Braht Researeh, 122 (1977) 551-555 ~) Elsevier/North-Holland Biomedical Press, Amsterdam - Printed in The Netherlands
55 l
Comments on reflex actions evoked by electrical stimulation of group II muscle afferents
A. LUNDBERG, K. MALMGREN and E. D. SCHOMBURG* Department of Physiology, University o/' Giiteborg, 400 33 GOteborg (Sweden) (Accepted November 19th, 1976)
In spinal cats electrical stimulation of group ll muscle afferents, irrespective of their muscle of origin, gives excitation in flexor and inhibition in extensor motoneurones, but sometimes the opposite actions dominate a,5,10. Recently, we postt, lated that the minimal linkage in excitatory group II pathways is disynaptic while the linkage in the corresponding inhibitory pathways is trisynaptic 8. However, Kirkwood and Sears 6, using spike triggered averaging (STA), found that impulses in secondary afferents produced homonymous monosynaptic EPSPs in ankle extensors and this finding has been confirmed 9. If adequate activity in secondaries evokes monosynaptic EPSPs then electrical stimulation of group I1 afferents would be expected to give the same effect. We have now re-analysed our material and indeed found previously overlooked evidence for homonymous monosynaptic group 1I EPSPs not only in extensor but also in flexor motoneurones which can be differentiated from the previously described interneuronally mediated EPSPs. Low spinal cats were anaesthetized with chloralose (50 mg/kg) and small doses of Nembutal (5-10 mg/kg) were added during the course of the experiments, lntracellular recording was made with citrate electrodes from motoneurones mainly from the knee flexor posterior biceps semitendinosus (PBSt) and ankle extensors gastrocnemius-soleus (G-S). We used the conventional technique of electrical stimulation of muscle nerves and stimulus strength is expressed in multiples of threshold for the nerve. The records in Fig. 1 show homonymous EPSPs in two PBSt motoneurones. The distinct group Ii EPSP in F - H with an onset ot about 2.7 msec after the incoming group I volley is the previously described presumed disynaptic group II EPSP - - in this case very large. Corresponding group I1 EPSPs were evoked alter about the same latency from other flexor and from extensor nerves. A similar though smaller late EPSP wave is found in the motoneurone in A - D but a close inspection of the records reveals an additional earlier action (downwards arrow in D) showing up as a small hump and a gradual slowing of the decay from the summit of the la EPSP with increasing Present address: Institute of Physiology, University of G6ttingen, G6ttingen, G.F.R.
552
A
PBSt 175
B
20
C~
2.75
D
.
H
i
4.0
4mY I
E
PBStl.5
~
~
2.25
G
.,
v
i
I
i
;~5.0
I
•
!
i
w
w
•
Ires Fig. 1. EPSPs evoked in flexor motoneurones by graded stimulation of the homon~mous nerve, A-D and F-H are from two different PBSt motoneurones, upper traces are intracellula~ recordings and lower traces incoming volleys recorded from the L7 dorsal root entry zone, Stimulus strengths are indicated in multiple of threshold for the nerve. Early monosynaptic group II EPSPs indicated by downward arrow in D and G, upward arrow signals onset of presumed disynaptic EPSPs. The very brief latency of the group li EPSP in D strongly suggests that it is mediated by fhsI conducting afferents but rather high stimulus strength is required to evoke the effects. Recordings fi'om primary afferents have revealed that some large group II afferents have high threshold (unpublished observations). strength of g r o u p 11 stimulation. Thus it a p p e a r s that the g r o u p II volley adds also a small early EPSP to the la EPSP. There is possibly a small early effect ( a r r o w ) also in the m o t o n e u r o n e in Fig, I E - H . [n record D the onset o f the g r o u p II EPSP occurs I msec after the incoming g r o u p I volley. A s s u m i n g that it i, evoked by fast s e c o n d a r y afferents c o n d u c t i n g at 70 m/sec (cf. legend) the central latency is a b o u t 0.8 msec showing m o n o s y n a p t i c transmission. C o r r e s p o n d i n g brief central latencies were f o u n d also in other m o t o n e u r o n e s which is s o m e w h a t surprising considering the slow intraspinal c o n d u c t i o n velocity in s e c o n d a r y afferents L Similar findings were m a d e in G-S m o t o n e u r o n e s as shown irl Fig. 2A--D, where the slowing o f the decay from the s u m m i t o f the la EPSP give~ evidence of a m o n o s y n a p t i c g r o u p li excitation as described a b o v e for the PBSt m o t o n e u r o n e . F o r c o m p a r i s o n are shown in F - H records from a n o t h e r G-S m o t o n e u r o n e without so clear evidence of a m o n o s y n a p t i c g r o u p 11 EPSP but in which is evoked the previously described p r e s u m e d d i s y n a p t i c EPSP which was found in a b o u t 15
