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GABA能神经元

GABA能神经元
GABA能神经元

Spontaneous and locomotor-related GABAergic input onto primary afferents in the neonatal rat

Silvia Fellippa-Marques,Laurent Vinay and Franc?ois Clarac

CNRS,UPR Neurobiologie et Mouvements(UPR9011),31chemin Joseph Aiguier,13402Marseille Cx20,France Keywords:antidromic discharges,bicuculline,presynaptic inhibition,spinal cord

Abstract

The in vitro brain stem±spinal cord preparation of neonatal rats(0±5days old)was used to examine the contribution of GABA A(g-aminobutyric acid)receptors to the spontaneous and locomotor-related antidromic?ring in the dorsal roots of neonatal rats. Spontaneous bursts of antidromic discharges were generated by the underlying afferent terminal depolarizations reaching spiking threshold.The number of antidromic action potentials increased signi?cantly in saline solution with Cl±concentration reduced to50% of control.Bath application of the GABA A receptor antagonist bicuculline,at low concentrations(1±2m M),or picrotoxin blocked the antidromic discharges in the dorsal roots almost completely.The increase in Cl±conductance was therefore mediated by an activation of GABA A receptors.Increasing the concentration of bicuculline to10±20m M never blocked these discharges further.On the contrary,in half of the preparations,the number of antidromic action potentials was higher in the presence of high concentrations of bicuculline(10±20m M)than in the presence of picrotoxin or low concentrations of bicuculline.This suggests that bicuculline,at high concentrations,may have other effects,in addition to blocking GABA A receptors.Dorsal root?ring was observed during?ctive locomotion induced by bath application of excitatory amino acids and serotonin.A rhythmical pattern was often demonstrated. Bicuculline at low concentrations caused a decrease of the antidromic discharge whereas,at high concentrations,bursts of discharges appeared.A double-bath with a barrier built at the L3level was then used to separate the mechanisms which generate locomotion from those mediating primary afferent depolarizations.Excitatory amino acids and serotonin were perfused in the rostral pool only.Decreasing the concentration of chloride in the caudal bath caused a sharp increase in the number of antidromic action potentials recorded from the L5dorsal root.These discharges,which were modulated in phase with the locomotor rhythm,were blocked by bicuculline.These data demonstrate the existence of a locomotor-related GABAergic input onto primary afferent terminals in the neonatal rat.

Introduction

It is well established that one form of presynaptic inhibition in the vertebrate spinal cord is associated with primary afferent depolariza-tion(PAD,Rudomin,1990;Rudomin et al.,1993;Alvarez-Leefmans et al.,1998).Suprathreshold depolarization triggers discharges that are antidromically conducted into peripheral nerves.This was?rst demonstrated by recording the reˉex response elicited in dorsal roots, by electrical stimulation of an adjacent dorsal root(`dorsal root reˉex',Toennies,1938;Barron&Matthews,1938a;see Kerkut& Bagust,1995for review).Antidromic discharges of primary afferents have been observed during locomotion in the cat(?ctive locomotion, Dubuc et al.,1988;Duenas et al.,1990;Gossard et al.,1991;and actual locomotion,Beloozerova&Rossignol,1994;1995;Rossignol et al.,1998)and in the rat(Pilyavskii et al.,1988).A spontaneous antidromic activity in the dorsal roots has been described in the in vitro spinal cord isolated from adult(Bagust et al.,1989;Chen et al., 1993)or young hamsters(Abdul-Razzak et al.,1994;see Kerkut& Bagust,1995for review).Antidromic discharges are also recorded from lumbar dorsal roots in the neonatal rat spinal cord in vitro (Kremer&Lev-Tov,1998;Vinay&Clarac,1999).

There is a wealth of evidence suggesting that g-aminobutyric acid (GABA),through the activation of GABA A receptors,plays a major role in the generation of PAD and therefore of antidromic discharges. Axo-axonic interactions between GABAergic terminals and primary afferents have been demonstrated(see Alvarez,1998for review). Activation of GABA A receptors increases membrane conductance to chloride ions,which leads to depolarization of afferent terminals.Both the GABA-evoked depolarization of terminals and PAD are reduced by GABA A receptor antagonists(Eccles et al.,1963;Levy,1975; Rudomin et al.,1981;Curtis&Lodge,1982).In addition,antidromic discharges elicited by stimulation of ventral descending pathways in the neonatal rat spinal cord in vitro are blocked by bath application of bicuculline,a GABA A receptor antagonist(Vinay&Clarac,1999). However,mechanisms other than activation of GABA A receptors have also been suggested to be responsible for PAD.In particular, PAD has been proposed to result from the transient increase in concentration of potassium ions in the extracellular space of the spinal cord,as a consequence of interneuronal activity(Barron& Matthews,1938b;see Vyklicky&Knotkova-Urbancova,1998for review).Support for this idea was provided recently by Kremer& Lev-Tov(1998)who described dorsal root afferent depolarization and antidromic?ring in isolated spinal cords of neonatal rats in the presence of bicuculline.

The aim of this study was to identify whether and to what extent the activation of GABA A receptors contributes to the spontaneous

Correspondence:Dr L.Vinay,as above.E-mail:vinay@https://www.sodocs.net/doc/ba18221309.html,rs-mrs.fr

Received29July1999,revised16September1999,accepted23September

1999

European Journal o Neuroscience,Vol.12,pp.155±164,2000?European Neuroscience Association

and locomotor-related antidromic?ring in dorsal roots of neonatal https://www.sodocs.net/doc/ba18221309.html,ing the in vitro brain stem±spinal cord preparation,we show that most of the spontaneous antidromic discharges disappear after application of low concentrations of bicuculline or picrotoxin(PTX). We also demonstrate a phasic GABAergic inˉuence on primary afferent terminals during?ctive locomotion.

Materials and methods

Experiments were performed on32Wistar rats[from postnatal day0 (P0),de?ned as the?rst24h after birth,to P5].All surgical and experimental procedures were made to minimize animal suffering and conformed to the guidelines from the French Ministry for Agriculture and Fisheries,Division of Animal Rights.The animals were anaesthetized with ether,decerebrated at a postcollicular level and eviscerated.They were pinned down onto a Petri dish continuously perfused with saline solution,containing the following substances(in m M):NaCl,130;KCl,4;CaCl2,3.75;MgSO4,1.3; NaH2PO4,0.58;NaHCO3,25;glucose,10,bubbled with a95%O2±5%CO2mixture,and adjusted to pH7.4.A dorsal craniotomy and laminectomy was performed.The brain stem,spinal cord and lumbar roots were then removed and pinned down with the ventral side up in the recording chamber.

