scholarly journals Reflex Effects of the Femoral Chordotonal Organ Upon Leg Motor Neurones of the Locust

1982 ◽  
Vol 101 (1) ◽  
pp. 265-285 ◽  
Author(s):  
L.H. FIELD ◽  
M. BURROWS

The femoral chordotonal organ (FCO) in a hind leg of a locust monitors the position and movement of the tibia about the femur. It consists of a group of sensory neurones embedded in connective tissue attached distally by two structures: the apodeme, which inserts close to the apodeme of the extensor tibiae muscle, and the flexor strand, which inserts at the base of the apodeme of the flexor tibiae muscle. The action of the apodeme and the flexor strand is reciprocal during movements of the tibia; the apodeme is stretched during flexion of the tibia whilst the flexor strand is relaxed. During extension, the apodeme is relaxed and the flexor strand is stretched. To analyse the reflex effects of this sense organ, all other sense organs of a hind leg were denervated. The apodeme of the FCO was then grasped between forceps, severed from its distal attachment site and its movements controlled by a function generator. The flexor strand remained intact and could be stimulated independently by moving the tibia. The different reflex effects mediated by the separate stimulation of the two components of the FCO were revealed by making intracellular recordings from the somata of leg motor neurones in the metathoracic ganglion. A movement stimulus to either component in a way that corresponded to tibial extension, excited flexor tibiae and inhibited extensor tibiae motor neurones. There was also an inter-joint effect whereby extension excited the depressor tarsi and inhibited the levator tarsi motor neurones. A flexion movement had the converse effects on these motor neurones. The effectiveness of the two components was dependent upon the velocity of the stimulus, the set position of the femoro-tibial joint at which the stimulus was applied, the initial direction of movement, and the activity of other neurones in the central nervous system. Slow motor neurones were depolarized more by low velocities of movement, whereas fast ones were depolarized more by high velocities. The two components produced their greatest effects at the set positions where they were most stretched; thus the apodeme was most effective when the joint was flexed, and the flexor strand when it was extended. Elicited movements of the hind legs or apparently spontaneous changes of excitability enhanced or masked the typical response of the motor neurones to stimulation of the FCO, indicating that the effects of this sense organ are not to be viewed as rigid, but as modifiable in the context of the behaviour of the animal. Note:

1996 ◽  
Vol 199 (3) ◽  
pp. 613-625
Author(s):  
T Jellema ◽  
W Heitler

The metathoracic fast extensor tibiae (FETi) motor neurone of locusts is unusual amongst insect motor neurones because it makes output connections within the central nervous system as well as in the periphery. It makes excitatory chemical synaptic connections to most if not all of the antagonist flexor tibiae motor neurones. The gain of the FETi-flexor connection is dependent on the peripheral conditions at the time of the FETi spike. This dependency has two aspects. First, sensory input resulting from the extensor muscle contraction can sum with the central excitatory postsynaptic potential (EPSP) to augment its falling phase if the tibia is restrained in the flexed position (initiating a tension-dependent reflex) or is free to extend (initiating a movement-dependent resistance reflex). This effect is thus due to simple postsynaptic summation of the central EPSP with peripheral sensory input. Second, the static tibial position at the time of the FETi spike can change the amplitude of the central EPSP, in the absence of any extensor muscle contraction. The EPSP can be up to 30 % greater in amplitude if FETi spikes with the tibia held flexed rather than extended. The primary sense organ mediating this effect is the femoral chordotonal organ. Evidence is presented suggesting that the mechanism underlying this change in gain may be specifically localised to the FETi-flexor connection, rather than being due to general position-dependent sensory feedback summing with the EPSP. The change in the amplitude of the central EPSP is probably not caused by general postsynaptic summation with tonic sensory input, since a diminution in the amplitude of the central EPSP caused by tibial extension is often accompanied by overall tonic excitation of the flexor motor neurone. Small but significant changes in the peak amplitude of the FETi spike have a positive correlation with changes in the EPSP amplitude, suggesting a likely presynaptic component to the mechanism of gain control. The change in amplitude of the EPSP can alter its effectiveness in producing flexor motor output and, thus, has functional significance. The change serves to augment the effectiveness of the FETi-flexor connection when the tibia is fully flexed, and thus to increase its adaptive advantage during the co-contraction preceding a jump or kick, and to reduce the effectiveness of the connection when the tibia is partially or fully extended, and thus to reduce its potentially maladaptive consequences during voluntary extension movements such as thrusting.


