Locations, associations and temporal evolution of intracranial arterial infundibular dilatations in children.

BACKGROUND: There are few data in the literature on the characteristics and natural history of intracranial arterial infundibular dilatations in children. METHODS: An institutional review board-approved retrospective review was performed of infundibula reported on MR angiography in patients <18 years of age at our tertiary pediatric institute from 1998 to 2016. Clinical data (age, sex, diagnosis, other vascular variants/pathologies) were recorded and images assessed for vessel of origin, infundibulum size and exact location. Ratios of infundibulum:parent artery were assessed at diagnosis and last follow-up. Temporal evolution to aneurysm was evaluated. RESULTS: We found 60 intracranial infundibula in 60 children (male:female=27:33; mean age 9.7±5.2 years, range 2-18 years,). Family history of aneurysms was present in 2/60 (3.3%). Syndromic association was found in 14/60 (23.3%), most frequently sickle cell disease (4/14=28.6%). Mean infundibulum size was 2.2±0.5 mm, with mean ratio to parent artery of 0.54±0.17. The most common location was on the P1-posterior cerebral artery (34/63=56.7%), whereas posterior communicating infundibula were seen in only 4/60 (6.7%) cases. Other cerebrovascular variants were seen in 12/60 (20%) patients. On follow-up imaging (in 32/60 patients over 86 patient-years, mean 32.3±35.7 months), no significant change in infundibulum:parent artery ratio was noted. None of the infundibular dilatations showed interval evolution to aneurysm. CONCLUSION: We present the largest reported cohort of pediatric intracranial arterial infundibula, which we found to be distinct from their adult counterparts with regard to location, etiology and temporal evolution. Growth over time and/or aneurysmal formation are rare, not necessitating frequent short-term imaging surveillance during childhood.

VEGF-dependent and PDGF-dependent dynamic neurovascular reconstruction in the neurohypophysis of adult mice.

Hypothalamo-neurohypophysial system (HNS) releases arginine vasopressin (AVP) and oxytocin (OXT) from axonal terminals of the neurohypophysis (NH) into blood circulation for controlling body fluid homeostasis and lactation. Chronic osmotic and suckling stimulations have been shown to cause neurovascular and neuroglial reconstruction in the NH of adult mammals and no study has been reported for vascular dynamics. The aim of this study was to elucidate the occurrence of continuous angiogenesis and growth factor-dependent neurovascular reconstruction in the NH of adult mice. Active proliferation of endothelial cells and oligodendrocyte progenitor cells (OPCs) was observed using the immunohistochemistry of bromodeoxyuridine and Ki-67. Vascular endothelial growth factor A (VEGFA) and VEGF receptor 2 (VEGFR2 (KDR)) were highly expressed at pituicytes and endothelial cells respectively. Moreover, prominent expression of platelet-derived growth factor B (PDGFB) and PDGF receptor beta was observed at OXT-containing axonal terminals and pericytes respectively. Administration of the selective tyrosine kinase inhibitor AZD2171 for VEGFRs and STI571 for PDGFRs significantly decreased proliferation of endothelial cells and OPCs. Moreover, AZD2171 treatment decreased vascular density by facilitating apoptosis of endothelial cells and the withdrawal of its treatment led to remarkable rebound proliferation of endothelial cells, so that vascular density rapidly returned to normal levels. AZD2171 decreased the density of both AVP- and OXT-containing axonal terminals, whereas STI571 selectively decreased the density of AVP-containing ones. Thus, this study demonstrates that the signaling pathways of VEGF and PDGF are crucial mediators for determining proliferation of endothelial cells and OPCs and the density of AVP- and OXT-containing axonal terminals in the HNS.

Direct and indirect roles of Fgf3 and Fgf10 in innervation and vascularisation of the vertebrate hypothalamic neurohypophysis.

The neurohypophysis is a crucial component of the hypothalamo-pituitary axis, serving as the site of release of hypothalamic neurohormones into a plexus of hypophyseal capillaries. The growth of hypothalamic axons and capillaries to the forming neurohypophysis in embryogenesis is therefore crucial to future adult homeostasis. Using ex vivo analyses in chick and in vivo analyses in mutant and transgenic zebrafish, we show that Fgf10 and Fgf3 secreted from the forming neurohypophysis exert direct guidance effects on hypothalamic neurosecretory axons. Simultaneously, they promote hypophyseal vascularisation, exerting early direct effects on endothelial cells that are subsequently complemented by indirect effects. Together, our studies suggest a model for the integrated neurohemal wiring of the hypothalamo-neurohypophyseal axis.

Tissue plasminogen activator and plasminogen are critical for osmotic homeostasis by regulating vasopressin secretion.

