1706 Neurobiology: Correction Proc. Natl. Acad. Sci. USA 85 (1988)

Correction. In the article "Nonsynaptic regulation of sen-sory-activity during movement in cockroaches" by FredericLibersat, Ronald S. Goldstein, and Jeffrey M. Camhi, whichappeared in number 22, November 1987, of Proc. Natl.Acad. Sci. USA (84, 8150-8154), the authors wish that thefollowing correction be noted. On p. 8153, column 1, line 2,the word "failures" should be replaced by "of pulsesevoking spikes".

Proc. Nati. Acad. Sci. USAVol. 84, pp. 8150-8154, November 1987Neurobiology

Nonsynaptic regulation of sensory activity during movementin cockroaches

(sensory feedback/Perplaneta americana/escape behavior/flight/locomotion)

FREDERIC LIBERSAT*, RONALD S. GOLDSTEIN, AND JEFFREY M. CAMHIDepartment of Zoology, Hebrew University, Jerusalem, Israel

Communicated by Thomas Eisner, July 6, 1987

ABSTRACT Here we describe a nonsynaptic mechanismfor filtering out potentially perturbing sensory feedback duringlocomotion. During flight, the cockroach moves its cerci, twoabdominal sensory appendages, about their joint with the bodyand holds them in place. The cerci bear highly sensitivewind-receptive hairs, which would be strongly stimulated byflight wind. Such wind could cause habituation of the synapticconnections from these cercal receptors onto interneuronsresponsible for the running escape response to an approachingpredator. We have found that the cercal displacement blocksone-third to one-half of the action potentials along the sensorynerve, possibly aiding in protection against such habituation.This block occurs if one experimentally displaces a cercus, andthe block persists in the complete absence of any connectionswith the central nervous system. The block appears to benonsynaptic and to result instead from mechanical pressure onthe nerve near the joint. The results suggest that activity inperipheral nerves in other animals may also be affected by theposition or movement ofjoints through which the nerves pass.

An important function of nervous systems is to control thesensory information recorded by its sensory receptors. Acase in point is seen during animal movements, when a richvariety of sensory feedback signals impinge on numerousreceptors. Some of these signals provide useful informationand are incorporated into the neural network controlling thebehavior (1-3). Others constitute sensory "noise" and couldperturb normal behavior if not filtered out. In fact, in a varietyof systems, potentially perturbing feedback is inhibitedsynaptically. The source ofthe inhibition is generally neuronsin the central nervous system. These can either (i) send theiraxons to the periphery and there inhibit the receptorsthemselves (4) or (ii) inhibit central neurons that are drivenby the receptors (5-8).We report here a form of filtering-out of the sensory

feedback from movement in cockroaches. This filteringconsists of a block of some action potentials traveling in asensory nerve. This block can occur in the absence of allconnections from the central nervous system and thereforedoes not result from central inhibition. In fact, the blockappears to be nonsynaptic and to be based rather uponmechanical stress on the sensory nerve that is imposed by theanimal itself.When a cockroach flies, both its movement through the air

and its wing movements should produce strong wind feed-back to the cerci, paired wind-responsive sensory append-ages. When not flying, the cockroach uses its cerci to evokewell-studied escape responses to very gentle air currentsgenerated by approaching predators (9). The strong wind-evoked feedback during flight, were it not filtered out, couldhabituate the escape behavior, rendering the insect defense-

less. It is the block of wind-evoked action potentials in thecercal sensory nerve that is studied here.

METHODS

Adult male Periplaneta americana were anesthetized withC02, and the legs, supra-anal plate, and wings were removed.After the medial cercal nerve (containing wind-receptoraxons), the lateral cercal nerve (containing motor axons tothe cercal muscles), and the nerve cord for recording (Fig.1A) were exposed, the preparation was perfused with cock-roach saline (10). The saline, containing 5.4 mM Ca2' and noMg2+, was replaced in some experiments with saline con-taining 5 mM Mg2' and no Ca2+.

Controlled wind stimuli were delivered from various di-rections toward the cercus by means of a wind stimulatordescribed previously (11). In various experiments, eitherintracellular or extracellular hook-electrode recordings weremade from sensory axons in the medial cercal nerve. Extra-cellular recordings were also made with hooks from the nervecord or the lateral cercal nerve. The medial or lateral cercalnerve also could be stimulated electrically, using hookelectrodes. In some experiments we recorded from the cercalnerve within the cercus by means of copper wires (diameter,50,m) inserted through tiny holes in the cuticle and fixedfirmly in place with cyanoacrylate glue. Standard recordingapparatus was used. All data were taped for subsequentanalysis, using a Hewlett-Packard instrumentation tape re-corder. The taped responses to wind stimuli were passedthrough a window discriminator, and action potentials ofselected amplitudes were counted electronically.