Monopolar stainless steel electrodes were placed in contact with the roots and insulated with vaseline,for recording of discharges (bandwidth,70Hz to1kHz).Dorsal root potentials were recorded to investigate the relationships between antidromic discharges and primary afferent depolarizations.For this purpose,dorsal roots were cut~2mm away from the spinal cord and the central stump was incorporated in a suction electrode?lled with normal saline and connected to an AC-coupled ampli?er(bandwidth,0.1Hz to1kHz). Data were collected through an Instrutech(NY,USA)ITC-16MAC interface on a Macintosh Quadra650(software programs from Axon Instruments,CA,USA).The number of action potentials was measured by using a software voltage discriminator(Fig.1B1, arrows)and peak detector.Antidromic discharges occurring sponta-neously in dorsal roots were recti?ed and integrated(time constant 5ms).Sections of traces(duration2s)including the bursts were duplicated,aligned at the burst onset and averaged(25±50bursts)to investigate the effect of low-chloride solutions on the spontaneous bursting dorsal root activity(Fig.3).

Fictive locomotion was elicited by bath application of N-methyl-D,L-aspartate(NMA,15±20m M)and serotonin(5-HT,10m M).A program was written to normalize the locomotor cycles and to sample the dorsal root antidromic discharges in100time intervals per locomotor cycle.The onset of the L2or L3ventral root burst on the right side was taken as time t=0for the resampling.A threshold was used for the detection of action potentials and the pattern of dorsal root discharges was identi?ed from30±100consecutive locomotor cycles.The number of antidromic action potentials was averaged over intervals of5±10%of the locomotor cycle(Figs6±8).Averages of the recti?ed ventral root activity were also plotted(Figs6B and8F). Results are presented in the text and?gures in the form of mean6SEM.The Mann±Whitney test was employed for statistical analysis when two groups were compared,and a one-way ANOVA with Tukey post test for more than two groups(Graphpad Prism2 Software,CA,USA).

Bicuculline methiodide and PTX were obtained from Sigma(MO, USA).A low-chloride solution was prepared by replacing NaCl in control saline with equimolar amounts of Na isethionate(Vinay& Clarac,1999).

Results

Spontaneous GABAergic antidromic dorsal root discharges Spontaneous activity recorded from lumbar dorsal roots consisted of bursts of action potentials separated by silent periods or continuous ?ring of action potentials(Figs1A and2A1,L5dorsal root). Motoneuron bursting episodes could be recorded from the ipsilateral ventral roots under these conditions.Motor activity,when present, was in phase with dorsal root discharge(Fig.1A).Note that the motor axons in the L3and L5ventral roots on one side burst simultaneously and not in the alternating manner characteristic of?ctive locomotion (Cazalets et al.,1992;Kiehn&Kjaerulff,1996).The interval between bursts was variable within a recording session(Fig.1B1 and B2,note that at least four ranges of intervals could be detected:2±3s;7±10s;16±23s;and28±32s).Recordings of a dorsal root in the neighbouring segment with a suction electrode showed that

F IG.1.Spontaneous bursts in ventral and dorsal roots.(A)Simultaneous

recordings from two ventral roots and one dorsal root on the same side of a P2

rat in vitro.(B1)Spontaneous burst activity recorded from the L5dorsal root of

a P4rat.The interval(in s)between two consecutive bursts is indicated below

the recording.Action potentials were detected by means of peak and level

detectors(horizontal arrows).(B2)Distribution of intervals between each

action potential recorded from the dorsal root(same root as in B1;n=670

action potentials taken into account)and all the subsequent ones occurring

within the next1±35s.

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depolarization occurred in phase with the bursts (lower trace in Fig.2A 1and A 2).The number of action potentials in a burst was proportional to the area of the dorsal root potential (Fig.2A 1and 2B,correlation coef?cient,r =0.94).Spontaneous discharges were there-fore generated by PAD reaching ?ring threshold.Discharges were antidromically conducted into the dorsal roots (Fig.2C).

We tested whether a Cl ±conductance was involved in generating antidromic action potentials by decreasing the concentration of Cl ±ions in the saline solution (Vinay &Clarac,1999).This should make the reversal potential for Cl ±currents in the afferent terminals become more positive,thereby increasing the amplitude of depolarizations and the probability of ?ring antidromic action potentials (Clarac &Cattaert,1996;Alvarez-Leefmans et al .,1998).The spontaneous dorsal root activity increased after replacing half of the NaCl in the normal solution by Na isethionate (compare Fig.3A 2with Fig.3A 1;Fig.3B).Bursts,after recti?cation and integration,were increased both in amplitude and duration in low Cl ±solutions [Fig.3C;699637ms (n =50)vs.554630ms (n =51)in control;P <0.01].This resulted in a signi?cant increase in the area of the bursts (+66%,P <0.001).A similar increase was observed in the three experiments tested in this way.There was a non-signi?cant trend towards an increase in burst frequency in low Cl ±solutions (Fig.3D,0.18Hz)compared with control (0.16Hz).These effects were reversible within 20±30min after the normal external concentration of Cl ±was restored (Fig.3A 3,B and D).These results indicate that the depolarizations which trigger antidromic action potentials are due to an increase in Cl ±conductance.

Bicuculline was applied to determine whether the increase in chloride conductance was mediated by an activation of GABA A receptors.The dorsal root activity was always sharply reduced in the presence of low concentrations of bicuculline (1±2m M ,n =9)as shown in Fig.4by the 3-min-long recordings (compare Fig.4A 3with Fig.4A 1and A 2,and Fig.4A 4and A 5)and the graph with the instantaneous burst frequency plotted against time (Fig.4B).However,a few antidromic discharges persisted in the presence of bicuculline at 1±2m M (Fig.4B).These may be due to non-GABA A receptor-mediated mechanisms or to an uncomplete blockade of GABA A receptors.Increasing the concentration of bicuculline to 10±20m M never blocked these discharges further (n =7).On the contrary,in three preparations,there was a signi?cant (P <0.05)increase in the number of antidromic action potentials per minute in the presence of high concentrations of bicuculline,compared with low concentrations (Fig.4C).Either no effect or a non-signi?cant trend towards an increase was observed in the remaining four experiments.The absence or existence of effects was not related to the age of animals.PTX (10m M ,n =4;20m M ,n =4),another GABA A -receptor antago-nist,was also tested.Antidromic discharges disappeared almost completely in the presence of PTX (Fig.5A 1,A 2and B;Table 1).Surprisingly,instead of decreasing further,the number of antidromic action potentials in the dorsal root increased after adding

bicuculline

100 ms

500 ms

100 μV 200 μV DRP area (μV .ms)

Spike-triggered averaging

N u m b e r o f a n t i d r o m i c a c t i o n p o t e n t i a l s

L5 DR

L4 DR prox.

L4 DR dist.