1985 ◽  
Vol 116 (1) ◽  
pp. 301-311 ◽  
Author(s):  
ULRICH BÄSSLER ◽  
EVA FOTH ◽  
GERHARD BREUTEL

On a slippery surface the forelegs of a decapitated stick insect walk forwards and the hindlegs, backwards. Animals with only forelegs but that are otherwise intact walk forwards, whereas animals with only hindlegs walk mostly backwards. Usually when intact animals start to walk, their hindlegs exert a rearwards thrust on the substrate, but occasionally the starting forces are directed forwards. A rampwise extension of the femoral chordotonal organ in the fixed foreleg of a walking animal first excites the flexor tibiae muscle (positive feedback). Towards the end of the ramp stimulus the activity of the flexor decreases, and the extensor tibiae motor neurones become strongly active. All experiments indicated that the inherent direction of movement of the metathorax is rearwards. In intact animals there must be a coordinating pathway from the prothorax to the metathorax that, together with the suboesophageal ganglion, induces the hindlegs to walk forwards.


1983 ◽  
Vol 105 (1) ◽  
pp. 127-145 ◽  
Author(s):  
ULRICH BÄSSLER ◽  
U. T. A. WEGNER

The denervated thoracic ventral nerve cord produces a motor output which is similar to that observed in the intact animal during irregular leg movements (seeking movements) or rocking, but not walking. When the nerves to some legs are left intact, and the animal walks on a wheel, the motor output in the protractor and retractor motor neurones of the denervated legs is modulated by the stepping frequency of the walking legs. The modulation is similar to that observed in the motor output to a not actually stepping leg of an intact walking animal. When only the crural nerve of one leg is left intact, stimulation of the trochanteral campaniform sensilli induces protractor and retractor motor output to that leg and the leg behind it. In this case the motor output to the ipsilateral leg is in phase. Stimulation of the femoral chordotonal organ influences activity in motor neurones of the extensor tibiae (FETi and SETi) but not those of the protractor and retractor coxae muscles. In a restrained leg of an intact animal stretching of the femoral chordotonal organ excites FETi and SETi as long as the other legs walk (as in a walking leg) and inhibits FETi and SETi (as in a seeking leg) when the other legs are unable to walk.


1977 ◽  
Vol 70 (1) ◽  
pp. 93-104 ◽  
Author(s):  
IAN FINDLAY ◽  
ALISTAIR MCVEAN

Limb autotomy results from the fracture of a preformed breakage plane within the second limb segment. Fracture is produced by the contraction of the large anterior levator (AL) muscle at the same time as its synergist, the posterior levator (PL) muscle. The AL force is thus directed on to a small portion of the breakage plane; withdrawal of this plug initiates cuticular fracture. Autotomy is a response to damage inflicted on the limb. In the absence of sensory information from the second limb segment there is less activity in the units serving the PL. It is shown that stimulation of the sense organ, cuticular stress detector one, provides feedback to PL motor neurones. The feedback is an integral part of the nervous control of limb autotomy.


1997 ◽  
Vol 200 (1) ◽  
pp. 93-100 ◽  
Author(s):  
T Matheson

Intact locusts (Schistocerca gregaria) respond to tactile stimulation of their folded wings with rhythmic scratching movements of the ipsilateral hindleg that are directed towards the site of stimulation. For example, sites near the base of a wing elicit anteriorly directed scratches, whereas sites near the distal end of a wing elicit posteriorly directed scratches. Locusts also scratch in response to tactile stimulation of a wing that is held outstretched in a posture similar to that normally adopted during flight, but they fail to alter their leg targeting to compensate for this changed position of the stimulus site. Instead, they scratch at an empty point in space near the abdomen, where the stimulus site would have been if the wing was folded in the resting posture. This inappropriate scratching does not result from mechanical constraints on the hindleg's movement, from stimulation of abdominal sensory receptors, or from an absence of sensory information from the outstretched wing. It also persists when the metathoracic ganglion that controls movements of the hindlegs is isolated from the remainder of the central nervous system (CNS). Targeted scratching of sites on the wings of locusts therefore appears to be fixed relative to body coordinates and does not take into account alterations of the target wing's position.