Histology was carried out on material fixed overnight in2.5% glutaraldehyde/1% paraformaldehyde/5% sucrose/0.1M phosphate buffer, pH 7.4, at room temperature. Tissueswere then dehydrated, embedded in plastic, cut at 4 tsm, andstained with methylene blue.

RESULTSControlled wind puffs from the front of the cockroach werepresented when the cerci were in their rest position, roughly600 laterally from the body (Fig. 1B, solid lines). These puffselicited very reproducible responses from the medial cercalnerve (12). This pattern of activity can be seen either inextracellular recordings from the whole nerve (Fig. 2A) or inintracellular recordings from axons in the nerve (Fig. 2C).As soon as a tethered cockroach begins flying, it moves

both cerci medially by 45-60° about the cercal joint with thebody and holds them there for the duration of the flight. Inorder to see the effect of such cercal displacement on theafferent response to wind, a cercus was moved with a minutepin and held parallel to the body by fixing the pin to thesubstrate. (The pin itself had no effect on the sensory

*To whom reprint requests should be addressed.

8150

The publication costs of this article were defrayed in part by page chargepayment. This article must therefore be hereby marked "advertisement"in accordance with 18 U.S.C. §1734 solely to indicate this fact.

Proc. Natl. Acad. Sci. USA 84 (1987) 8151

A B

4717

Supra anal plate

FIG. 1. Experimental arrangement. (A) Locations of hook elec-trodes, intracercal wire electrodes glued to cuticle, and microelec-trode used in various combinations in this study. A6, sixth abdominalganglion; med. and lat. n, medial and lateral cercal nerves; abd. conn,abdominal connectives. (B) Geometry of stimulator relative to cercusat rest (solid-line arrow and cercus) and when displaced (dashedlines). Dot shows location of pin used to hold displaced cercus.

response, as shown by recordings made when the cercus wasnot displaced but rested against the pin.) The wind tube was

A_~~~lo-k_ A i~dm,IL__

~ ~ -

FIG. 2. Responses of cercal sensory axons to wind stimuli. In Aand B, top traces show responses to wind, recorded extracellularlyfrom the medial cercal nerve. Roughly 30 msec after a trigger pulseto the wind stimulator (bottom trace in each panel), a burst of actionpotentials begins. By use of a window discriminator, the number ofspikes that crossed a criterion line (immediately below nerve trace)during a 200-msec interval were counted. Each is shown as a dot; thenumber of dots is 128 in A and 91 in B. C and D show intracellularrecords, both from the same axon in the cercal nerve (differentpreparation than A and B). (A and C) Cercus in relaxed position. (Band D) Cercus displaced with a pin. Time calibration for all traces,20 msec; voltage calibration for C and D, 60 mV.

also rotated about the animal to retain the same angle ofstimulation (Fig. 1B, dashed lines). Fig. 2B shows that thewind-evoked response was now reduced. (The response wasalso reduced when the wind tube was not rotated with thecercus.) The reduction, a mean of 34% (Fig. 3A, bar 2), wasstatistically significant (P < 0.05, analysis of variance) andoccurred in each of the nine animals tested. This reductionwas repeatable within the same animal for as long as it wastested (3 hr), as determined by repeatedly displacing andreleasing the cercus. The reduction was also evident inintracellular recordings from sensory axons (Fig. 2 C and D;Fig. 3A, bar 3). We found the response to be reduced asquickly after cercal displacement as we tested it (less than 1sec) and to be restored to normal within a few seconds aftercercal release.To determine whether the reduction in sensory activity

might occur when the animal actively displaces its cerci, westimulated the lateral cercal nerve with repetitive pulses. Thisevoked a medial-directed movement of the cercus like thatmade by the animal during flight (Fig. 1B, dashed cercus),which persisted for the duration of the stimulus. We againrotated the wind tube (Fig. 1B, dashed tube). Cercal move-ment produced in this way also produced a significantreduction of the sensory response (Fig. 3A, bar 4).Two observations demonstrate that the sensory reduction

did not result from displacement of the cercus to a positionwhere the wind was blocked by other body parts or by therecording apparatus. First, when air was drawn into thestimulator tube, and thus came from behind the animal,where nothing could block its flow, a typical displacement-