L5 DR (rectified)L4 DRP

L4 DRP

A 1

A 2

B

C

10 ms

F I

G .2.Spontaneous depolarizations of primary afferent terminals and antidromic discharges.(A 1)Simultaneous recordings made from the L5(stainless steel electrode placed in contact with the root)and the L4(suction electrode)dorsal roots showed that discharges were associated with primary afferent depolarizations.(A 2)Averages of the discharges (recti?ed trace)and dorsal root potentials.Recordings were triggered by the action potentials detected in the L5dorsal root (n =276).(B)Number of action potentials in a burst (L5)plotted against the area of the depolarization (above the baseline)recorded from the adjacent dorsal root (L4).Correlation coef?cient of the regression line,r =0.94.(C)Two electrodes were placed in contact with the L4dorsal root to record spontaneous antidromic activity at both proximal (prox.)and distal (dist.)levels.Data recording was triggered by action potentials detected by the distal electrode (averaging of 450events).Action potentials were propagated in a proximo-distal direction with a conduction time of ~4±5ms between the two electrodes (interval between the vertical dotted lines).

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(20m M )to the PTX (20m M )-containing saline solution (Fig.5A 2,A 3and B).This increase was observed for all the dorsal roots recorded during the four experiments tested and was signi?cant in two preparations (Table 1).The effects of bicuculline at 20m M were reversible as shown by the reduction of the antidromic discharges after decreasing the concentration of bicuculline (Fig.4C)or removing bicuculline from the bath (Fig.5B,Table 1).

These results show that the spontaneous antidromic activity results almost exclusively from the activation of GABA A receptors.A difference in the blockade of this activity was observed between PTX and bicuculline,suggesting that the latter,at high concentrations,may have other effects,in addition to blocking GABA A receptors.Locomotion-related antidromic dorsal root discharges

Dorsal roots were recorded during ?ctive locomotion induced by adding excitatory amino acids and serotonin to the saline solution (n =13).Fictive locomotion was characterized by:(i)the bursts of activity in the right and left ventral roots alternating in a given segment (Fig.6A and B,recti?ed activity);and (ii)the L2/L3ventral roots on one side bursting in phase and the L5ventral root bursting in antiphase (Cazalets et al .,1992;Kiehn &Kjaerulff,1996).Dorsal root ?ring was observed under these conditions in all the experiments.The discharge rarely appeared,at ?rst sight,to be related with the motor activity (Fig.6A,note the irregular ?ring in the L3dorsal root).However,a rhythmical pattern was often demonstrated after detailed analysis including normalization of the locomotor cycles and resampling of the dorsal root antidromic discharges (see Materials and methods).The graph at the bottom of Fig.6B shows a signi?cant decrease in the discharge during the motor burst in the homonymous ventral root on the same side (10±20%of the cycle;see also arrows in Fig.6A).The discharge of seven dorsal roots (four L2,one L3and two L5)recorded in ?ve experiments was analysed.A signi?cant rhythmic modulation of the discharge was observed in ?ve dorsal roots (P <0.05).No characteristic pattern of discharge could be revealed.

The contribution of GABA A receptors to these discharges during ?ctive locomotion was evaluated by applying bicuculline (1±20m M ,n =18).At low concentrations (1±2m M ,n =13),bicuculline resulted in a signi?cant (P <0.001)decrease of the antidromic discharge (Fig.7A 2and B 2continuous line;760.5action potentials per cycle,n =30)as compared with control (Fig.7A 1,B 1and B 2dotted line;12.660.6action potentials per cycle,n =30).Bursts of antidromic discharges appeared when the concentration of bicuculline was increased (Fig.7A 3and B 3).In the experiment illustrated in Fig.7,these bursts occurred at the cycle onset (vertical dotted line in Fig.7A 3,time t =0in Fig.7B 3).Such a strong modulation of dorsal root activity was observed in each of the ?ve preparations

perfused

F I

G .3.Involvement of chloride conductance in the spontaneous antidromic activity.(A 1±A 3)The spontaneous antidromic activity was enhanced in low-chloride saline solution (A 2)when compared with normal saline (A 1,control and A 3,washout).(B)Mean (6SEM)number of antidromic action potentials in the L5dorsal root in low-chloride saline solution compared with normal saline (control and after washout).(C)Average of 50bursts of antidromic action potentials recorded in normal (control)and low-chloride (50%Cl ±)saline solutions.Traces were recti?ed and integrated (time constant,5ms).The sections of traces including bursts were duplicated and aligned at burst onset before averaging.Note the increase in amplitude and duration in low-chloride saline indicating a higher number of action potentials.(D)A slight,non-signi?cant,increase in the burst frequency was observed in low-chloride saline.

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with high concentrations of bicuculline (10±20m M ).These ?ndings indicate that antidromic discharges may be recorded from dorsal roots following the activation of the spinal cord by excitatory amino acids and serotonin and the disinhibition by bicuculline.However,they do not give any indication on whether primary afferent terminals receive a phasic input from GABAergic interneurons during ?ctive locomo-tion.

Because of the interaction of bicuculline with the locomotor rhythm (Fig.7;Cazalets et al .,1994;Cowley &Schmidt,1995;Kremer &Lev-Tov,1997;see also Bertrand &Cazalets,1999),we separated the mechanisms which generate locomotion from those mediating primary afferent depolarizations.The recording chamber was partitioned into two pools with a barrier built at the L3±L4level so that each pool could be perfused separately (Fig.8A,n =4experiments).The central pattern generators for locomotion were activated by perfusing excitatory amino acids and serotonin only in the rostral bath (Cazalets et al .,1995;1996),and the L5dorsal roots were recorded in the caudal bath in the absence of the tonic pharmacological activation by these two substances.A rhythmic bursting discharge was recorded from the L2ventral roots (Fig.8B±F,top two traces).Antidromic discharges were recorded from the L5dorsal roots in normal saline solution.Only a slight modulation of the discharge with a decreased activity at ~60%of the cycle (Fig.8B,

lower trace and Fig.8F continuous trace at the bottom of the graph)could be observed.Decreasing the concentration of chloride in the caudal bath caused a sharp increase in the number of antidromic action potentials recorded from the L5dorsal root (Fig.8C and F,compare traces `B'and `C').In addition,the discharge was strongly modulated with a peak occurring at the end of the cycle (signi?cant difference between the peak and the minimum with P <0.001).Adding bicuculline (1m M )to the low-chloride solution in the caudal bath blocked the discharges almost completely (Fig.8D).The number of action potentials in the different phases of the locomotor cycle was smaller than that in normal saline solution (Fig.8F,compare traces `D'and `B').These effects were reversible (Fig.8E and F,trace `E').Similar results were obtained in the four preparations tested.These data establish the existence of a locomotor-related GABAergic input onto primary afferent terminals in the neonatal rat.

