Abstract
Neuronal networks generating coordinated rhythmic motor activity such as locomotion are already functional at birth in the mouse spinal cord, suggesting that these neuronal networks develop during prenatal stages. Indeed, as early as embryonic day (E)12.5, periodic spontaneous motor activity could be observed in the mouse fetus (Suzue (1996) Neurosci. Lett. 218:131-134). We examined the neuronal mechanisms of rhythmic motor activity during early fetal period, using isolated spinal cord preparations taken from mouse fetuses at E13. In these preparations, periodic spontaneous bursts (PSB) recorded from lumbar ventral roots were abolished by simultaneous blockade of glutamate, glycine and GABAA receptors, while they were not abolished by blockade of glutamate receptors, a excitatory device in the matured neuronal network. Bath-application of glycine or GABA evoked burst activity in the ventral roots, suggesting that these neurotransmitters exert excitatory effects during this period to generate PSB. Moreover, whole cell patch clamp recordings in ventral horn neurons revealed that high intracellular Cl− concentration is causing excitation by these amino acids at this stage. Such excitatory synaptic inputs via glycine and GABAA receptors during the early fetal period may play an important role in development of neuronal circuit. [Jpn J Physiol 54 Suppl:S21 (2004)]