In the study of the phenomena of anaphylaxis there are certain points on which some measure of agreement seems to have been attained. In the case of anaphylaxis to soluble proteins, with which alone we are directly concerned in this paper, the majority of investigators probably accept the view that the condition is due to the formation of an antibody of the precipitin type. Concerning the method, however, by which the presence of this antibody causes the specific sensitiveness, the means by which its interaction with the antibody produces the anaphylactic shock, there is a wide divergence of conception. Two main currents of speculation can be discerned. One view, historically rather the earlier, and first put forward by Besredka (1) attributes the anaphylactic condition to the location of the antibody in the body cells. There is not complete unanimity among adherents of this view as to the nature of the antibody concerned, or as to the class of cells containing it which are primarily affected in the anaphylactic shock. Besredka (2) himself has apparently not accepted the identification of the anaphylactic antibody with a precipitin, but regards it as belonging to a special class (sensibilisine). He also regards the cells of the central nervous system as those primarily involved in the anaphylactic shock in the guinea-pig. Others, including one of us (3), have found no adequate reason for rejecting the strong evidence in favour of the precipitin nature of the anaphylactic antibody, produced by Doerr and Russ (4), Weil (5), and others, and have accepted and confirmed the description of the rapid anaphylactic death in the guinea-pig as due to a direct stimulation of the plain-muscle fibres surrounding the bronchioles, causing valve-like obstruction of the lumen, and leading to asphyxia, with the characteristic fixed distension of the lungs, as first described by Auer and Lewis (6), and almost simultaneously by Biedl and Kraus (7). But the fundamental conception of anaphylaxis as due to cellular location of an antibody, and of the reaction as due to the union of antigen and antibody taking place in the protoplasm, is common to a number of workers who thus differ on details.


1995 ◽  
Vol 198 (7) ◽  
pp. 1589-1601 ◽  
Author(s):  
F Kuenzi ◽  
M Burrows

The hair plate proprioceptors at the thoraco-coxal joint of insect limbs provide information about the movements of the most basal joint of the legs. The ventral coxal hair plate of a middle leg consists of group of 10-15 long hairs (70 microns) and 20-30 short hairs (30 microns). The long hairs are deflected by the trochantin as the leg is swung forward during the swing phase of walking, and their sensory neurones respond phasically during an imposed deflection and tonically if the deflection is maintained. Selective stimulation of the long hairs elicits a resistance reflex that rotates the coxa posteriorly and is similar to that occurring at the transition from the swing to the stance phase of walking. The motor neurones innervating the posterior rotator and adductor coxae muscles are excited, and those to the antagonistic anterior rotator muscle are inhibited. By contrast, selective stimulation of the short hairs leads only to a weak inhibition of the anterior rotator. The excitatory effects of the long hairs are mediated, in part, by direct connections between their sensory neurones and particular motor neurones. A spike in a sensory neurone elicits a short-latency depolarising postsynaptic potential (PSP) in posterior rotator and adductor motor neurones whose amplitude is enhanced by hyperpolarising current injected into the motor neurone. When the calcium in the saline is replaced with magnesium, the amplitude of the PSP is reduced gradually, and not abruptly as would be expected if an interneurone were interposed in the pathway. Several sensory neurones from long hairs converge to excite an individual motor neurone, evoking spikes in some motor neurones. The projections of the sensory neurones overlap with some of the branches of the motor neurones in the lateral association centre of the neuropile. It is suggested that these pathways would limit the extent of the swing phase of walking and contribute to the switch to the stance phase in a negative feedback loop that relieves the excitation of the hairs by rotating the coxa backwards.


1982 ◽  
Vol 96 (1) ◽  
pp. 325-341
Author(s):  
MALCOLM BURROWS

Simultaneous intracellular recordings have been made from the two expiratory, and from the two inspiratory motor neurones which have their axons in the unpaired median nerves of the thoracic ganglia. Each motor neurone has an axon that branches to innervate muscles on the left and on the right side of one segment. The expiratory neurones studied were those in the meso- and meta-thoracic ganglia which innervate spiracular closer muscles. The depolarizing synaptic potentials underlying the spikes during expiration are common to the two closer motor neurones in a particular segment. Similarly, during inspiration when there are usually no spikes, the hyperpolarizing, inhibitory potentials are also common to both motor neurones. The synaptic input to the neurones can be derived from four interneurones; two responsible for the depolarizing potentials during expiration and two for the inhibitory potentials during inspiration. The inspiratory neurones studied were those in the abdominal ganglia fused to the metathoracic ganglion which innervate dorso-ventral abdominal muscles. During inspiration the two motor neurones of one segment spike at a similar and steady frequency. The underlying synaptic input to the two is common. During expiration, when there are usually no spikes, the hyperpolarizing synaptic potentials are also common to both neurones. In addition they match exactly the depolarizing potentials occurring at the same time in the closer motor neurones. The same set of interneurones could be responsible. No evidence has been revealed to indicate that the two closer, or the two inspiratory motor neurones of one segment are directly coupled by electrical or chemical synapses. The morphology of both types of motor neurone is distinct from that of other motor neurones in these ganglia. Both types branch extensively in both the left and in the right areas of the neuropile.


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