Discussion

Spontaneous and locomotor-related GABAergic activity in dorsal root afferents

The present study has revealed that spontaneous antidromic activity is propagated in dorsal roots of isolated spinal cord preparations (Fig.1).This activity is associated with primary afferent

depolariza-

F I

G .4.The antidromic activity is due to the activation of GABA A receptors.(A 1±A 5)Spontaneous bursting activity in the L5dorsal root (A 1,A 2;note that each vertical line is a burst)is almost completely blocked by application of bicuculline (2m M )in the saline solution (A 3,note the absence of activity during the 3-min recording).Effects are reversible (A 4,A 5).A 2and A 5are enlargements of the sections of traces between vertical dotted lines in A 1and A 4,respectively.(B)Instantaneous burst frequency before,during and after the application of bicuculline.(C)Mean (6SEM)number of antidromic action potentials in the L4dorsal root in another experiment at two different concentrations of bicuculline (2and 20m M )compared with normal saline (control and after washout of bicuculline).Note the signi?cant (<0.001)increase in the discharge in the presence of 20m M of bicuculline compared with 2m M .This increase is reversible (right 2m M histogram).

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tions (Fig.2)and is due to an increase in chloride conductance (Fig.3).In addition,most of the action potentials disappeared in the presence of bicuculline at low concentrations (1±2m M )or PTX

(Figs 4and 5)demonstrating that they are generated by GABAergic mechanisms.High concentrations of bicuculline (10±20m M )caused an increase of the antidromic ?ring when compared with the activity in the presence of either PTX or low concentrations of bicuculline (Figs 4and 5).This may correspond to non-GABAergic effects of bicuculline (see below).

60 s

B

A 1

A 2

A 3

control

PTX

PTX

PTX +bicuculline PTX 20 μM +bicuculline 20 μM

PTX 20 μM

control

left L4 DR

100N u m b e r o f a c t i o n p o t e n t i a l s / m i n .

200300400500600700F IG .5.Bicuculline triggers some spontaneous bursting activity in dorsal roots.(A 1±A 3)Four-minutes-long dorsal root recordings in normal saline solution (A 1),after addition of PTX (A 2),and under both PTX and bicuculline (A 3).(B)The number of antidromic action potentials was decreased signi?cantly (P <0.001)in the presence of GABA A receptor antagonists when compared with control.However,antidromic discharges were signi?cantly (P <0.001)more numerous in the presence of both antagonists than in the presence of PTX alone.The activity decreased after washout of bicuculline (no signi?cant difference under PTX before and after bicuculline;P >0.05).T ABLE 1.One-way

ANOVA

with a Tukey's multiple comparison test of antidromic activity in the presence of PTX and bicuculline (BIC)

Number of action potentials per minute (+record duration in minutes)Dorsal PTX vs.PTX +BIC PTX +BIC Experiment root Control PTX

PTX +BIC PTX (wash)

control vs.control vs.PTX 1Right L2234639.3(5)6164.8(12)132614.6(12)*******1Right L4394610.1(7)5468.5(12)190621.8(12)*********2Left L3108622.3(4)860.9(12)2163.7(12)******NS 2Left L5292630.1(5)2061.6(12)3163.1(12)******NS 3Left L515866.2(16)2668.5(12)36617.4(12)561.5(8)******NS 4Right L4371616.3(16)2567.5(12)101629.1(12)43617.6(8)*******4

Left L4

493622.4(16)

56613.4(12)

228641.6(12)

81622.2(8)

***

***

***

Data are shown as means 6SEM,with the number of minutes of recording taken into account in parentheses.Four experiments were performed.NS,non-signi?cant;*P <0.05;**P <0.01;***P <0.001.

right L3 VR

right L3 VR right L3 DR

right L3 DR

N u m b e r o f a c t i o n p o t e n t i a l s

left L3 VR

left L3 VR

cycle (%)

A

B

F I

G .6.Locomotor-related modulation of the antidromic discharges.(A)The antidromic discharges in the dorsal root decreased (arrows)shortly after the burst onset in the ventral root on the same side (indicated by vertical dotted lines).(B)Cycles were normalized and onset of the right ventral root burst was taken as time t =0for average.Averaged recti?ed activities in the two opposite ventral roots are shown (n =120cycles).The normalized locomotor cycle is represented twice.Dorsal root activities were sampled over 30cycles and averaged in 100time intervals per locomotor cycle.The number of antidromic action potentials is averaged over intervals of 10%of the locomotor cycle (6SEM).Note the signi?cant (P <0.01)decrease in the discharge at 10±20%of the cycle,when compared with the next interval.

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The spontaneous activity consisted of periodic bursts and was therefore probably triggered by a centrally generated rhythm.Motor activity sometimes accompanied the dorsal root bursts indicating the existence of neuronal connections which coactivate the motoneurons and the primary afferent terminals.Alternatively,`antidromic'discharges in dorsal roots may have postsynaptic effects in lumbar motoneurons and ?rst-order interneurons.This hypothesis is under investigation.When present,the motor bursts in the L3and L5ventral roots on the same side were not in antiphase,suggesting that the central pattern generator for locomotion was either inactive or active partially (Cazalets et al .,1992;Kiehn &Kjaerulff,1996).The relationships between the network driving the spontaneous activity and the locomotor network remain to be elucidated.Spontaneous rhythmic motor activity is a property of the developing spinal cord (Gu et al .,1994in Xenopus ;O'Donovan &Landmesser,1987;Chub &O'Donovan,1998;Milner &Landmesser,1999in the chick;Nishimaru et al .,1996;Nakayama et al .,1999in the rat).Spontaneous network-driven activity has also been described in other parts of the central nervous system (CNS)during development (see Feller,1999for recent review;Ho &Waite,1999in the trigeminal system;Ben-Ari et al .,1989in the hippocampus;see Wong,1999for review on the visual system).The spontaneous GABAergic dorsal root discharges demonstrated in the present study may play a role in some developmental processes,e.g.central path?nding,axon extension,synapse formation or maturation of the peripheral receptors.However,spontaneous antidromic discharges are not found only in immature systems as they also occur in the adult hamster spinal cord in vitro (Bagust et al .,1989;Chen et al .,1993).Antidromic discharges were recorded during ?ctive locomotion (see also Kremer &Lev-Tov,1998).A phasic modulation of the discharge could be detected in some dorsal root recordings,demonstrating a locomotion-related input to the interneurons which mediate antidromic discharges (Fig.6).The antidromic activity was decreased by perfusion of bicuculline,at low concentrations,over the whole spinal cord preparation.However,the contribution of GABA A receptors to antidromic discharges recorded during ?ctive locomotion could not be identi?ed in such conditions.A direct effect of bicuculline on the dorsal root discharge may,indeed,be masked by a concomitant action on the locomotor rhythm (Cazalets et al .,1994;Cowley &Schmidt,1995;Kremer &Lev-Tov,1997),which may thereby modulate the intensity of antidromic discharges.The existence of a locomotion-related GABAergic input to primary afferent terminals was demonstrated by partitioning the recording chamber into two pools (Fig.8).This avoided actions of bicuculline on the locomotor rhythm.Antidromic discharges were enhanced in low-chloride solution indicating that the amplitude of locomotor-

