title: Regulation of EphB1 expression by dopamine signaling.
abstract: The Eph family tyrosine kinase receptors and their ligands have been implicated in axon guidance and neuronal migration during development of the nervous system. In the current study, we aim to characterize the nature of changes in EphB1 receptor expression following increases or decreases in dopamine activity. Neonatal mice (P3) were injected with 6-hydroxydopamine and allowed 13 days to recover. These animals show a profound depletion of dopamine in all areas assayed, with a corresponding dose-dependent decrease in EphB1 expression. Day 3 pups were also injected either chronically (P3-P16) or acutely (P3 only) with cocaine to determine how enhancing dopamine signaling would affect EphB1 signal density. It was found that both treatments significantly increased expression of EphB1 in the cortex, striatum and substantia nigra. Finally, animals were treated prenatally (E15-E17) with cocaine and sacrificed on P7. These animals also showed an increase in EphB1 signal density, but only in the dopaminergic terminal areas in the cortex and striatum. These studies indicate that dopamine activity regulates developmental expression of the tyrosine kinase receptor EphB1.
authors.affiliation: Department of Psychology, Rutgers University, 152 Frelinghuysen Road, Piscataway, NJ 08854, USA.
authors.forename: A K
authors.initials: AK
authors.lastname: Halladay
authors.forename: Y
authors.initials: Y
authors.lastname: Yue
authors.forename: L
authors.initials: L
authors.lastname: Michna
authors.forename: D A
authors.initials: DA
authors.lastname: Widmer
authors.forename: G C
authors.initials: GC
authors.lastname: Wagner
authors.forename: R
authors.initials: R
authors.lastname: Zhou
mesh_terms: D015102:3,4-Dihydroxyphenylacetic Acid / Q000032:analysis; D000818:Animals; D000831:Animals, Newborn; D002540:Cerebral Cortex / Q000737:chemistry / Q000187:drug effects / Q000378:metabolism; D003042:Cocaine / Q000494:pharmacology; D019970:Cocaine-Related Disorders / Q000378:metabolism; D003342:Corpus Striatum / Q000737:chemistry / Q000187:drug effects / Q000378:metabolism; D004298:Dopamine / Q000032:analysis / Q000378:metabolism*; D018765:Dopamine Uptake Inhibitors / Q000494:pharmacology; D036387:Ephrin-B1; D005260:Female; D015870:Gene Expression / Q000187:drug effects / Q000502:physiology; D006719:Homovanillic Acid / Q000032:analysis; D017403:In Situ Hybridization; D008565:Membrane Proteins / Q000235:genetics* / Q000378:metabolism; D051379:Mice; D008815:Mice, Inbred Strains; D009410:Nerve Degeneration / Q000139:chemically induced / Q000378:metabolism; D016627:Oxidopamine; D011247:Pregnancy; D012333:RNA, Messenger / Q000032:analysis; D015398:Signal Transduction / Q000187:drug effects / Q000502:physiology*; D013378:Substantia Nigra / Q000737:chemistry / Q000187:drug effects / Q000378:metabolism; D013565:Sympatholytics
chemical_list: D018765:Dopamine Uptake Inhibitors; D036387:Ephrin-B1; D008565:Membrane Proteins; D012333:RNA, Messenger; D013565:Sympatholytics; D015102:3,4-Dihydroxyphenylacetic Acid; D016627:Oxidopamine; D003042:Cocaine; D004298:Dopamine; D006719:Homovanillic Acid