The Development and Response to Injury of Neonatal Rat Hindlimb Motoneurones and Their Afferent Connections: A Morphological Study

Development of motor function extends into the first three postnatal weeks in rats, and is correlated with maturation of spinal motoneurones and their afferent inputs. This study examined the normal development of somatodendritic morphology of identified ankle flexor motoneurones and the effect of nerve injury on the morphology and survival of cells. The effect of nerve injury upon motoneurone synaptic connectivity was also examined. Retrogradely labelled motoneurones were injected with fluorescent dyes. One to three days after birth, the soma and dendrites of these motoneurones were covered in filopodial and lamellipodial processes. After four postnatal days there was an elimination of these processes which proceeded from the soma to the distal dendrites. By nine days after birth, these structures were found only distally. There was no significant growth of the soma during the first postnatal week. After common peroneal (CP) nerve injury on postnatal day two, elimination of processes from the soma and proximal dendrites was halted some cells showed evidence of dendritic sprouting. Other motoneurones displayed features associated with neuronal degeneration. However, there was no significant difference in soma area of injured motoneurones compared with control motoneurones. Finally, two to three months later only 48-69% of the injured motoneurones survived. The effect of nerve injury on the distribution of parvalbumin immunoreactive primary afferent fibres and descending serotonergic fibres in the ventral horn was studied. Within five days after nerve injury, there was a decrease in the density of parvalbumin immunoreactivity around the injured CP motoneurone pool. In contrast, the density of serotonergic fibres was apparently unaltered. The somatodendritic surface of rat flexor motoneurones matures during the first week of postnatal life. Injury during the critical period arrests the maturation of the cell, and results in death of motoneurones