Presynaptic inhibition of the monosynaptic reflex following the stimulation of nerves to extensor muscles of the ankle

1967 ◽  
Vol 4 (1) ◽  
pp. 34-42 ◽  
Author(s):  
M. Decandia ◽  
L. Provini ◽  
H. Táboříková
1969 ◽  
Vol 205 (2) ◽  
pp. 329-339 ◽  
Author(s):  
J. D. Gillies ◽  
J. W. Lance ◽  
P. D. Neilson ◽  
C. A. Tassinari

2006 ◽  
Vol 32 (1) ◽  
pp. 74-80 ◽  
Author(s):  
B. S. Shenkman ◽  
E. V. Lyubaeva ◽  
D. V. Popov ◽  
A. I. Netreba ◽  
O. S. Tarasova ◽  
...  

1981 ◽  
Vol 90 (1) ◽  
pp. 85-100
Author(s):  
CHARLES H. PAGE

Postural extensions of the abdomen of the crayfish, Procambarus clarkii, could be evoked by mechanical stimulation of a single thoracic leg. Movement of a single leg joint was sufficient to initiate an extension response. Vigorous abdominal extensions were initiated either by depression of the whole leg (WLD) or by flexion of the mero-carpal joint (MCF). Weaker extension responses were obtained by depression of the thoracic-coxal and coxo-basal joints. Similar stimulation of the chelipeds did not elicit an abdominal extension response. Single-frame analysis of motion pictures of crayfish responding to WLD or MCF stimulation of a 2nd thoracic leg showed that the responses evoked by the two different stimulus situations were nearly identical. They differed principally in the responses of the leg located contralateral to the stimulated leg. Movements of most of the cephalic, thoracic and abdominal appendages accompanied the abdominal extension response. Only the eyes remained stationary throughout the response. The mean values of the latencies for the initiation of appendage movement ranged from 125 to 204 ma; abdominal movement had a mean latency of about 220 ms. The abdominal extension reflex resulted from the activity of the tonic superficial extensor muscles. The deep phasic extensor muscles were silent during the response. The mean latencies for the initiation of superficial extensor muscle activity by WLD and MCF stimulation were 53·7 and 50·0 ms respectively.


1986 ◽  
Vol 55 (1) ◽  
pp. 113-130 ◽  
Author(s):  
R. Kretz ◽  
E. Shapiro ◽  
E. R. Kandel

We have examined the synaptic conductance mechanisms underlying presynaptic inhibition in Aplysia californica in a circuit in which all the neural elements are identified cells (Fig. 1). L10 makes connections to identified follower cells (RB and left upper quadrant cells, L2-L6). These connections are presynaptically inhibited by stimulating cells of the L32 cluster (4). L32 cells produce a slow inhibitory synaptic potential on L10. This inhibitory synaptic potential is associated with an apparent increased membrane conductance in L10. Both the inhibitory postsynaptic potential (IPSP) and the conductance increase are voltage dependent; the IPSP could not be reversed by hyperpolarizing the membrane potentials to - 120 mV. The hyperpolarization of L10 induced by L32 reduces the transmitter output of L10 and thereby contributes to presynaptic inhibition. However, this hyperpolarization accounts for about 30% of the effect because presynaptic inhibition can still be observed even when the hyperpolarization of L10 by L32 is prevented by voltage clamping. When L10 is voltage clamped, stimulation of L32 produces a slow outward synaptic current associated with an apparent increased conductance. Both the synaptic current and conductance change measured under clamp are voltage dependent, and the outward current could not be reversed. This synaptic current is not mediated by an increase in C1- conductance. It is sensitive to external K+ concentration, especially at hyperpolarized membrane potentials. With L10 under voltage clamp, stimulation of L32 also reduces a slow inward current in L10. This current has time and voltage characteristics similar to those of the Ca2+ current. Presynaptic inhibition is still produced by L32 when L10 is voltage clamped, and transmitter release is elicited by depolarizing voltage-clamp pulses. This component of presynaptic inhibition, which accounts for approximately 70% of the inhibition, appears to be due to a decrease in the Ca2+ current in the presynaptic neuron.


Toxicon ◽  
1989 ◽  
Vol 27 (4) ◽  
pp. 431-438 ◽  
Author(s):  
K. Takano ◽  
F. Kirchner ◽  
B. Tiebert ◽  
P. Terhaar

2013 ◽  
Vol 109 (8) ◽  
pp. 2118-2128 ◽  
Author(s):  
Patrick M. Sonner ◽  
David R. Ladle

Sensory feedback is critical for normal locomotion and adaptation to external perturbations during movement. Feedback provided by group Ia afferents influences motor output both directly through monosynaptic connections and indirectly through spinal interneuronal circuits. For example, the circuit responsible for reciprocal inhibition, which acts to prevent co-contraction of antagonist flexor and extensor muscles, is driven by Ia afferent feedback. Additionally, circuits mediating presynaptic inhibition can limit Ia afferent synaptic transmission onto central neuronal targets in a task-specific manner. These circuits can also be activated by stimulation of proprioceptive afferents. Rodent locomotion rapidly matures during postnatal development; therefore, we assayed the functional status of reciprocal and presynaptic inhibitory circuits of mice at birth and compared responses with observations made after 1 wk of postnatal development. Using extracellular physiological techniques from isolated and hemisected spinal cord preparations, we demonstrate that Ia afferent-evoked reciprocal inhibition is as effective at blocking antagonist motor neuron activation at birth as at 1 wk postnatally. In contrast, at birth conditioning stimulation of muscle nerve afferents failed to evoke presynaptic inhibition sufficient to block functional transmission at synapses between Ia afferents and motor neurons, even though dorsal root potentials could be evoked by stimulating the neighboring dorsal root. Presynaptic inhibition at this synapse was readily observed, however, at the end of the first postnatal week. These results indicate Ia afferent feedback from the periphery to central spinal circuits is only weakly gated at birth, which may provide enhanced sensitivity to peripheral feedback during early postnatal experiences.


1995 ◽  
Vol 73 (6) ◽  
pp. 2578-2583 ◽  
Author(s):  
C. A. Pratt

1. The functional organization of heterogenic reflexes produced by activation of extensor force receptors (Golgi tendon organs) was studied in intact cats during stationary stance. Intramuscular stimulation (200 Hz, 20 ms) of hindlimb extensor muscles via chronically implanted electrodes was used to evoke weak muscle contractions and naturally activate Golgi tendon organ Ib afferents while cats stood unrestrained with each paw on a moveable triaxial force plate. 2. Intramuscular stimulation of every hindlimb extensor muscle tested in this study evoked excitatory responses that were widely distributed among hindlimb extensor muscles. Source and target specializations in the functional organization of this positive force feedback system were also observed. For example, stimulation of ankle extensors typically excited extensors and flexors at the ankle and hip (but not knee), whereas stimulation of hip extensors typically excited only extensors at all three joints. In addition, intramuscular stimulation of either lateral (LG) or medial (MG) gastrocnemius consistently inhibited soleus while exciting other extensors at the ankle and more proximal joints. 3. The electromyographic (EMG) reflex responses described above are attributed to the natural (via muscle contraction) activation of extensor group Ib afferents. Direct activation of intramuscular afferents by the stimulus was unlikely because there was no evidence that Ia afferents, which have the lowest electrical thresholds, were activated. Both the observed inhibition of the synergist, soleus, and the excitation of the antagonist, tibialis anterior, produced by gastrocnemius stimulation are opposite to the reflex effects that would be produced at the ankle by activation of gastrocnemius Ia afferents.(ABSTRACT TRUNCATED AT 250 WORDS)


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