, Francois Clarac, and Daniel Cattaert. Antidromic modulation of a proprioceptor sensory discharge in crayfish. J. Neurophysiol. 78: 1180–1183, 1997. In the proprioceptive neurons...
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Chloride conductance produces both presynaptic inhibition and Antidromic spikes in primary afferents.
Brain Research, 1994Co-Authors: Daniel Cattaert, A. El Manira, François ClaracAbstract:Primary afferents from a crayfish leg proprioceptor display both primary afferent depolarizations (PADs) and Antidromic spikes. PADs are generated by activation of GABA receptors and produce presynaptic inhibition, while the Antidromic spikes do not elicit any synaptic effect in the postsynaptic neurons. The aim of the present study was to investigate the ionic mechanisms that allow PADs to produce Antidromic spikes and to test whether GABA can produce similar effects. Intracellular recordings from the sensory axon terminals within the ganglion where PAD are produced were performed. Lowering the extracellular chloride concentration resulted in an increase in PAD amplitude, which was then capable of producing Antidromic spikes. Local application of GABA close to the axon terminal also resulted in production of Antidromic spikes. We conclude that Antidromic spikes may result from the activation of a GABA-mediated increase in chloride conductance that also produces PADs. Therefore PADs and Antidromic spikes may represent two aspects of the same GABAergic inhibitory mechanism that gate sensory transmission.
Raju Metherate - One of the best experts on this subject based on the ideXlab platform.
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thalamic stimulation largely elicits orthodromic rather than Antidromic cortical activation in an auditory thalamocortical slice
Neuroscience, 2001Co-Authors: Heather J Rose, Raju MetherateAbstract:Stimulation of the medial geniculate body in an auditory thalamocortical slice elicits a short-latency current sink in the middle cortical layers, as would be expected following activation of thalamocortical relay neurons. However, corticothalamic neurons can have axon collaterals that project to the middle layers, thus, a middle-layer current sink could also result from Antidromic activation of corticothalamic neurons and their axon collaterals. The likelihood of thalamic stimulation activating corticothalamic neurons would be reduced substantially if the corticothalamic pathway was not well preserved in the slice, and/or if the threshold for Antidromic activation was significantly higher than for orthodromic activation. To determine the prevalence and threshold of Antidromic activation, we recorded intracellularly from day 14-17 mouse brain slices containing infragranular cortical neurons while stimulating the medial geniculate or thalamocortical pathway. Antidromic spikes were confirmed by spike collision and characterized according to spike latency "jitter" and the ability to follow a high-frequency (100 Hz) stimulus train. The ability to follow a 100-Hz tetanus was a reliable indicator of Antidromic activation, but both Antidromic and orthodromic spikes could have low jitter. Thalamic stimulation produced Antidromic activation in two of 69 infragranular cortical neurons (<3%), indicating the presence of Antidromic activity, but implying a limited corticothalamic connection in the slice. Antidromic spikes in 13 additional neurons were obtained by stimulating axons in the thalamocortical pathway. The Antidromic threshold averaged 214+/-40.6 microA (range 6-475 microA), over seven times the orthodromic threshold for medial geniculate-evoked responses in layer IV extracellular (28+/-5.4 microA) or intracellular (27+/-5.6 microA) recordings. We conclude that medial geniculate stimulation activates relatively few corticothalamic neurons. Conversely, low-intensity thalamic stimulation strongly activates thalamocortical neurons. Thus, at low-stimulus intensities, the auditory thalamocortical slice can be used to probe mechanisms of thalamocortical function with limited Antidromic activation of corticothalamic neurons.
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thalamic stimulation largely elicits orthodromic rather than Antidromic cortical activation in an auditory thalamocortical slice
Neuroscience, 2001Co-Authors: Heather J Rose, Raju MetherateAbstract:Abstract Stimulation of the medial geniculate body in an auditory thalamocortical slice elicits a short-latency current sink in the middle cortical layers, as would be expected following activation of thalamocortical relay neurons. However, corticothalamic neurons can have axon collaterals that project to the middle layers, thus, a middle-layer current sink could also result from Antidromic activation of corticothalamic neurons and their axon collaterals. The likelihood of thalamic stimulation activating corticothalamic neurons would be reduced substantially if the corticothalamic pathway was not well preserved in the slice, and/or if the threshold for Antidromic activation was significantly higher than for orthodromic activation. To determine the prevalence and threshold of Antidromic activation, we recorded intracellularly from day 14–17 mouse brain slices containing infragranular cortical neurons while stimulating the medial geniculate or thalamocortical pathway. Antidromic spikes were confirmed by spike collision and characterized according to spike latency ‘jitter’ and the ability to follow a high-frequency (100 Hz) stimulus train. The ability to follow a 100-Hz tetanus was a reliable indicator of Antidromic activation, but both Antidromic and orthodromic spikes could have low jitter. Thalamic stimulation produced Antidromic activation in two of 69 infragranular cortical neurons ( We conclude that medial geniculate stimulation activates relatively few corticothalamic neurons. Conversely, low-intensity thalamic stimulation strongly activates thalamocortical neurons. Thus, at low-stimulus intensities, the auditory thalamocortical slice can be used to probe mechanisms of thalamocortical function with limited Antidromic activation of corticothalamic neurons.