5 s

right L3 VR right L5 DR

left L3 VR control

bicuculline 1μM

bicuculline 20μM

A 1

A 2

A 3

control

cycle (%)

N u m b e r o f a c t i o n p o t e n t i a l s

N u m b e r o f a c t i o n p o t e n t i a l s

N u m b e r o f a c t i o n p o t e n t i a l s

B 1

F I

G .7.Locomotor-related dorsal root bursting activity in the presence of bicuculline.(A 1±A 3)Simultaneous recordings from two opposite ventral roots and one dorsal root in the same segment during ?ctive locomotion induced by bath application of NMA (17m M )and serotonin (10m M )before (A 1)and after the addition of bicuculline at various concentrations (A 2,1m M ;A 3,20m M ).(B 1±B 3)Mean (6SEM)number of action potentials during the different phases of the locomotor cycle (10%-bins;30cycles averaged).The discharge was modulated in normal saline solution (B 1;signi?cant difference between 15%and 35%,and between 35%and 65%of the cycle with P <0.01and P <0.001,respectively).The number of action potentials per cycle was signi?cantly lower in the presence of bicuculline 1m M (B 2,continuous trace)compared with control (B 1,B 2,dotted trace).Phasic discharges were recorded at the cycle onset (0±20%)in the presence of bicuculline 20m M (B 3).

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related primary afferent depolarizations was increased.These occurred,as revealed by the maximum of discharge in low-chloride solution,during the L3motor burst on the ipsilateral side which is in phase with the activity in the ˉexor muscles (Kiehn &Kjaerulff,1996).Interestingly,muscle spindle primary afferents from both ˉexor and extensor muscles as well as cutaneous afferents recorded during ?ctive locomotion in the decerebrate cat have been shown to be maximally depolarized during the ˉexor phase (Gossard et al .,1989;1991;Gossard,1996).

A tonic GABAergic input may also depolarize primary afferent terminals during ?ctive locomotion.However,this issue could not be handled in our experiments because of the tonic activation of the

interneurons which mediate PADs and antidromic discharges,by the bath application of NMA and 5-HT.

Bicuculline-insensitive antidromic activities in dorsal roots The present results con?rm the presence of antidromic discharges under bicuculline (Kremer &Lev-Tov,1998).The antidromic ?ring in the presence of bicuculline does not involve activation of GABA B receptors,5-HT 2/5-HT 1C receptors,and metabotropic glutamate receptors of the groups II and III (Kremer &Lev-Tov,1998).A mechanism involving potassium transients was suggested to be the major cause of bicuculline-resistant antidromic bursts and was proposed to modulate intraspinal afferents not only during

disinhibi-

F I

G .8.Locomotor-related GABA A receptor-mediated depolarizations of primary afferent terminals.(A)Experimental arrangement with two separate pools;locomotor activity induced by bath application of NMA and 5-HT in the rostral pool was recorded from the L2ventral roots on both sides,whereas a L5dorsal root was recorded in the caudal pool.(B±E)Antidromic activity in the L5dorsal root increased when the concentration of chloride in the caudal bath was decreased (C,E).This activity was blocked by bicuculline (D).(F)The top two traces are averages of recti?ed ventral root activities over 54cycles that were normalized with onset of L2ventral root burst taken as time t =0.The graph plots the mean number of antidromic action potentials in the L5dorsal root in the different experimental conditions shown in B±E (5%-bins).Two cycles are represented.***P <0.001.

162S.Fellippa-Marques et al .

ó2000European Neuroscience Association,European Journal of Neuroscience ,12,155±164

tion by bicuculline but also during locomotion and other motor activities(Kremer&Lev-Tov,1998).However,the comparison made in the present study between the effects of bicuculline at high concentrations and those of PTX or bicuculline at low concentrations (Fig.5,Table1)raises the question whether the activities recorded in the presence of bicuculline are resistant to or triggered by this antagonist.Answering this question is of relevance before consider-ing a possible physiological role of potassium transients.Spontaneous rhythmic motor bursts are also triggered by bicuculline(Bracci et al., 1996a;b;Kremer&Lev-Tov,1997).

Bicuculline methiodide may have two effects on the spinal cord.The?rst effect,at low concentrations,is the blockade of GABA A receptors which causes a disinhibition of spinal neurons and a blockade of primary afferent depolarizations thereby decreasing the probability of antidromic?ring.Similar effects are evoked by PTX.It is likely that the second effect of bicuculline,obtained with higher concentrations,is not related to its ability to block GABA A receptors.Bicuculline has been shown to prolong calcium-dependent action potentials of mouse dorsal root ganglion and spinal cord neurons in cell culture(Heyer et al., 1982),and to potentiate NMDA-induced burst?ring in dopamine neurons(Johnson&Seutin,1997)by an apamin-like action on the spike afterhyperpolarization(AHP,Seutin et al.,1997;see also Shi&Rayport,1994in nucleus accumbens neurons).The blockade of a calcium-activated current by bicuculline does not involve the action of any neurotransmitter but is mediated by a direct block of apamin-sensitive small-conductance(SK)potas-sium channels(Debarbieux et al.,1998in various brain regions). The antagonistic action of bicuculline methiodide on SK channels may potentiate the burst?ring of disinhibited interneurons, thereby leading to the release of an unidenti?ed neurotransmitter acting on primary afferent terminals or to potassium transients. The potentiation of neuronal discharge may be highly dependent on the level of activity in the spinal cord.This may account for the observation that the modulation of antidromic discharges by high concentrations of bicuculline is stronger when tested during ?ctive locomotion(Fig.7,increase observed in all the prepara-tions)than when tested under`spontaneous'conditions(Fig.4, signi?cant increase of the discharges observed in half of the preparations).The effect on the excitability of neurons,in addition to the well-known blockade of GABA A receptors,should be considered when interpreting the data obtained with bicuculline methiodide.The action of bicuculline on neuronal?ring and calcium-activated potassium currents is not reproduced by PTX (Johnson&Seutin,1997;Seutin et al.,1997;Debarbieux et al., 1998).This may account for the higher number of antidromic discharges recorded in the presence of bicuculline when compared with PTX.