55 l
Comments on reflex actions evoked by electrical stimulation of group II muscle afferents
A. LUNDBERG, K. MALMGREN and E. D. SCHOMBURG* Department of Physiology, University o/' Giiteborg, 400 33 GOteborg (Sweden) (Accepted November 19th, 1976)
In spinal cats electrical stimulation of group ll muscle afferents, irrespective of their muscle of origin, gives excitation in flexor and inhibition in extensor motoneurones, but sometimes the opposite actions dominate a,5,10. Recently, we postt, lated that the minimal linkage in excitatory group II pathways is disynaptic while the linkage in the corresponding inhibitory pathways is trisynaptic 8. However, Kirkwood and Sears 6, using spike triggered averaging (STA), found that impulses in secondary afferents produced homonymous monosynaptic EPSPs in ankle extensors and this finding has been confirmed 9. If adequate activity in secondaries evokes monosynaptic EPSPs then electrical stimulation of group I1 afferents would be expected to give the same effect. We have now re-analysed our material and indeed found previously overlooked evidence for homonymous monosynaptic group 1I EPSPs not only in extensor but also in flexor motoneurones which can be differentiated from the previously described interneuronally mediated EPSPs. Low spinal cats were anaesthetized with chloralose (50 mg/kg) and small doses of Nembutal (5-10 mg/kg) were added during the course of the experiments, lntracellular recording was made with citrate electrodes from motoneurones mainly from the knee flexor posterior biceps semitendinosus (PBSt) and ankle extensors gastrocnemius-soleus (G-S). We used the conventional technique of electrical stimulation of muscle nerves and stimulus strength is expressed in multiples of threshold for the nerve. The records in Fig. 1 show homonymous EPSPs in two PBSt motoneurones. The distinct group Ii EPSP in F - H with an onset ot about 2.7 msec after the incoming group I volley is the previously described presumed disynaptic group II EPSP - - in this case very large. Corresponding group I1 EPSPs were evoked alter about the same latency from other flexor and from extensor nerves. A similar though smaller late EPSP wave is found in the motoneurone in A - D but a close inspection of the records reveals an additional earlier action (downwards arrow in D) showing up as a small hump and a gradual slowing of the decay from the summit of the la EPSP with increasing Present address: Institute of Physiology, University of G6ttingen, G6ttingen, G.F.R.
552
A
PBSt 175
B
20
C~
2.75
D
.
H
i
4.0
4mY I
E
PBStl.5
~
~
2.25
G
.,
v
i
I
i
;~5.0
I
•
!
i
w
w
•
Ires Fig. 1. EPSPs evoked in flexor motoneurones by graded stimulation of the homon~mous nerve, A-D and F-H are from two different PBSt motoneurones, upper traces are intracellula~ recordings and lower traces incoming volleys recorded from the L7 dorsal root entry zone, Stimulus strengths are indicated in multiple of threshold for the nerve. Early monosynaptic group II EPSPs indicated by downward arrow in D and G, upward arrow signals onset of presumed disynaptic EPSPs. The very brief latency of the group li EPSP in D strongly suggests that it is mediated by fhsI conducting afferents but rather high stimulus strength is required to evoke the effects. Recordings fi'om primary afferents have revealed that some large group II afferents have high threshold (unpublished observations). strength of g r o u p 11 stimulation. Thus it a p p e a r s that the g r o u p II volley adds also a small early EPSP to the la EPSP. There is possibly a small early effect ( a r r o w ) also in the m o t o n e u r o n e in Fig, I E - H . [n record D the onset o f the g r o u p II EPSP occurs I msec after the incoming g r o u p I volley. A s s u m i n g that it i, evoked by fast s e c o n d a r y afferents c o n d u c t i n g at 70 m/sec (cf. legend) the central latency is a b o u t 0.8 msec showing m o n o s y n a p t i c transmission. C o r r e s p o n d i n g brief central latencies were f o u n d also in other m o t o n e u r o n e s which is s o m e w h a t surprising considering the slow intraspinal c o n d u c t i o n velocity in s e c o n d a r y afferents L Similar findings were m a d e in G-S m o t o n e u r o n e s as shown irl Fig. 2A--D, where the slowing o f the decay from the s u m m i t o f the la EPSP give~ evidence of a m o n o s y n a p t i c g r o u p li excitation as described a b o v e for the PBSt m o t o n e u r o n e . F o r c o m p a r i s o n are shown in F - H records from a n o t h e r G-S m o t o n e u r o n e without so clear evidence of a m o n o s y n a p t i c g r o u p 11 EPSP but in which is evoked the previously described p r e s u m e d d i s y n a p t i c EPSP which was found in a b o u t 15