Systemic osmotic homeostasis is regulated mainly by neuroendocrine system of arginine-vasopressin (AVP) in mammalians. In the present study, we demonstrated that the immunoreactivity of tissue plasminogen activator (tPA) was observed specifically at neurosecretory granules of AVP-positive magnocellular terminals and that of plasminogen was seen at astrocytes in the neurohypophysis (NH). Both tPA and plasminogen knockout (KO) mice revealed higher plasma osmolarity upon water deprivation, a chronic osmotic stimulation, as compared with their wild-type (WT) animals, indicating abnormal osmotic control in these KO mice. tPA KO mice but not plasminogen ones revealed lower ability in secreting AVP into the blood circulation upon an acute osmotic stimulation. Both tPA and plasminogen KO animals showed lower ability in secreting AVP into the blood circulation upon a chronic osmotic stimulation. The recombinant tPA was able to promote the release of AVP from isolated NH. Chronic osmotic stimulation decreased the laminin expression level of neurohypophysial microvessel in WT mice but not in plasminogen KO ones. We suggest that AVP secretion is critically regulated by tPA-dependent facilitation of AVP release from terminals and plasminogen-dependent increase of AVP permeability across microvessels possibly via laminin degradation.

Perivascular cells increase expression of ciliary neurotrophic factor following partial denervation of the rat neurohypophysis.

The expression of ciliary neurotrophic factor (CNTF) was investigated immunocytochemically during the axonal degeneration and collateral axonal sprouting response that follows partial denervation of the rat neurohypophysis. A significant increase in the number of CNTF-immunoreactive (CNTF-ir) cells was observed in the neurohypophysis of partially denervated animals compared to age-matched sham-operated controls by 5 days post-denervation, remaining elevated throughout the 30 day post-denervation period. Stereometric assessment of the numbers of CNTF-ir cells within the partially denervated neurohypophysis demonstrated a 36% increase by 3 days following denervation reaching 130% of control values by 10 days post-lesion. The cell numbers remained elevated throughout the 30 day post-lesion period suggesting that CNTF may play a role in the neurosecretory axonal sprouting process known to occur between 10 and 30 days post-denervation. Subsequent preparations pairing anti-CNTF with antibodies against ED1, CR3, p75 low affinity neurotrophin receptor (p75(LNGFR)), and S100beta, demonstrated that CNTF was exclusively localized in a phenotypically-distinct population of perivascular cells. The association of perivascular cells with phagocytic activity was confirmed by dual-label fluorescence microscopy showing the colocalization of P75(LNGFR)-ir and OX-42-ir in cells expressing the ED-1 antigen. No increase in CNTF-ir was observed in non-injured animals in which heightened levels of neurosecretory activity were induced physiologically. These results suggest that increased CNTF-ir occurs in response to conditions which induce high levels of phagocytic activity by perivascular cells in the axotomized neurohypophysis which is sustained throughout a period in which axonal sprouting is known to occur in the partially denervated neurohypophysis.

The circumventricular organs: an atlas of comparative anatomy and vascularization.

The circumventricular organs are small sized structures lining the cavity of the third ventricle (neurohypophysis, vascular organ of the lamina terminalis, subfornical organ, pineal gland and subcommissural organ) and of the fourth ventricle (area postrema). Their particular location in relation to the ventricular cavities is to be noted: the subfornical organ, the subcommissural organ and the area postrema are situated at the confluence between ventricles while the neurohypophysis, the vascular organ of the lamina terminalis and the pineal gland line ventricular recesses. The main object of this work is to study the specific characteristics of the vascular architecture of these organs: their capillaries have a wall devoid of blood-brain barrier, as opposed to central capillaries. This particular arrangement allows direct exchange between the blood and the nervous tissue of these organs. This work is based on a unique set of histological preparations from 12 species of mammals and 5 species of birds, and is taking the form of an atlas.

Histologic study of the human pituitary gland in acute traumatic brain injury.

PURPOSE: Approximately 25% of patients with traumatic brain injury (TBI) may develop partial or complete hypopituitarism. The causative mechanisms involved in its development are not clear. To the authors' knowledge, there have been no recent morphologic studies of the pituitary following TBI. METHODS: To characterize the resultant histologic changes, this study investigated the pituitaries of 42 patients who died following a motor vehicle accident, all from the Mayo Tissue Registry. Twelve patients died instantly at the scene of the accident (Group I) whereas 30 survived between 3 hours and 7 days (Group II). All pituitary specimens were obtained at autopsy, formalin-fixed and paraffin-embedded. Hematoxylin-eosin sections cut in horizontal or sagittal plane were examined light-microscopically. RESULTS: No infarction was noted in the pituitary specimens from group I. In group II, 13 of 30 (43%) showed acute infarcts of varying size. The extent of infarction in group II ranged from focal to sub-total necrosis involving 90% of the adenohypophysis. CONCLUSIONS: Underlying adenohypophysial pathology in patients dying after TBI is acute infarction. Loss of large numbers of adenohypophysial cells causes reduced secretion of adenohypophysial hormones and may contribute to post-traumatic hypopituitarism.

