scholarly journals Differential presynaptic inhibition of actions of group II afferents in di‐ and polysynaptic pathways to feline motoneurones

2002 ◽  
Vol 542 (1) ◽  
pp. 287-299 ◽  
Author(s):  
E. Jankowska ◽  
U. Slawinska ◽  
I. Hammar
2005 ◽  
Vol 49 ◽  
pp. 45-56 ◽  
Author(s):  
Christopher J. Price ◽  
Theofanis Karayannis ◽  
Balázs Zoltán Pál ◽  
Marco Capogna

1977 ◽  
Vol 120 (3) ◽  
pp. 459-468 ◽  
Author(s):  
Christoph Fromm ◽  
Joachim Haase ◽  
Elmar Wolf

2010 ◽  
Vol 103 (2) ◽  
pp. 616-622 ◽  
Author(s):  
B. Friemert ◽  
S. Franke ◽  
A. Gollhofer ◽  
L. Claes ◽  
M. Faist

The hamstring reflex response has been suggested to play a substantial role in knee joint stabilization during anterior tibial translation. The present study was performed to determine which afferent pathways contribute to the hamstring reflex as well as the potential effects of specific afferent pathways on functional knee stability. Short- and medium-latency hamstring reflexes (SLR and MLR) were evoked by anterior tibial translation in 35 healthy subjects during standing with 30° knee flexion. Nerve cooling, tizanidine, and ischemia were employed to differentiate afferent pathways. Two hours of thigh cooling ( n = 10) resulted in a significant increase in MLR latency and, to a lesser extent, SLR latency. No significant changes were recorded in reflex sizes or maximum tibial translation. The ingestion of tizanidine ( n = 10), a suppressor of group II afferents, strongly reduced the MLR size while SLR size or latency of both reflex responses was not significantly affected. Maximum tibial translation was unchanged [5.3 ± 1.9 to 4.8 ± 2 (SD) mm; P = 0.410]. Ischemia in the thigh ( n = 15) led to a highly significant depression in SLR size (89 ± 4%; P < 0.001) but only a slight and not significant decline of MLR size. In these subjects maximum tibial translation increased significantly (6.9 ± 1.6 to 9.4 ± 3.2 mm; P = 0.028). It is concluded that the hamstring SLR is mediated by Ia afferents, while group II afferents mainly contribute to the MLR. Suppression of SLR may increase maximum anterior tibial translation, thus indicating a possible functional role of Ia afferents in knee joint stabilization.


1999 ◽  
Vol 82 (6) ◽  
pp. 2947-2955 ◽  
Author(s):  
Chunyi Zhang ◽  
John T. Schmidt

Presynaptic inhibition is one of the major control mechanisms in the CNS. Previously we reported that adenosine A1 receptors mediate presynaptic inhibition at the retinotectal synapse of goldfish. Here we extend these findings to metabotropic glutamate receptors (mGluRs) and report that presynaptic inhibition produced by both A1 adenosine receptors and group II mGluRs is due to Gi protein coupling to inhibition of N-type calcium channels in the retinal ganglion cells. Adenosine (100 μM) and an A1 (but not A2) receptor agonist reduced calcium current ( I Ca2+) by 16–19% in cultured retinal ganglion cells, consistent with their inhibition of retinotectal synaptic transmission (−30% amplitude of field potentials). The general metabotropic glutamate receptor (mGluR) agonist 1S,3R-1-amino-cyclopentane-1,3-dicarboxylic acid (1S,3R-ACPD, 50 μM) and the selective group II mGluR receptor agonist (2S,2′R,3′R)-2-(2′,3′-dicarboxy-cyclopropyl)glycine (DCG-IV, 300 nM) inhibited both synaptic transmission and I Ca2+, whereas the group III mGluR agonistl-2-amino-4-phosphono-butyrate (l-AP4) inhibited neither synaptic transmission nor I Ca2+. When the N-type calcium channels were blocked with ω-conotoxin GVIA, both adenosine and DCG-IV had much smaller percentage effects on the residual 20% of I Ca2+, suggesting effects mainly on the N-type calcium channels. The inhibitory effects of A1 adenosine receptors and mGluRs were both blocked by pertussis toxin, indicating that they are mediated by either Gi or Go. They were also inhibited by activation of protein kinase C (PKC), which is known to phosphorylate and inhibit Gi. Finally, when applied sequentially, inhibition by adenosine and DCG-IV were not additive but occluded each other. Together these results suggest that adenosine A1 receptors and group II mGluRs mediate presynaptic inhibition of retinotectal synaptic transmission by sharing a pertussis toxin (PTX)–sensitive, PKC-regulated Gi protein coupled to N-type calcium channels.


2010 ◽  
Vol 104 (4) ◽  
pp. 1872-1883 ◽  
Author(s):  
E. Jankowska ◽  
P. Krutki ◽  
I. Hammar

Strong evidence that premotor interneurons provide ventral spinocerebellar tract (VSCT) neurons with feedback information on their actions on motoneurons was previously found for Ia inhibitory interneurons and Renshaw cells, while indications for similar actions of other premotor interneurons were weaker and indirect. Therefore the aim of the present study was to reexamine this possibility with respect to interneurons relaying actions of group Ib afferents from tendon organs and group II afferents from muscle spindles. In all, 133 VSCT neurons in the L3–L5 segments (including 41 spinal border neurons) were recorded from intracellularly in deeply anesthetized cats to verify that stimuli applied in motor nuclei evoked monosynaptic inhibitory postsynaptic potentials (IPSPs) attributable to stimulation of axon collaterals of premotor interneurons. IPSPs were found in over two thirds of the investigated neurons. When intraspinal stimuli were preceded by stimuli applied to a muscle nerve at critical intervals, IPSPs evoked from motor nuclei were considerably reduced, indicating a collision of nerve volleys in axons of interneurons activated by group I and group II afferents. In individual VSCT neurons monosynaptic IPSPs were evoked from both biceps–semitendinosus and gastrocnemius–soleus motor nuclei, in parallel with disynaptic IPSPs from group Ib and group II as well as group Ia afferents. These observations indicate that individual VSCT neurons may monitor the degree of inhibition of both flexor and extensor motoneurons by premotor interneurons in inhibitory pathways from group Ib and group II afferents to motoneurons. They may thus be providing the cerebellum with feedback information on actions of these premotor interneurons on motoneurons.


1995 ◽  
Vol 487 (1) ◽  
pp. 211-220 ◽  
Author(s):  
M C Perreault ◽  
M J Angel ◽  
P Guertin ◽  
D A McCrea

1985 ◽  
Vol 1 ◽  
pp. S51 ◽  
Author(s):  
Norio Ishizuka ◽  
Toshinori Hongo ◽  
Norio Kudo ◽  
Shigeto Sasaki ◽  
Masayuki Yamashita ◽  
...  

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