A B

10

80

2090 _ 42A2

I. 1an Na X

I2 3 4 5 67 8 9 2 3

FIG. 3. Wind response under various test conditions. A hatchedbar represents the mean, and the line its standard deviation, of thenumber of action potentials counted with the cercus displaced,expressed as a percentage of that counted with the cercus in itsnormal position (solid bars). Bars 2-8 in A and bar 2 in B aresignificantly different from their controls (P < 0.05, analysis ofvariance). At least 10 stimuli were presented with the cercus in eachof the normal, displaced, and released normal positions in eachanimal. Controls were means of responses in the initial and finalnormal positions. (A) Bar 1: control. Bar 2: extracellular responsewhen the cercus was displaced and held by a pin; n = 9 animals. Bar3: intracellular response of wind-sensitive primary afferent axons;cercus was held by a pin; n = 5 animals. Bar 4: extracellular responsewhen displacement of the cercus was evoked by stimulation of thelateral (motor) cercal nerve; n = 3 animals. Bar 5: extracellularresponse to wind withdrawn into the stimulator; cercus held by a pin;n = 3 animals. Bar 6: same as bar 4, except that a pin was placed justmedial to the cercus to prevent cercal movement during motor nervestimulation; n = 3 animals. Bar 7: extracellular response with thesensory nerve left completely slack, to prevent stress on the receptorcells in the cercus; cercus was held by a pin; n = 3 animals. Bar 8:extracellular response with both the medial and lateral cercal nervescut near the terminal ganglion to prevent efferent activity; cercus washeld by a pin; n = 6 animals. Bar 9: extracellular response with thetissues at the base of the cercus dissected away; cercus was held bya pin; n = 4 animals. (B) Recordings made by hook electrodes in thesame position along the medial cercal nerve as in A and simulta-neously inside the cercus (Fig. 1A). Cercus was held by a pin. Bar 1:control. Bar 2: nerve response. Bar 3: intracercal response. (n = 3animals.)

Neurobiology: Libersat et al.

8152 Neurobiology: Libersat et al.

induced reduction occurred (Fig. 3A, bar 5). Second, when aminute pin was placed medial to the cercus, mechanicallypreventing its movement, the reduction still occurred uponstimulation of the lateral nerve (Fig. 3A, bar 6). In these trialsthe wind tube was not rotated.A possible explanation for the reduction is that when the

cercus is displaced, due to the anchoring effect of the hookelectrodes or the microelectrode-support stage, the sensorynerve might pull on receptor endings within the cercus.(Conceivably, such a pulling could also occur during electri-cal stimulation of the lateral nerve and blocking of cercalmovement with the pin.) Such pulling could affect thesensory response in unpredictable ways. However, thisexplanation of the sensory reduction is ruled out because,when the sensory nerve is cut near ganglion A6 (Fig. 1A) andthe nerve is left completely slack, the reduction still occurs(Fig. 3A, bar 7; compare to bar 2, which involved the sameextracellular recording technique and the same method ofcercal displacement).

Inhibition emanating from the central nervous system canbe ruled out as the source of the reduction in sensory activity.Cutting both the medial and the lateral cercal nerves (Fig.lA), which provide the only innervation of the cercus andsurrounding tissues, near ganglion A6 leaves the reductionunaffected (Fig. 3A, bar 8; compare to bar 2, which involvedthe same recording and cercal-displacement methods).The above results demonstrate that both the source of the

reduction and the location of its effect must be peripheral. Wenext wished to localize the site of the effect on the sensoryresponse. Two experiments suggest that this site is locatednear the point where the sensory nerve emerges from thecercus. First, we recorded from the medial cercal nervewithin the cercus near its base (Fig. 1A). Such recordingsshow no significant reduction in the sensory response to windupon cercal displacement (Fig. 3B, bar 3); yet simultaneousrecordings from the nerve made, as before, inside the bodycavity (Fig. LA) show typical reductions (Fig. 3B, bar 2). Thisresult also supports the previous findings that neither block-ing of the wind nor a pulling on receptors causes the sensoryreduction. Second, we dissected the medial cercal nerve freefrom its surrounding tissues near the cercal joint. Now thewind response recorded central to the joint was not reducedby displacing the cercus (Fig. 3A, bar 9).Having localized the site of action of the filtering effect to