In conclusion,it is quite clear that the spinal cord of the newborn rat is able to generate action potentials,which are propagated antidromically in dorsal root afferents,in some extreme conditions, e.g.bath application of excitatory amino acids and serotonin and/or bicuculline at high concentrations (Kremer&Lev-Tov,1998and the present study).However,the existence of these GABA A receptor-independent discharges in the absence of these pharmacological tools remains to be shown.The present study has demonstrated a locomotor-related GABAergic inˉuence on primary afferent terminals.Whether the observed PADs are associated with presynaptic inhibition of the mono-synaptic reˉex will be investigated further.Acknowledgements

We thank Dr N.Martin for computer programming and Dr J.-R.Cazalets,Dr P.Domenici and F.Brocard for critical reading of the manuscript.This study was supported by grants from the Centre National d'Etudes Spatiales(CNES, France)and the French Institute on Spinal Cord Research(I.R.M.E.).

Abbreviations

5-HT,serotonin;AHP,afterhyperpolarization;CNS,central nervous system; GABA,g-aminobutyric acid;NMA,N-methyl-D,L-aspartate;NMDA,N-methyl-D-aspartate;P,postnatal day;PAD,primary afferent depolarization; PTX,picrotoxin;SK channels,small-conductance potassium channels.

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日产风神蓝鸟汽车说明书用户手册

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4.7紧急定车附加费用计算如下:r临时定车在原有单价的基础上加收一定比例的紧急 附加费,比例如下:提前12小时--3%,提前8小时--6%,提前4小时--10%,提前2小时--15%,提前1小时--20%,提前30分钟--25%,提前15分钟--30% 4.8一般用车由车队队长根据用车标准安排车型种类,有特殊要求的应经办公室主任审 批在车辆使用申请表上注明 4.9车辆使用人根据工作需要,确需改变目标和路线的要事先向办公室主任申请,同意 后方可实施 4.10夜间确保至少有一辆车,为两公司的生产服务,须做到随叫随到 4.11神马实业股份有限公司的办公用车交由集团公司一并管理 5车辆使用流程C-15-05-001

S60系列机器简易操作手册

S60系列喷码机简易操作手册    开机操作: 1、喷码机电源开关位于机箱左上边。接通喷码机电源。  左侧蓝色指示灯亮起,这时表示机器开始启动,  方可松开按键(图1);   2、等待约半分钟直到系统启动初使化完毕,液晶屏幕图像出现,图1  3、在机器启动到稳定状态的过程中,先显示伟迪捷LOGO图案,  然后才进入待机界面; 4、此时机器开始运转,但泵没有运转, 机器无法喷印信息,属于待机状态。 机器显示屏进入 “主菜单”界面(图2)。    运行操作: 当机器处于待机状态时,在键盘左侧按墨线开/关键图2 2~3秒的时间,状态栏显示即变为"开机",等待约2分钟,墨线指示灯变为常亮,状态栏显示:正在喷印。现在喷码机已经做好打印信息的准备。由印字触发信号(光电眼等)触发后进行印字。    停止、喷印操作: 需要机器停止喷印时,直接在“主画面”界面按 停止打印键, 此处会自动变换为开始打印,同时墨线指示灯熄灭, 机器将自动处理回到待喷印状态。 如需机器喷印时,只需在此界面重新按开始打印键即可。 关机操作: 1、用户需要关闭机器时,在键盘左侧 按住墨线开/关键2~3秒的时间. 状态栏提示:关机  1、约两分钟后状态栏显示变为"喷码机关闭"。墨线绿色指示灯停止闪烁并保持熄灭状态.  2、.按下机箱左边的电源开关,关闭喷码机电源(如图1)。    选择信息操作: 在键盘“主题菜单键”界面中按进入信息读取界面,使用 键选择所需信息的文件名,然后在菜单栏中选择读取到编辑栏 ,即所需信息显示在编辑界面中,按菜单栏中的打印信息 ,则喷码机现在喷印的内容即为所选择的信息内容。  墨水、溶剂的添加操作: 当机器屏幕左侧的“橙色报警指示”灯亮时,同时在屏幕左上角报警栏 显示溶剂液位低或者墨水液位低时,则需要补充墨水或溶剂,用户需要打开机器墨水箱盖,拧开墨水缸或者溶剂缸的盖子,加入相应型号的墨水或者溶剂即可。同时,随着液位的上升,警报消除。

TORO301铲运机维护手册

TORO 301维护手册

目录 页数概述 维修和润滑 安全预防 润滑 注油容积 维护项目 注意事项 工作50小时后对维护保养 维护和润滑项目 油压测试

概述 在操作机器以前先阅读安全操作与维修手册! 这一点对于那些偶尔在TORO铲运机上 工作的人尤为重要。 严格遵守操作规程! 工作人员不得留松散长发、不得穿宽大服装更不得 戴珠宝耳环以免受伤。 必须穿着工作服和其它劳保服装。 不得对设备随意改造,以免影响设备的安全性能。 在对设备进行改造、调整安全装置和阀以及焊接车架前, 向供应商或制造商咨询。 零件必须与制造商的技术规范对应, 只有原装零件才被担保。 报告失火位置并使用灭火器 为了进行维护检测,应使用工作场地的设备使工作顺利 完成。 Toro铲运机上的每一个维护和修理工作只能按照说明书 规定由专职人员完成。 电器部件必须由电工维修、液压部件必须由有经验的专 职人员维修。 在进行维护、调整和检测时,仔细检查零件,必要时按 照说明书的要求进行更换。 在铲运机行走时或发动机工作是不得进行清洗、调整、 修理或作业。

维护和润滑 概述 Toro301铲运机是按照矿山的艰难条件和要求来设计的。按照保养周期的要求经常进行维护确保设备无故障地正常和经济的工作是非常重要的。当按照保养周期的要求经常进行维护以后,你会很容易地发现,在设备隐患还未出现时已经被修理好了。这就是以小的维护成本,将故障降到最低限度。 手册的一下章节指出了保养位置和周期,并强烈建议使用者按照道依茨(DEUTZ)柴油机维护手册进行有关的保养。 电器系统的防护 电焊前,发电机和主开关电缆必须断开,如果配有自动润滑中心及其它电器设备(如遥控器等)都必须断开。 在用水、蒸汽喷头和其它清洗设备进行清洗前,盖好发电机、接线盒及电器柜。 清洗后拿开盖。 安全注意事项 为保养工作留下足够的安全空间,在保养和修理期间一定要保证柴油机不会被突然地起动。在进行预防性维护前通知所有工作人员。 无论何时需要在铰接点处工作时,都要在前后车架之间装上安全锁止棒以防突然转向。在以举起的大臂下工作前先要: 1、倒空铲斗; 2、对大臂进行牢固支撑; 3、关闭发动机。 按照说明书的要求,遵守“开”和“关”机的程序。 保持手柄和踏板干净。 所有维护工作完成后,拧紧所有紧固件。马上装好所有已经拆卸的安全装置。 安照安全和环保的要求处置所有垃圾和被更换元件。

