HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Enríquez-Denton, M. Articles by Hultborn, H. Search for Related Content PubMed PubMed Citation Articles by Enríquez-Denton, M. Articles by Hultborn, H.

Presynaptic control of transmission along the pathway mediating disynaptic reciprocal inhibition in the cat

M. Enríquez-Denton, J. Nielsen, M.-C. Perreault, H. Morita, N. Petersen and H. Hultborn

1. In cat lumbar motoneurones, disynaptic inhibitory postsynaptic potentials (IPSPs) evoked by stimulation of antagonist motor nerves were depressed for at least 150 ms following conditioning stimulation of flexor (1·7-2 times threshold (T)) and ankle extensor (5T) nerves. The aim of the present study was to investigate the possibility that this depression is caused by presynaptic inhibitory mechanisms acting at the terminals of group I afferent fibres projecting to the Ia inhibitory interneurones and/or the terminals of these interneurones to the target motoneurones.

2. Conditioning stimulation of flexor, but not ankle extensor, nerves evoked a depression of the monosynaptic Ia excitatory postsynaptic potentials (EPSPs) recorded intracellularly in Ia inhibitory interneurones. This depression lasted between 200 and 700 ms and was not accompanied by a depression of the monosynaptic EPSPs evoked by stimulation of descending pathways. These results suggest that flexor, but not ankle extensor, group I afferent fibres can modulate sensory transmission at the synapse between Ia afferent fibres and Ia inhibitory interneurones.

3. Conditioning stimulation of flexor muscle nerves, extensor muscle nerves and cutaneous nerves produced a long-lasting increase in excitability of the terminals of the Ia inhibitory interneurones. The increase in the excitability of the terminals was not secondary to an electrotonic spread of synaptic excitation at the soma. Indeed, concomitant with the excitability increase of the terminals there were signs of synaptic inhibition in the soma.

4. The unitary IPSPs induced in target motoneurones following the spike activity of single Ia inhibitory interneurones were depressed by conditioning stimulation of muscle and cutaneous nerves. Since the conditioning stimulation also evoked compound IPSPs in those motoneurones, a firm conclusion as to whether unitary IPSP depression involved presynaptic inhibitory mechanism of the terminals of the interneurones could not be reached.

5. The possibility that the changes in excitability of the Ia interneuronal terminals reflect the presence of a presynaptic inhibitory mechanism similar to that operating at the terminals of the afferent fibres (presynaptic inhibition) is discussed.1. In cat lumbar motoneurones, disynaptic inhibitory postsynaptic potentials (IPSPs) evoked by stimulation of antagonist motor nerves were depressed for at least 150 ms following conditioning stimulation of flexor (1·7-2 times threshold (T)) and ankle extensor (5T) nerves. The aim of the present study was to investigate the possibility that this depression is caused by presynaptic inhibitory mechanisms acting at the terminals of group I afferent fibres projecting to the Ia inhibitory interneurones and/or the terminals of these interneurones to the target motoneurones.

6. Conditioning stimulation of flexor, but not ankle extensor, nerves evoked a depression of the monosynaptic Ia excitatory postsynaptic potentials (EPSPs) recorded intracellularly in Ia inhibitory interneurones. This depression lasted between 200 and 700 ms and was not accompanied by a depression of the monosynaptic EPSPs evoked by stimulation of descending pathways. These results suggest that flexor, but not ankle extensor, group I afferent fibres can modulate sensory transmission at the synapse between Ia afferent fibres and Ia inhibitory interneurones.

7. Conditioning stimulation of flexor muscle nerves, extensor muscle nerves and cutaneous nerves produced a long-lasting increase in excitability of the terminals of the Ia inhibitory interneurones. The increase in the excitability of the terminals was not secondary to an electrotonic spread of synaptic excitation at the soma. Indeed, concomitant with the excitability increase of the terminals there were signs of synaptic inhibition in the soma.

8. The unitary IPSPs induced in target motoneurones following the spike activity of single Ia inhibitory interneurones were depressed by conditioning stimulation of muscle and cutaneous nerves. Since the conditioning stimulation also evoked compound IPSPs in those motoneurones, a firm conclusion as to whether unitary IPSP depression involved presynaptic inhibitory mechanism of the terminals of the interneurones could not be reached.

9. The possibility that the changes in excitability of the Ia interneuronal terminals reflect the presence of a presynaptic inhibitory mechanism similar to that operating at the terminals of the afferent fibres (presynaptic inhibition) is discussed.

This article has been cited by other articles:

				G. Courtine, S. J. Harkema, C. J. Dy, Y. P. Gerasimenko, and P. Dyhre-Poulsen Modulation of multisegmental monosynaptic responses in a variety of leg muscles during walking and running in humans J. Physiol., August 1, 2007; 582(3): 1125 - 1139. [Abstract] [Full Text] [PDF]

				A. Jackson, S. N. Baker, and E. E. Fetz Tests for presynaptic modulation of corticospinal terminals from peripheral afferents and pyramidal tract in the macaque J. Physiol., May 15, 2006; 573(1): 107 - 120. [Abstract] [Full Text] [PDF]

				S. Rossignol, R. Dubuc, and J.-P. Gossard Dynamic Sensorimotor Interactions in Locomotion Physiol Rev, January 1, 2006; 86(1): 89 - 154. [Abstract] [Full Text] [PDF]

				G. Nafati, A. Schmied, and C. Rossi-Durand Changes in the Inhibitory Control Exerted by the Antagonist Ia Afferents on Human Wrist Extensor Motor Units During an Attention-Demanding Motor Task J Neurophysiol, April 1, 2005; 93(4): 2350 - 2353. [Abstract] [Full Text] [PDF]

				H. S. Pyndt, M. Laursen, and J. B. Nielsen Changes in Reciprocal Inhibition Across the Ankle Joint With Changes in External Load and Pedaling Rate During Bicycling J Neurophysiol, November 1, 2003; 90(5): 3168 - 3177. [Abstract] [Full Text] [PDF]

				M. Enriquez-Denton, H. Morita, L.O.D. Christensen, N. Petersen, T. Sinkjaer, and J. B. Nielsen Interaction Between Peripheral Afferent Activity and Presynaptic Inhibition of Ia Afferents in the Cat J Neurophysiol, October 1, 2002; 88(4): 1664 - 1674. [Abstract] [Full Text] [PDF]