Glutamatergic innervation of the hypothalamic median eminence and posterior pituitary of the rat.

Recent studies have localized the glutamatergic cell marker type-2 vesicular glutamate transporter (VGLUT2) to distinct peptidergic neurosecretory systems that regulate hypophysial functions in rats. The present studies were aimed to map the neuronal sources of VGLUT2 in the median eminence and the posterior pituitary, the main terminal fields of hypothalamic neurosecretory neurons. Neurons innervating these regions were identified by the uptake of the retrograde tract-tracer Fluoro-Gold (FG) from the systemic circulation, whereas glutamatergic perikarya of the hypothalamus were visualized via the radioisotopic in situ hybridization detection of VGLUT2 mRNA. The results of dual-labeling studies established that the majority of neurons accumulating FG and also expressing VGLUT2 mRNA were located within the paraventricular, periventricular and supraoptic nuclei and around the organum vasculosum of the lamina terminalis and the preoptic area. In contrast, only few FG-accumulating cells exhibited VGLUT2 mRNA signal in the arcuate nucleus. Dual-label immunofluorescent studies of the median eminence and posterior pituitary to determine the subcellular location of VGLUT2, revealed the association of VGLUT2 immunoreactivity with SV2 protein, a marker for small clear vesicles in neurosecretory endings. Electron microscopic studies using pre-embedding colloidal gold labeling confirmed the localization of VGLUT2 in small clear synaptic vesicles. These data suggest that neurosecretory neurons located mainly within the paraventricular, anterior periventricular and supraoptic nuclei and around the organum vasculosum of the lamina terminalis and the preoptic area secrete glutamate into the fenestrated vessels of the median eminence and posterior pituitary. The functional aspects of the putative neuropeptide/glutamate co-release from neuroendocrine terminals remain to be elucidated.

Differential diagnosis of the infundibular dilation and aneurysm of internal carotid artery: assessment with fusion imaging of 3D MR cisternography/angiography.

Fusion imaging of 3D MR cisternography/angiography was used for the assessment of the vascular bulging finding detected by MR angiography from the viewpoint of the outer wall configuration of the corresponding internal carotid artery depicted by MR cisternography. With a fusion image, useful information was obtained to distinguish an infundibular dilation and enlarged origin of the normal posterior communicating artery from an aneurysm. This imaging technique can be a feasible addition to a noninvasive screening of cerebrovascular lesions with MR angiography alone.

Metabolic indices shift in the hypothalamic-neurohypophysial system during lactation: implications for interpreting their relationship with neuronal activity.

Metabolic indices of neuronal activity are thought to predict changes in the frequency of action potentials. There are stimuli that do not shift action potential frequency but change the temporal organization of neuronal firing following modifications of excitatory inputs by inhibitory synaptic activation. To our knowledge it is unknown whether this kind of stimulus associates with adjustments of metabolic markers of neuronal activity. Here, we used the hypothalamic-neurohypophysial system of lactating rats to address whether shifts in the temporal organization of neuronal firing relate with modifications of metabolic markers of neuronal activity. Cytochrome oxidase activity, (3)H-2-deoxyglucose uptake, and the area occupied by blood vessels increased in the paraventricular nucleus and neurohypophysis of lactating rats, as compared with their virgin counterparts. Taken together, these results suggest that metabolic demands denote shifts in the temporal organization of action potentials related with the adjustment of excitatory synaptic activation, and support that changes in metabolic markers do not necessarily reflect shifts in the frequency of action potentials.

Idiopathic central diabetes insipidus is associated with abnormal blood supply to the posterior pituitary gland caused by vascular impairment of the inferior hypophyseal artery system.