高空作业车使用说明书

高空作业车使用说明书 一、概述 湖北楚胜汽车高空作业车以东风小霸王、江铃五十铃、福田奥铃、东风140、东风145 系列等底盘(也可采用其他车辆改装),全回转三折臂式液压多功能工程作业车,它能将工作人员平稳,安全的送到14-20 米的高空作业,进行维修、安装、清洗、摄影、造船、化工、电力、剪枝、更换路灯及其他工程抢修作业。该车的主臂上还设有起重结构,故该车的使用领域较宽。 该车驾驶室外型美观,内部舒适,可载(座)3-6 人,整车外形尺寸小于国内同类产品,整车移动方便,能适合狭窄的地段,小街小巷作业。该车的上臂、下臂、回转和起重液压系统均为独特无级调速系统,具有节能和动作灵活,平稳安全可靠的特点。该车的支腿分单独、可调,能实现整车在平路上调平。该车液压和电器控制系统均设有各种限位装置及发动机紧急熄火装置。能在操作人操作失误,出现故障自动切断电源或紧急停止发动机,及时停止危险动作,确保安全可靠。该车电动操作系统均采用防水开关,避免了开关易进水,锈蚀漏电的问题,工作斗采用管状工作斗,外形美观,在工作斗和转台实行双位置操作,使用方便,维修简便,安全可靠。 二、结构简图(如图1):

三、操作步骤 步骤1.根据如下指示牌先伸出后横,然后伸出后左右脚及前左右脚,如图2: 步骤2.按住上述操作指示牌的“升臂操作”换向阀向里推,然后准备操作各臂; 步骤3.操作各臂时分为站臂操作和吊栏操作

步骤4.操作各臂时最先升小臂举升一定角度,如图3: 步骤5.然后将二臂举升一定角度,如图4: 步骤6.再将大臂举升一定角度,如图5: 步骤7.将小臂油缸伸出到最大高度,如图6: 步骤8.接着再将二臂举升一定角度,如图7:

850使用说明书

1机械部分 1.1主要用途和适用范围 高速立式加工中心(V850)是配有CNC系统的三轴联动的加工中心。 该机床可实现铣削、镗孔、扩孔、铰孔、钻孔等多工序的自动工作循环;可精确、高效地完成平面内各种复杂曲线的凸轮、样板、压模、弧形槽等零件的自动加工。本机床是钻、铣、镗多功能为一体的金属加工机床。 本机床控制部分采用SIEMENS802D交流伺服数控系统或三菱E60S交流伺服数控系统。运动轴均采用精度较高有预紧力的零间隙滚珠丝杆,机床输出力矩大,工作稳定可靠,机床主轴转速高,运动轴除自动外还可手动操作。 本机床基本上能满足百分之八十左右零件的铣削、钻削要求。机床适用性广泛,对各种较复杂曲线的凸轮、模板、模具、工具和刀具等零件的半精加工和精加工尤为适宜。 本机床三轴联动,并可控制第四轴,含有RS232接口,可与计算机联接加工复杂工件。 本机床适用于工业机械制造、仪器仪表、纺织、轻工等行业。 1.2机床的基本参数 工作台面积(长×宽)mm 1025mm×525mm 刀库 BT40-16 主轴锥度 ISO.40(BT40) 工作台纵向行程 800mm 工作台横向行程 500mm 工作台垂向行程 500mm 主轴转速范围 200-8000rpm 主轴最高转速 10000rpm X、Y、Z快速移动速度 10000mm/min X、Y、Z进给速度 10-3000mm/min T型槽宽×槽数(mm) 18×3 主电机功率 7.5kW

进给电机 X、Z向1.5KW(伺服),Y向2KW(伺服) 最小设定单位 0.005/0.001mm 定位精度 0.01mm 重复定位精度± 0.005mm 工作气压 0.4-0.6MPa 机床最大承载重量 400kg 机床外形尺寸(长×宽×高) 3060mm×1900mm×2200mm 机床重量 4200kg 1.3高速雕刻基本参数(选件) 高速电主轴转速范围:3000-25000r/min 功率: 3KW 安装夹头 ER20 1.4激光切割、雕刻基本参数(选件) 1.5.1主轴传动说明 主轴运动由主轴伺服电机直接由主轴伺服驱动控制电机轴,通过同步带轮驱动主轴旋转,使传速从200-10000rev/min范围内无级调速。 1.5.2进给运动及说明 进给运动分为X轴(纵向)、Y轴(横向)、Z轴(垂直)三向。 X、Y、Z三个方向进给均采用伺服电机,通过弹性联轴器驱动丝杆带动移动部件,完成各个方向进给运动.

43s Chinese Simply Guide

RELIABILITY·TOTAL SOLUTIONS PROVIDER 43S 简明使用指南

安全信息 警告注意事项 警告事项表示对用户健康 和安全的潜在危险。 致命电压 接通电源后,喷码机存在 致命电压,只有经培训和授权的人员才能进行维护操作。 眼睛防护 此标志提醒您:在进行任 何如墨水、溶剂和清洗剂有关的操作时,必须佩戴已核准的眼镜防护装置 火灾危险 墨水、溶剂、清洗剂是易挥发,易燃物,必须遵照当地的规定储存和处理。 此标志提醒您:在进行任何如墨水、溶剂和清洗剂有关的操作时,必须佩戴已核准的手部防护装置 手部防护 注意事项。 在使用喷码机之前必须阅读这些 本页包含重要的危险注意事项, 危险信息

切勿… × 使用非伟迪捷公司指 定耗材,否则将失去保修资格; × 在喷码机、墨水、溶剂 和清洗剂附近抽烟或使用明火; × 吸入过量的溶剂; × 让墨水、溶剂沾染眼睛 和皮肤; × 让墨水或溶剂进入本 地的排水系统; 务必… √ 佩戴防护眼镜和手套;√ 将墨水、溶剂和清洗剂存储在原厂容器中,放置在通风良好的储存室,避免阳光直射,环境温度为0~50℃; √ 根据本地法规回收废墨水,废溶剂和清洗材料; √ 在通风良好的区域工作; 与墨水、溶剂和清洗剂有关的医疗注意事项,请参阅本指南后面的“墨水、溶剂相关急救措施” 墨水、溶剂和清洗剂注意事项

如果没有“原料安全数据表”请向伟迪捷当地分支机构索取建议 操作者应该: √接受急救培训,并了 解使用可燃物和/或 毒性物质工作时可能 产生的后果; √持有“原料安全数据 表”。这些材料说明在 需要急救时应该采取 的医护行动; 眼睛沾染 用干净的自来水冲洗眼 睛至少15分钟,然后立 即就医治疗。 皮肤沾染 脱下被沾染的衣服,用香 皂和水冲洗被沾染的皮 肤区域。不要用清洗剂清 洗皮肤上的墨水。 墨水、溶剂相关急救措施…

