The development of the hypophysial portal system in the White-crowned Sparrow,Zonotrichia leucophrys gambelii

Summary The development of the hypophysial portal system has been studied in 35 embryos and 45 nestlings of the White-crowned Sparrow. The primordium of the hypophysis is vascularized by the infundibular (primary) capillary plexus, supplied by the right and left infundibular arteries, which, in the embryo, are constant branches of the right and left internal carotid arteries.The cellular proliferation and differentiation of the pars distalis into rostral and caudal lobes is accompanied by a penetration of portal vessels from the infundibular (primary) capillary plexus into these lobes beginning on the fifth day of incubation. The cellular proliferation of the rostral lobe of the pars distalis and development of the rostral group of the portal vessels precedes that of the caudal lobe of the pars distalis and the development of the caudal group of the portal vessels.The periglandular vessels, which originate in younger embryos from the infundibular (primary) capillary plexus, apparently become a part of the portal vessels.The portal vessels are the sole blood supply to the developing pars distalis of the White-crowned Sparrow; there is no evidence of a direct arterial supply at anytime during embryonic development. The neural-lobe artery appears at the end of incubation as a secondary branch of the right and left infundibular arteries. The rostral and caudal groups of the portal vessels are well-developed at the end of incubation (17–29 mm CRL) when aldehyde-fuchsin positive neurosecretory material first appears in the supraoptic and paraventricular nuclei, in the median eminence and in the neural lobe.The differentiation of the median eminence into rostral and caudal divisions begins at the end of the nestling period although its adult form is not achieved until later. The formation of the portal zone begins at the end of incubation (17–29 mm CRL) and is completed by the time of fledging.Dedicated to Professor Dr. W. Bargmann in honor of his 60th birthday.The investigations reported herein were supported by a research grant (HE 07240 NEUA) from the National Institutes of Health to Professor Vitums, by funds for biological and medical research made available by State of Washington Initiative Measure No 171 to Professor Vitums, by a research grant from the Deutsche Forschungsgemeinschaft to Professor Oksche, by aresearch grant (NB 01353) from the National Institutes of Health to Professor Farner, and by a Research Career Development Award from the National Institute of Arthritis and Metabolic Diseases (5 K 3 AM-18,370) to Professor King. We are grateful to Professor Bargmann for his generosity in making available the facilities of the Anatomisches Institut Kiel for this investigation. We wish to thank Frau Karin Graap and Mrs. Dianne Reno for technical assistance and Miss Janice Austin for the preparation of the drawings.