Z Wiesenfeldhallin - One of the best experts on this subject based on the ideXlab platform.
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nk 1 but not nk 2 tachykinin receptors mediate plasma extravasation induced by Antidromic c fiber stimulation in rat hindpaw demonstrated with the nk 1 antagonist cp 96 345 and the nk 2 antagonist men 10207
Neuroscience Letters, 1992Co-Authors: Carljohan Dalsgaard, C A Maggi, Z WiesenfeldhallinAbstract:The effects of intradermal injection of CP-96,345 and Men 10207, selective antagonists for NK-1 and NK-2 tachykinin receptors, respectively, on the extravasation of plasma protein induced by Antidromic stimulation of unmyelinated sensory fibers in the sciatic nerve was studied in rat hindpaw. Activation of unmyelinated fibers by Antidromic sciatic nerve stimulation (1 Hz, 5 min) consistently evoked a localized plasma extravasation of Evans blue on the skin area of the hindpaw innervated by the sciatic nerve, which was not inhibited by intradermal injection of saline or Men 10207 (9 and 35 nmol). In contrast, CP-96,345 (3 and 9 nmol, but not 1 nmol), injected intradermally 15 min prior to nerve stimulation dose-dependently inhibited this response. Plasma extravasation induced by intravenously injected substance P was also inhibited by CP-96,345. Since CP-96,345 is a highly selective antagonist for NK-1 tachykinin receptors, it is suggested that the plasma extravasation induced by Antidromic C-fiber stimulation and by systemically applied tachykinins is mediated by NK-1 tachykinin receptors.
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spantide ii a novel tachykinin antagonist and galanin inhibit plasma extravasation induced by Antidromic c fiber stimulation in rat hindpaw
Neuroscience, 1991Co-Authors: Z Wiesenfeldhallin, Ha R Kanson, Karl Folkers, Ho T KfeltAbstract:Abstract The effect of intradermal injection of Spantide II, a novel tachykinin antagonist and the neuropeptide galanin on neurogenic plasma extravasation induced by Antidromic stimulation of C-fibers in the sciatic nerve was examined in the hindpaws of rats. Activation of C-fibers by Antidromic sciatic nerve stimulation (2 Hz, 5 min) consistently evoked a localized plasma extravasation of Evans Blue in the skin area of the hindpaw innervated by the sciatic nerve. Intradermal injection of 3 nmol Spantide II significantly inhibited this response. The plasma extravasation was nearly totally abolished when the concentration of Spantide II was increased to 9 nmol. Intradermal injection of 1.5 and 15 nmol galanin also inhibited plasma extravasation. Intradermal injection of 9 nmol Spantide II effectively blocked the plasma extravasation in the hindpaw induced by 8 nmol intravenous substance P. Plasma extravasation induced by intravenous substance P was also inhibited by the higher, but not by the lower, dose of galanin injected intradermally. The present results indicate that Spantide II, a potent non-toxic tachykinin antagonist, effectively blocks the neurogenic plasma extravasation induced by Antidromic C-fiber stimulation, thus supporting the view that tachykinins play an important role in this neurogenic inflammatory process. It is further shown that galanin, a naturally occurring neuropeptide present in primary afferents, also inhibits C-fiber activation-evoked plasma extravasation, indicating an interaction between galanin and tachykinins in the peripheral terminals of primary afferents, possibly through both pre- and postsynaptic mechanisms.
François Clarac - One of the best experts on this subject based on the ideXlab platform.
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Antidromic discharges of dorsal root afferents in the neonatal rat
Journal of Physiology-paris, 1999Co-Authors: Laurent Vinay, Frederic Brocard, Silvia Fellippamarques, François ClaracAbstract:Abstract Presynaptic inhibition of primary afferents can be evoked from at least three sources in the adult animal: 1) by stimulation of several supraspinal structures; 2) by spinal reflex action from sensory inputs; or 3) by the activity of spinal locomotor networks.The depolarisation in the intraspinal afferent terminals which is due, at least partly, to the activation of GABAA receptors may be large enough to reach firing threshold and evoke action potentials that are Antidromically conducted into peripheral nerves. Little is known about the development of presynaptic inhibition and its supraspinal control during ontogeny. This article, reviewing recent experiments performed on the in vitro brainstem/spinal cord preparation of the neonatal rat, demonstrates that a similar organisation is present,to some extent, in the new-born rat. A spontaneous activity consisting of Antidromic discharges can be recorded from lumbar dorsal roots. The discharges are generated by the underlying afferent terminal depolarizations reaching firing threshold. The number of Antidromic action potentials increases significantly in saline solution with chloride concentration reduced to 50% of control. Bath application of the GABAA receptor antagonist, bicuculline (5–10 μM) blocks the Antidromic discharges almost completely. Dorsal root discharges are therefore triggered by chloride-dependent GABAA receptor-mediated mechanisms; 1) activation of descending pathways by stimulation delivered to the ventral funiculus (VF) of the spinal cord at the C1 level; 2) activation of sensory inputs by stimulation of a neighbouring dorsal root; or 3) pharmacological activation of the central pattern generators for locomotion evokes Antidromic discharges in dorsal roots. VF stimulation also inhibited the response to dorsal root stimulation. The time course of this inhibition overlapped with that of the dorsal root discharge suggesting that part of the inhibition of the monosynaptic reflex may be exerted at a presynaptic level. The existence of GABAA receptor-independent mechanisms and the roles of the Antidromic discharges in the neonatal rat are discussed.