TORO400E电动铲运机操作手册

(译文仅供参考,如有异议,以原文为准)

此页空白

操作手册

? SANDVIK TAMROCK 公司,TORO铲运机分部 11/2004

前言 感谢您选购了TORO铲运机。 本手册有助于您熟悉TORO铲运机及其预期的用途。您将要使用的TORO 400 E 铲运机是电动的胶轮铲运机,外形低矮,适于井下采矿使用。 每一位司机在操作之前都应通晓此铲运机,并完全掌握操作手册、保养手册和通用安全规程的内容。本手册包含了关于部件、仪表和控制装置安全使用的资料。保养手册中对定期保养做了详细说明。只有经过正规培训的人员才允许操作此铲运机。 在对TORO铲运机的不断研究和开发过程中,有可能已对铲运机做了某些改动,本手册中没有包含关于这方面的内容。 如果铲运机安装了如遥控装置那样的选装设备,您应当熟悉选装设备的单独说明书,有关操作使用方法在说明书中有详细说明。 所有负责TORO 400E工作的人员,包括对TORO 400E进行操作、运 输、维修的人员,都必须阅读和使用本手册。 驾驶室内必须固定放有此手册,以备TORO 铲运机的操作人员随时使用。 始终要遵守国家有关事故预防和环境保护的强制性法规。此外还必须遵守普遍公认的有关安全和职业工作方面的技术法规。 需要保养和修理时,建议您与离得最近的Sandvik Tamrock授权服务部门联系。我们的维修人员技术熟练,经验丰富,备有专用工具,能完成最需要的保养和修理任务。 通过正确使用并按照保养手册的内容去做,可以指望您的铲运机能得到高度利用并延长使用寿命。

前言 (3) 合格声明 (5) 1. 铲运机介绍 (6) 1.1. 预期的用途 (6) 1.2. 推荐的作业条件 (6) 1.3. 技术详情 (7) 1.3.1. 噪声强度和噪声辐射 (7) 1.3.2. 型号牌 (7) 2. 安全说明 (8) 2.1. 设备上的警告标牌 (8) 2.2. 伤害危险的警告 (8) 2.3. 损坏设备或器材的警告 (8) 2.4. 阅读使用手册或保养手册 (8) 2.5. 操作安全规程 (9) 2.6. 使用或保养工作中的主要危险 (10) 2.7. 不允许铲运机作业的方式和条件 (11) 2.8. 警告标志 (12) 2.9. 防火 (14) 2.10.紧急停机和停机装置 (16) 2.11.紧急出口 (17) 2.12.锁定装置 (17) 3.13. 安全设备 (20) 3. 操作说明 (21) 3.1. 仪表和控制装置 (21) 3.2. 符号牌和安全注意事项 (32) 3.3. 起动电动机之前的常规检查 (33) 3.4. 进入驾驶室和起动电动机 (35) 3.5. 行驶之前的常规检查 (38) 3.6. 行驶 (40) 3.6.1.坡度 (40) 3.6.2.司机的视界 (41) 3.6.3.行驶操作 (42) 3.6.4.制动 (43) 3.7. 停车和停止电动机 (44) 3.8. 寒冷气候下作业 (45) 3.9. 牵引 (46) 3.10.运输铲运机 (48) 3.11.存放条件说明 (49) 3.12.起吊方法和起吊点 (50) 4. 装载、搬运和卸载 (51) 4.1. 作业期间的危险区域 (51) 4.2. 装载 (51) 4.3. 搬运 (54) 4.4. 卸载 (56) 4.5. 遥控行驶(选装) (56) 5. 故障诊断 (58) 6. 技术规格 (60)

伟迪捷激光喷码机使用标准操作规程 2

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一、结构特点 混凝土搅拌运输车(以下简称搅拌车)由底盘和上装部分两大总成组成。上装部分由搅拌筒、副车架、进出料装置、操作系统、液压系统、电气系统、供水系统及护栏等组成。具体结构见下图所示: 利用内置的叶片不断的对混凝土进行强制搅动,使它在一定的时间内(最长不超过90分钟)不产生凝固现象,从而使搅拌运输车到达工地后还能满足使用要求。

二、性能介绍 1.搅拌筒 搅拌筒是整个搅拌运输车的关键部件,作为存储混凝土的容器,对防止其固化、离析起着决定性的作用。它由拌筒体、托轮等组成。 筒体由前锥段、后锥段、圆柱段、封头、叶片、进料小锥、滚道等组焊而成。前端与减速机连接在一起,后部经过托轮支撑在副车架上。托轮起支撑滚筒体的作用,由支座、轴承座、轴、轴承等做成。 搅拌筒的壳体及叶片都由高强度钢板制作而成,具有更高的耐磨性。封头整体一次旋压成形,与加强板焊接后具有足够的刚度与强度。 进料小锥直接影响到整车的进料速度,速度太快,会产生离析现象,而进料速度太慢,又影响工作效率。因此,进料小锥设计呈漏斗状,大口径,进料速度保持在3.2 ,可确保顺利进料,防止混凝土溢出。 滚道为锻件,整体锻造而成。在整个筒体焊完后,再加工外圈,以保证同轴度要求。 经过优化设计的搅拌筒,具有可靠地结构刚度,良好的耐磨性能,流畅地进出料,极低的残留量,即可搅拌混凝土,又可搅动输送预拌混凝土,决无出料离析现象,确保了混凝土的质性

能。 2.副车架 搅拌车副车架是主要的承重部分,作业时的载荷几乎都是经过它来支撑,加上在行驶中由于路面的颠簸和加、减速形成的冲击载荷,都对副车架的结构提出很高的要求。 整个副车架由主梁、前台支撑架、后台支撑架组成。 主梁采用整体箱型结构梁,从根本上增强了它的抗扭、抗折、抗拉性能,保证了刚性要求,在两根主梁之间加装辅助横梁,调整主梁各段的刚性,让载荷在副车架整个长度上更均匀的分布。 在行驶过程中不可避免会遇到特殊情况而采取紧急制动,由此所带来的惯性是非常大的,加上搅拌筒本身有一定的倾角,因此副车架前台承受的载荷相对来说要大得多,而这一部分载荷主要加在联接减速机与前支撑座的六个螺栓上,为防止螺栓发生被剪断而酿成事故,在前支撑台加装止推挡块,式螺栓不受到减切力的影响,确保车辆运行中的安全。 为满足搅拌车的填充率,搅拌筒还要满足一定的倾角要求。搅拌筒、减速机和前台支撑架在装配后已经固连为一体,由于制造的误差有可能后台支撑架在装配后满足不了倾角的要求,无法对搅拌筒产生有效的支撑。这时整个结构就相当于一个悬臂梁。这对于减速机来说会产生很大的扭转力矩。为防止由此给减速机

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