Reduced Renshaw recurrent inhibition after neonatal sciatic nerve crush in rats.
Renshaw recurrent inhibition (RI) plays an important gated role in spinal motion circuit. Peripheral nerve injury is a common disease in clinic. Our current research was designed to investigate the change of the recurrent inhibitory function in the spinal cord after the peripheral nerve crush injury in neonatal rat. Sciatic nerve crush was performed on 5-day-old rat puppies and the recurrent inhibition between lateral gastrocnemius-soleus (LG-S) and medial gastrocnemius (MG) motor pools was assessed by conditioning monosynaptic reflexes (MSR) elicited from the sectioned dorsal roots and recorded either from the LG-S and MG nerves by antidromic stimulation of the synergist muscle nerve. Our results demonstrated that the MSR recorded from both LG-S or MG nerves had larger amplitude and longer latency after neonatal sciatic nerve crush. The RI in both LG-S and MG motoneuron pools was significantly reduced to virtual loss (15-20% of the normal RI size) even after a long recovery period upto 30 weeks after nerve crush. Further, the degree of the RI reduction after tibial nerve crush was much less than that after sciatic nerve crush indicatig that the neuron-muscle disconnection time is vital to the recovery of the spinal neuronal circuit function during reinnervation. In addition, sciatic nerve crush injury did not cause any spinal motor neuron loss but severally damaged peripheral muscle structure and function. In conclusion, our results suggest that peripheral nerve injury during neonatal early development period would cause a more sever spinal cord inhibitory circuit damage, particularly to the Renshaw recurrent inhibition pathway, which might be the target of neuroregeneration therapy.
The Department of Neurology, Shanghai Ninth People's Hospital Affiliated Shanghai Jiao Tong University School of Medicine, Shanghai 200011, China.
Liang
L
Shu
The Department of Neurology, Shanghai Ninth People's Hospital Affiliated Shanghai Jiao Tong University School of Medicine, Shanghai 200011, China.
Jingjing
J
Su
The Department of Anaesthesia, The Fifth People's Hospital of Shanghai, Fudan University, Shanghai 200240, China.
Lingyan
L
Jing
The Department of Neurology, Shanghai Ninth People's Hospital Affiliated Shanghai Jiao Tong University School of Medicine, Shanghai 200011, China.
Ying
Y
Huang
The Department of Neurology, Shanghai Ninth People's Hospital Affiliated Shanghai Jiao Tong University School of Medicine, Shanghai 200011, China.
Yu
Y
Di
The Department of Anaesthesia, The Fifth People's Hospital of Shanghai, Fudan University, Shanghai 200240, China.
Lichao
L
Peng
The Department of Neurology, Shanghai Ninth People's Hospital Affiliated Shanghai Jiao Tong University School of Medicine, Shanghai 200011, China.
Jianren
J
Liu
D000818:Animals; D000831:Animals, Newborn / Q000502:physiology*; D004558:Electric Stimulation; D055724:Electrophysiological Phenomena / Q000502:physiology; D006614:Hindlimb / Q000294:innervation; D006735:Horseradish Peroxidase; D008297:Male; D009046:Motor Neurons / Q000502:physiology; D018482:Muscle, Skeletal / Q000294:innervation / Q000502:physiology; D009409:Nerve Crush; D009416:Nerve Regeneration / Q000502:physiology; D009433:Neural Inhibition / Q000502:physiology*; D051381:Rats; D017208:Rats, Wistar; D012023:Reflex, Monosynaptic / Q000502:physiology; D012584:Sciatic Nerve / Q000473:pathology*; D013979:Tibial Nerve / Q000502:physiology
D006735:Horseradish Peroxidase