Abstract
Motoneurons MN-1 and MN-3 in the moth Manduca sexta go through 3 distinct phases during postembryonic life. During larval life their neuritic fields show allometric growth in concert with larval growth. Larval neurites are then lost during the larval-pupal transition, which is followed by the outgrowth of adult-specific neurites during adult development. In MN-1, the adult-specific arbor typically results from the outgrowth of neurites ipsilateral to the cell body. However, in a small percentage of cells, ipsilateral branches are not present and contralateral branches extend across the midline to fill the vacant space. This altered form of MN-1 is thought to result from the early failure of ipsilateral neurite extension. The steroid hormones, the ecdysteroids, are responsible for the outgrowth of adult neurites. The onset of the latter is correlated with the ecdysteroid increase that promotes adult differentiation and does not occur under conditions such as diapause, in which the normal steroid rise is absent. Artificial replacement of ecdysteroids, however, induces the adult-specific growth. This action of ecdysteroids to cause a change in neuronal form requires the absence of juvenile hormone (JH). Application of JH mimics prior to the onset of the program of adult outgrowth blocks this outgrowth. MN-1 and MN-3 show different times of JH sensitivity, which appear to be correlated with different times of neurite outgrowth. It is concluded that the role of JH is to maintain the status quo of central neurons and prevent changes in form in response to ecdysteroids. In the absence of JH, the ecdysteroids can then exert morphogenetic changes, but the nature of these actions, neurite outgrowth or regression, is likely a function of the developmental history of the cell.
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