PROPERTIES OF ECTOPIC NEURONS INDUCED BY XENOPUS NEUROGENIN1 MISEXPRESSION

We have examined cells cultured from ectoderm-misexpressing Neurogenin 1 (Ngn1) to describe better the extent to which this gene can control aspects of neuronal phenotype including motility, morphology, excitabi lity, and synaptic properties. Like primary spinal neurons which norma lly express Ngn1, cells in Ngn1-misexpressing cultures exhibit a motil ity-correlated behavior called circus movements prior to neuritogenesi s. Misexpression of Neuron also causes circus movements and later neur onal differentiation. GSK3 beta, which inhibits NeuroD function in viv o, blocks both Ngn1-induced and NeuroD-induced neuronal differentiatio n, while Notch signaling inhibits only Ngn1-induced neuronal different iation, confirming that Neuron is downstream of Ngn1 and insensitive t o Notch inhibition. While interfering with NeuroD function in ventral ectoderm inhibits both circus movements and neuronal differentiation, such inhibition in the neural plate inhibits only neuronal differentia tion, suggesting that additional factors regulate circus movements in the neural ectoderm. Ngn1-misexpressing cells extend N-tubulin-positiv e neurites and exhibit tetrodotoxin-sensitive action potentials. Unlik e the majority of cultured spinal neurons, however, Ngn1-misexpressing cells do not respond to glutamate and do not form functional synapses with myocytes, suggesting that these cells are either like Rohon-Bear d sensory neurons or are not fully differentiated.