ALTERATIONS IN GENICULATE GANGLION PROTEINS FOLLOWING FUNGIFORM RECEPTOR DAMAGE

Previous anatomical studies in rat have shown that damage produced to fungiform receptors of the anterior tongue at postnatal age 2 (P2) alt ers the growth and ramification of primary gustatory axons in the rost ral nucleus of the solitary tract (NST). Studies employing artificial rearing (AR) procedures, which functionally deprive rat pups of oroche mical stimulation during critical periods of postnatal life, produce s imilar alterations in the development of primary gustatory axons in th e NST. Therefore, orochemical stimulation during rat's early postnatal life is necessary for normal development of primary gustatory axons i n the rostral NST. One hypothesis concerning receptor-damage effects a nd AR effects is that receptor damage during critical periods of devel opment may alter the regulation (i.e. transcription/translation) and/o r distribution (i.e. transport) of proteins in geniculate ganglion neu rons, thereby affecting growth of primary gustatory axons in the rostr al NST. Specific aims of the present experiments were to comprehensive ly examine electrophoretic profiles of geniculate ganglion proteins fo llowing P2 receptor damage and late (> P40) receptor damage. Results s how that concentrations-of particular geniculate ganglion proteins are differentially altered following P2 receptor damage and late receptor damage, and that early receptor damage and late receptor damage produ ces distinct effects on the electrophoretic profiles of particular cla sses of proteins. Between the ages of P7-P38, P2 receptor damage lower s ganglion concentration of an acidic membrane glycoprotein designated as Al, with an apparent M(r) of 64-67 kDa and a pi of 4.8-5.2. P2 rec eptor damage also lowers ganglion concentrations of GAP-43. P2 recepto r damage produces transient decreases in ganglion concentrations of NF -160, NF-200, and 8 additional acidic proteins. Three of these protein s may correspond to peripheral nerve sheath proteins analyzed in previ ous studies of the sciatic nerve, and one of these proteins may corres pond to a 24 kDa growth-associated protein characterized in regenerati ng optic nerve. The time-course for changes observed in ganglion prote ins following P2 damage was consistent with that observed for normal a natomical development of primary gustatory axons in both the lingual e pithelium and NST. Receptor damage produced at P40 and later yielded d ifferent patterns of changes in geniculate ganglion proteins. Late rec eptor damage produced a transient increase in ganglion concentrations of NF-160, NF-200, GAP-43 and four additional acidic proteins within t he 29-57 kDa M(r) range. Late receptor damage also produced a transien t decrease in the concentrations of protein Al and a 30 kDa protein th at was not affected by P2 damage. Therefore, proteins that were prefer entially affected by P2 damage may be involved in the regulation of in itial axonal growth within the Lingual epithelium and NST, as opposed to the structural repair or maintenance of extant axons. Relationships between normal anatomical development in peripheral and central compo nents of primary gustatory axons are discussed in relation to availabi lity of particular cytoskeletal and growth-associated proteins.