The temporal correspondence between neuroanatomical and neurophysiological development of peripheral and central gustatory neurons has suggested that morphological development of the first-order central gustatory relay, located in the rostral nucleus of the solitary tract (NST), may be dependent on afferent input from peripheral gustatory pathways. The objective of the present study was to determine the effects of perinatal receptor damage on development of gustatory recipient zones within the rostral and intermediate NST. Results show that damage induced to fungiform receptors of the anterior tongue at postnatal day 2 (P2) alters normal development of NST terminal fields associated with the chorda tympani nerve (CT) and greater superficial nerve (GSP), and that alterations in the CT/GSP terminal field persist in adulthood after peripheral gustatory receptors have regenerated. Damage induced to fungiform receptors at P2 does not alter the normal development of glossopharyngeal terminal fields in the intermediate NST. Receptor damage produced at P10 and P20 is without effect on normal development of the CT/GSP terminal field. Thus, fungiform receptor damage at P2 produces specific alterations in the development of NST terminal fields that receive projections from the facial-intermediate nerve, and receptor damage effects are only obtained during a critical period of postnatal development. P2 receptor damage has the overall effect of eliminating caudally directed migration of CT/GSP axons to additional projection neurons that establish connections with the second-order central gustatory relay located in the parabrachial nucleus (PBN). Behavioral studies were conducted to determine the functional consequences of early receptor damage. Results from behavioral studies show that bilateral damage to fungiform papillae at P2 alters normal adult preferences to low and intermediate concentrations of NaCl and sucrose tastes, yet aversions to citric acid and quinine HCl are not obviously affected. Therefore, anatomical alterations in the CT/GSP terminal field produced by P2 receptor damage are accompanied by specific changes in adult taste preference responses.