the region of the cercal joint, we can divide the possiblemechanisms of the displacement-induced reduction in sen-sory activity into two general types: (i) a mechanism based onsynapses, in which some peripheral mechanoreceptors thatsense cercal position (13) would make en passant inhibitorysynapses on the wind sensory axons in the cercal nerve nearthe cercal joint, and (ii) mechanical effects such as pinchingor stretching of the sensory nerve upon cercal displacement.To help distinguish between synaptic and mechanical

mechanisms, we recorded sensory activity while replacingthe normal saline with saline without Ca2 . If the reductionwere mediated by chemical synapses, the lack of Ca2+ shouldprevent the displacement of the cercus from reducing sensoryactivity. In each of six experiments, in the presence of salinewithout Ca2+, cercal displacement still induced typical re-ductions (Fig. 4A, hatched bar 2; compare to controls-hatched bars 1 and 3). To demonstrate that zero-Ca2` salineblocks chemical synapses in this preparation, the wind-evoked activity of giant interneurons was simultaneouslyrecorded. The giant interneurons are activated by the wind-sensory cells in the sixth abdominal ganglion, A6, apparentlythrough nicotinic cholinergic synapses (14). In zero-Ca2lsaline the giant-interneuron response with the cercus in itsrest position was reduced by roughly 80% (Fig. 4A, solid bar2; compare to solid bars 1 and 3).

A~,100

a) 80 l60

u0 40-_ _

o 20 -__

2 3

B

< r,2 rn3 c, E A6

FIG. 4. Tests for synaptic and mechanical mechanisms of action-potential block. (A) Effect of zero-Ca2+ saline on the displacement-induced reduction of sensory neuron response and on the simulta-neous response of giant intemeurons to wind stimuli. Extracellularrecordings were made just before changing the saline (bars 1), 45 minafter changing (bars 2), and 45 min after returning to normal (5.4mMCa21) saline (bars 3). Each bar represents data from six cockroaches,with at least five wind stimuli for each. Displacement-inducedreduction in the response of the sensory neurons (hatched bars) wasunaffected by zero-Ca2+ saline. In contrast, the number of large-amplitude action potentials, primarily from giant intemeurons,recorded in the nerve cord (solid bars) with the cerci in the restingposition was dramatically reduced by the zero-Ca2+ saline, and thisreduction was largely reversible. The lack of full reversibilitypresumably resulted from habituation and/or deterioration of thepreparation during the time (about 2 hr) since the start of thedissection. (B) Equivalent circuit (neglecting capacitance) represent-ing a sensory axon, and the experimental arrangement to test theeffect of cercal displacement on component resistances. See text forexplanation. Square pulse in circle, extracellular stimulating hookelectrodes; arrow in circle, intracellular recording electrode; ril andri2, internal (axonal core) resistances; rmi and rm2, membraneresistances; ro, and ro2, external resistances; A6, sixth abdominalganglion; large arrows, current paths.

Support for a mechanical basis for the sensory reductionwas obtained using the experimental arrangement shown inFig. 4B. The equivalent circuit shown represents a singlesensory axon. With the cercus displaced, extracellular stim-ulus pulses (square pulse on figure) were delivered to thenerve. The stimulus voltage was adjusted so that roughly 80%oof the pulses each evoked an action potential. The currentflow is shown by the long arrows. The action potential wouldbegin at resistor rm3 and was recorded intracellularly (shortarrow), close to ganglion A6. The test was as follows. Uponrelease of the cercus, if there were a net decrease in theinternal resistance (ril), external resistance (rol), and mem-brane resistance (rml) at the cercal base, the current strengththrough the membrane resistance rm3 would decrease, be-cause more of the total current would be shunted through thereduced resistances, leaving less current available to crossrm3. As a result, the likelihood that the same strength ofapplied stimulus pulses would evoke action potentials wouldbe lower. [Calculations based on the equivalent circuit shownindicate that these intuitive expectations are quantitativelyupheld (I. Segev, personal communication).] Thus, less than80% of the pulses would now evoke an action potential. Thisexperiment provides an extremely sensitive test for resis-tance changes at a distance. It thus permitted us to studyevents at the cercal joint without disturbing its local mechan-ical properties.

