Transmitter phenotypic expressions is a dynamic cellular process governed by multiple interactions with the neuronal environment. During sympathoadrenal development the arrival of presynaptic nerve terminals at the adrenal chromaffin cell (in the immediate postnatal period), coincides with the acquisition and subsequent development of a variety of transmitter biosynthetic capacities. Data discussed herein supports the contention that synaptic connections serve a central role in triggering the ontological cascade. Disruption of the normal timing of innervation events is detrimental to subsequent function and results in permanent deficiencies in development. In addition, alteration of transmitter biosynthetic regulatory mechanisms appears to reside at the level of gene expression. In view of this, additional molecular approaches are necessary to further elucidate the fundamental basis of neuronal transmitter phenotypic plasticity. Our approach to this problem represents a logical extension of previous research in this area and ultimately, will involve characterizing transcription activator molecules important in transmitter gene expression at various ontological ages.