Long term depression of the recurrent inhibition of monosynaptic spinal reflexes after sciatic nerve crush in adult rats.
- Author:
Liang SHU
1
;
You-Rong DONG
;
Wei-Hong YAN
;
Yu ZHAI
;
Yun WANG
;
Wei LI
Author Information
1. Shanghai Ninth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai 200011, China.
- Publication Type:Journal Article
- MeSH:
Animals;
Long-Term Synaptic Depression;
physiology;
Male;
Motor Neurons;
physiology;
Nerve Crush;
Nerve Regeneration;
physiology;
Neuronal Plasticity;
physiology;
Neurons, Afferent;
physiology;
Rats;
Rats, Wistar;
Reflex, Monosynaptic;
physiology;
Sciatic Nerve;
injuries;
physiopathology;
Spinal Cord;
physiopathology;
Spinal Nerve Roots;
physiopathology
- From:
Acta Physiologica Sinica
2011;63(4):291-299
- CountryChina
- Language:Chinese
-
Abstract:
Sciatic nerve injury is a common disease of peripheral nerve in clinic. After nerve injury, there are many dysfunctions in motoneurons and muscles following regeneration. Previous studies mostly investigated the aspects related to the injured nerve, and the effect on the recurrent inhibition (RI) pathway of spine following regeneration was not fully understood. Following reinnervation after temporary sciatic nerve crush, the functional alteration of RI was studied. In adult rats, RI between lateral gastrocnemius-soleus (LG-S) and medial gastrocnemius (MG) motor pools was assessed by conditioning monosynaptic reflexes (MSRs) elicited from the cut dorsal roots and recorded from either the LG-S or MG nerves by antidromic stimulation of the synergist muscle nerve. The following results were obtained. (1) The RI of MSRs in rats was almost lost (<5 weeks) after sciatic nerve crush. Although the RI partially recovered following reinnervation (6 weeks), it remained permanently depressed (up to 14 weeks). (2) Sciatic nerve crush on one side did not affect the contralateral RI. (3) Sciatic nerve crush did not induce any motoneuron loss revealed by immunohistochemistry. Peripheral nerve temporary disconnection causes long term alterations in RI pathway which make up motoneuron's function enhance for the alteration of muscle power and suggests that peripheral nerve injury induces long term plastic changes in the spinal motoneuron circuitry.