Proc. Natl. Acad. Sci. USA 84 (1987)

Proc. Natl. Acad. Sci. USA 84 (1987) 8153

In a total of nine trials from three impaled axons in twodifferent animals, the percent failures (means, with ranges inparentheses) were as follows: cercus displaced, 81% (67-92%); cercus released, 25% (8-32%); cercus displaced again,83% (37-100%). The differences between the mean uponrelease and those both before and after release were highlysignificant (P < 0.0001, paired t test). This suggests that whenthe animal displaces its cercus (the opposite of the releasefrom displacement that was used in this test), one or more ofthe three resistances (internal, external, or membrane)' in-creases at the cercal joint.Of these three resistances, an increase of the membrane

resistance would not be expected to block action potentials.Rather, such an increase would cause the local membrane toproduce a larger than normal depolarization in response tothe action currents from an arriving action potential. Thus anincrease in membrane resistance could not account for theobserved action-potential block. However, an increase ineither the internal or external resistance could contribute toan action-potential block, since these would restrict actioncurrents of an arriving action potential from proceeding alongthe axon. One would in fact expect that squeezing orstretching a nerve might increase locally both the internalresistance (by reducing the axonal cross-sectional area) andthe extracellular resistance (by reducing the extracellularspace).

Is the requisite anatomical arrangement for mechanicalsqueezing or stretching of the nerve present at the cercaljoint? Careful dissection reveals that the medial cercal nervecomes into contact with the cuticle at a constriction of thecercus found at the joint. Cross-sections at this point of sixcerci fixed in the displaced position showed the nerve to betightly sandwiched' between the cuticle on its medial side andmuscles on its lateral side. In contrast, cross-sections of threecerci fixed in the resting position showed no contact of thenerve with the cercal muscles in this area. (One of these threewas from an animal whose opposite cercus had been dis-placed before fixation.) In spite of the sandwiching of thenerve in the displaced cerci, we find no evidence for flatten-ing of the nerve or any of its axons. Thus, although thefixation undoubtedly influences the structural details, itappears that rather gentle mechanical effects may be respon-sible for the action-potential block that we find in the nerve.

DISCUSSIONThe results ofthis paper reveal a form ofregulation ofsensoryactivity that has two novel features. First, the sensoryregulation, occurring in the periphery, does not require anyneural connections from the central nervous system. Rather,it can be obtained by experimental cercal displacement afterisolation of all central connections. Of course in normalbehavior this regulation is produced by central activation ofmotor axons traveling in the lateral cercal nerve, but theirrole appears to be only that of producing the cercal move-ment. In most other known cases of sensory regulation in theperiphery, the control results from projections from thecentral nervous system (4, 15). The second novel feature isthat the mechanism of regulation appears to be nonsynapticand based upon mechanical forces on the medial cercalnerve.The evidence for nonsynaptic regulation is three-fold.

First, since the block of action potentials occurs in theabsence of central connections, any synaptic basis for theblock would have to be from one group of sensory neurons,that detect the position of the cercus, onto the axons of themedial cercal nerve. We are not aware of a single example ininsects of sensory-to-sensory synaptic connections along aperipheral nerve. On the other hand, we have been able to

demonstrate histologically a mechanical arrangement thatcould potentially account for the action-potential block.The second indication that synapses are not involved is

that zero-Ca2l saline, though it did largely block chemicalsynaptic activation of the giant interneurons, did not affectthe sensory reduction produced by cercal displacement.Given that the cercus in its rest position shows large freespaces around the medial cercal nerve, it seems likely that thezero-Ca2+ saline had ready access to the outside of this nerve.Moreover, it is likely that the zero-Ca2+ saline penetrated thesensory nerve at least as readily as it did the terminalganglion, since the cockroach has a blood-brain barrier thatis very effective around the ganglia, and much less so aroundperipheral nerves (16).The third argument against a synaptic effect comes from

the electrical stimulation experiment of Fig. 4B. The resultssuggest a net increase in three resistances near the cercaljoint-the internal, external, and membrane resistances. Byfar the best-known type of synaptic inhibition is chemicalinhibition that operates by decreasing the membrane resis-tance of the postsynaptic cell. If such synapses were respon-sible for the action-potential block in the medial cercal nerve,they should produce a reduction of the membrane resistanceupon cercal displacement and an increase upon cercal re-lease. Thus, in our experiment such a synapse shouldproduce an increased likelihood of evoking an action poten-tial upon cercal release. This is the opposite of the result weobtained.Two other types of synaptic inhibition are also known,

though rare. One, chemical inhibition operating by an in-crease in the resistance of the postsynaptic membrane (17,18), could account for the results ofthe experiment of Fig. 4B.However, such an increase of the membrane resistancewould not be expected to block action potentials along thenerve. This is because, as mentioned above, an increase ofmembrane resistance would cause a larger than normaldepolarization in response to the action currents from anarriving action potential. The second alternative type ofsynaptic inhibition, electrical inhibition, is known from onlyone example (19). An electrical inhibitory synapse does notaffect the resistances shown in Fig. 4B and thus could notaccount for the result of this experiment.A possible mechanism for action-potential block, other