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Antidromic Modulation of a Proprioceptor Sensory Discharge in Crayfish
Journal of neurophysiology, 1997Co-Authors: Michelle Bévengut, François Clarac, Daniel CattaertAbstract:Bevengut, Michelle, Francois Clarac, and Daniel Cattaert. Antidromic modulation of a proprioceptor sensory discharge in crayfish. J. Neurophysiol. 78: 1180–1183, 1997. In the proprioceptive neurons...
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Chloride conductance produces both presynaptic inhibition and Antidromic spikes in primary afferents.
Brain Research, 1994Co-Authors: Daniel Cattaert, A. El Manira, François ClaracAbstract:Primary afferents from a crayfish leg proprioceptor display both primary afferent depolarizations (PADs) and Antidromic spikes. PADs are generated by activation of GABA receptors and produce presynaptic inhibition, while the Antidromic spikes do not elicit any synaptic effect in the postsynaptic neurons. The aim of the present study was to investigate the ionic mechanisms that allow PADs to produce Antidromic spikes and to test whether GABA can produce similar effects. Intracellular recordings from the sensory axon terminals within the ganglion where PAD are produced were performed. Lowering the extracellular chloride concentration resulted in an increase in PAD amplitude, which was then capable of producing Antidromic spikes. Local application of GABA close to the axon terminal also resulted in production of Antidromic spikes. We conclude that Antidromic spikes may result from the activation of a GABA-mediated increase in chloride conductance that also produces PADs. Therefore PADs and Antidromic spikes may represent two aspects of the same GABAergic inhibitory mechanism that gate sensory transmission.
Glenn J Giesler - One of the best experts on this subject based on the ideXlab platform.
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spinothalamic and spinohypothalamic tract neurons in the cervical enlargement of rats iii locations of Antidromically identified axons in the cervical cord white matter
Journal of Neurophysiology, 1994Co-Authors: Robert J Dado, James T Katter, Glenn J GieslerAbstract:1. Fifty-five neurons in the cervical enlargement (C6-C8) of urethan-anesthetized rats were Antidromically activated from the contralateral posterior diencephalon. In all cases, Antidromic thresholds were < or = 30 microA. The locations of the axons of these neurons within the white matter of segments C2-C6 were determined by tracking systematically using a second Antidromic stimulating electrode. 2. The recording locations of 51 neurons were marked and recovered. Twenty neurons were recorded in the superficial dorsal horn (SDH) and 31 were in the deep dorsal horn (DDH). Eighty-three lowest threshold points for Antidromic activation within the white matter of segments C2-C6 were determined for these 51 neurons. The mean Antidromic threshold at these points was 9.5 +/- 0.5 (SE) microA. For 26 neurons, the lowest threshold point for Antidromic activation was determined at one segmental level. We also attempted to determine whether individual axons maintained their position as they ascended through the cervical cord white matter. In 25 cases, lowest threshold points were determined at two or more segmental levels. 3. In segments C5-C6, 88% (7/8) of the lowest threshold points of the examined axons were located in the contralateral ventral funiculus, indicating that the majority of examined axons crossed the midline within one or two segments. 4. In segments C3-C4, 32% (14/44) of all examined axons were found in the dorsal lateral funiculus (DLF) and 66% (29/44) were within the ventral quadrant [ventral lateral funiculus (VLF) and ventral funiculus (VF)]. Sixty-nine percent (11/16) of the axons of neurons recorded in the SDH were located in the contralateral DLF and 31% (5/16) were located in the ventral quadrant (VQ). In contrast, only 11% (3/28) of the axons of neurons recorded in the DDH were located in the contralateral DLF and 86% (24/28) were located in the VQ. Therefore, in segments C3-C4, the locations of axons differed significantly. Those from neurons recorded in the SDH were located primarily in the DLF and those from neurons recorded in the DDH were located principally in the VQ. 5. In segment C2, 74% (23/31) of all examined axons were found in the DLF, 23% (7/31) were in the VQ, and 3% (1/31) were in the dorsal horn. Thus, the percentage of all examined axons in the DLF in C2 was approximately 2.5 times greater than it was in C3-C4.(ABSTRACT TRUNCATED AT 400 WORDS)
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Physiological characterization of spinohypothalamic tract neurons in the lumbar enlargement of rats.
Journal of neurophysiology, 1991Co-Authors: Rami Burstein, Robert J Dado, Kenneth D. Cliffer, Glenn J GieslerAbstract:1. Ninety-six neurons in the lumbar enlargement of urethananesthetized rats were Antidromically activated from the contralateral hypothalamus. The Antidromic stimulating electrode was moved systema...