than either a synaptic inhibition or a mechanical effect thatdirectly alters internal or external resistances, would be localaccumulation of extracellular K+, which exits from the axonswith each action potential. Sequestering of extracellular K+could conceivably result from an altered spatial relationshipamong axons and glia upon cercal displacement. In fact, K+accumulation is known to block action potentials in cock-roaches (20). However, one would expect such an extracel-lular accumulation to produce a depolarization, owing to thealtered equilibrium potential of K+, that would produce adecrease in membrane resistance (rmi) owing to membranerectification. However, since the experiment of Fig. 4Bsuggests an increased resistance upon cercal displacement,no such K+ mechanism appears to occur in the displacedcercus.The cercal displacements that we imposed in studying

sensory responses to wind resemble closely those producedby the animal itself during flight. In fact, during flight itselfthere is a mean reduction of 41% in the number of wind-evoked action potentials in the medial cercal nerve, relativeto trials during rest (F.L., unpublished data).What is the significance to the animal of this reduction of

sensory input? Is a roughly 40% reduction sufficient to playa useful role? The displacement-induced block of actionpotentials described here probably is not the only means bywhich the animal reduces its responses to wind during flight.For instance, a chordotonal organ activated by cercal dis-

Neurobiology: Libersat et al.

8154 Neurobiology: Libersat et al.

placements like those studied here is known to produceinhibitory postsynaptic potentials in interneurons driven bythe cercal wind-sensory cells (13). Moreover, in crickets,during both walking and flying, the giant intemeurons oflargest diameter that are driven by cercal wind receptors aresubjected to strong synaptic inhibition (5). This occurs also inwalking cockroaches (21, 22). Though the question has notbeen investigated for flying cockroaches, it seems likely thathere too there would be inhibition of the giant interneurons.[During walking and running escapes, the cockroach does notdisplace its cerci, so the action-potential block described hereprobably does not occur at such times (J.M.C., unpublisheddata).] Thus, there may be at least three levels of inhibitorycontrol on the escape system during flight, together exertinga potent effect. Preliminary evidence shows that the roughly40% reduction in sensory activity produced by cercal dis-placement gives rise to a comparable decrease in the wind-evoked responses ofthe giant interneurons (R.S.G. and F.L.,unpublished data).The purpose of this sensory reduction could be to prevent

habituation of the escape circuit by the strong flight winds.Most of the habituation in this system, within this species, isknown to occur postsynaptic tothe giant interneurons, withinthe thoracic ganglia, though some habituation also occurs atthe first, sensory-to-interneuron, synapse (11, 23). Thus,since all three forms of reduction of wind responses precedethe major site of habituation, they could' all aid in protectingthe escape circuitry from habituation. However, only themechanism described in this paper clearly precedes, and thuscould protect, the first synapse in the escape circuit (thesensory-to-interneuron synapse) from habituation. In thecrayfish escape system, protection from habituation appearsto result from presynaptic inhibition of the terminals ofsensory axons (6). This possibility has not been investigatedin cockroaches.The present study has general implications for the design

of nervous systems. Many peripheral nerves pass throughjoints where they may be subjected to constriction duringnormal movements. Our results suggest that such constric-tions might block nerve activity. It is noteworthy that thecockroach's cercal nerve is not obviously flattened by cercaldisplacement; a fairly gentle mechanical disturbance may besufficient to produce the action-potential block. Thus, evena slight squeeze on a peripheral nerve, such as might occurmoment to moment during normal movements, could alterimpulse traffic in both sensory and motor axons. Therefore,those who study activity in peripheral nerves may need totake account of the positions and movements particularly of

limb joints and determine which impulses successfully crossthese possibly risky locations. As a further implication,chronic nerve pinch in human subjects can have drasticeffects upon impulse conduction (24). The displacement-induced block of action potentials studied here may providea model system for examining the mechanisms of such nervepinch injury.

We thank I. Parnas, I. Segev, R. Werman, and Y. Yarom forhelpful discussions and for reviewing the manuscript. This work wassupported by Grant NS20932 from the National Institute of Neuro-logical and Communicative Disorders and Stroke and Grant 84-00178from the U.S.-Israel Binational Science Foundation.

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