Central diabetes insipidus (CDI) has been linked to vascular central nervous system damage, although the pathophysiology of the mechanism has never been perfectly understood. Indeed, the vascular system of human pituitary gland has rarely been the subject of rigorous investigation except at postmortem. Recently, studies of pituitary gland blood supply have been carried out by means of a time evaluation of pituitary gland enhancement with noninvasive dynamic magnetic resonance (MR) imaging after contrast medium injection. In the present study, we decided to investigate the status of posterior pituitary blood supply by evaluating vascular pituitary patterns in a group of 19 patients with idiopathic CDI in whom previous standard MR imaging had failed to identify causal specific lesions. The control group was composed of 55 subjects with a median age of 12 yr (range, 4.2-17 yr) who had idiopathic isolated GH deficiency and normal pituitary morphology and 15 young adults (18-25 yr) who had normal pituitary gland and no endocrine dysfunction. Nineteen patients (12 females and seven males), ranging in age at the time of diagnosis of CDI from 0.5-14.9 yr (median, 5 yr), were examined with dynamic MR imaging between 1990 and 1997 at a median age of 14.1 yr (range, 5.0-26.3 yr). CDI was diagnosed according to clinical findings of polyuria and polydipsia, water deprivation test, and desmopressin acetate therapeutic trial. All of the patients had permanent CDI and were being treated with satisfactory results with desmopressin, two to three times daily, either intranasally or orally. The previous MR imaging findings of the 19 CDI patients had shown the absence of posterior pituitary hyperintensity, normal pituitary stalk, and normal anterior pituitary size. Enhancement of the straight sinus, representing a temporal reference point and occurring in normal subjects simultaneously to that of the posterior pituitary gland, was observed in all subjects after iv gadopentetate dimeglumine administration, with no substantial differences between patients and controls. However, the enhancement of the posterior pituitary lobe occurred simultaneously with the enhancement of the straight sinus in all of the controls but in only 14 of the 19 patients with CDI. In the remaining five patients, the enhancement of the straight sinus was not associated with the expected contrast enhancement of the posterior pituitary gland, suggesting abnormal blood supply to the posterior pituitary lobe. This is in keeping with vascular impairment of the inferior hypophyseal artery system and suggests that abnormal blood supply to the posterior pituitary gland is associated with what, until now, has been considered idiopathic CDI.

Non-sprouting angiogenesis in neurohypophysis after traumatic injury of the cerebral cortex. Electron-microscopic studies.

OBJECTIVES: Angiogenesis comprises two different mechanisms: endothelial sprouting and intussusceptive microvascular growth. The sprouting process is based on endothelial cell migration, proliferation and tube formation. Intussusceptive microvascular growth divides existing vessel lumens by formation and insertion of endothelial columns into the vessel lumen. The morphological features of microvessels of cerebral cortex and neurohypophysis were evaluated in a model of the cerebral traumatic injury. METHOD: The observations were conducted seven days after induction of cortical trauma. Traumatic injury was induced in the fronto-temporal region of cerebral cortex in general anesthesia with 20mg/kg ketamine hydrochloride. RESULTS: Seven days after traumatic brain injury in sections from cerebral cortex and neurohypophysis we can observe morphological features of angiogenesis. Endothelium of the cerebral cortex possesses high endotheliocytes tightly connected and enveloped by amorphous basement membrane-like material. Transcapillary pillars tightly connected with neighbouring endothelial cells split the newly formed vessels and branching takes place. In neurohypophysis we can observe all stages of non-sprouting angiogenesis: proliferation endothelial cells on the inside mother vessel, splitting newly formed blood vessels by transcapillary pillars directed into the vessel lumen, maturation of endothelium and network formation. CONCLUSION: The mechanical injuries directly induced angiogenesis not only in cerebral cortex, but also in neurohypophysis. Our studies show that mechanism of angiogenesis is not the same as observed previously in neurohypophysis after focal cerebral ischemia (Neuroendocrinology Letters 2001; 22:87 92). This study indicates that mechanism of angiogenesis can depend on kind of induction.

Focal ischemia in the cerebral cortex has an effect on the neurohypophysis. I. Ultrastructural changes in capillary vessels of the neurohypophysis after focal ischemia of the cerebral cortex.

OBJECTIVES: In our investigations we have reported that photochemical reaction leading to brain ischemia can also be precipitated with visible light from a non-coherent light source. It was revealed that focal cerebral ischemia after photochemical reaction cause the alterations in the capillaries ultrastructure and perivascular spaces of the barrier-competent regions of the brain. The purpose of this study is to first characterize the ultrastructural morphological consequences of photochemically induced ischemia in the cerebral cortex on the capillaries of neurohypophysis as the barrier-free region of the brain. METHOD: We used a model of ischemic brain damage due to obliteration of microvessels following the photochemical reaction. Rats were treated with an intravenous injection of rose bengal and irradiated from a halogen lamp source through an intact cranium to precipitate microvascular damage. Material for electron microscopic studies were sampled from the neurohypophysis 1 and 4 days after irradiation (4 animals in each group) in experimental group and 1 and 4 days after a rose bengal injection in control group. RESULTS: Investigations in transmission electron microscopy revealed platelet aggregation on the endothelium preceded by its early ultrastructural damage. In the capillaries of the neurohypophysis, one and four days after irradiation, numerous microthrombi adhering to the damaged endothelium were present. The capillary vessels contained a continuous, rather than a fenestrated endothelium. The basement membrane was thickened, blurred and locally multiplicated. CONCLUSION: Our results show that experimentally-induced thrombosis of cortical microvessels leads to alterations in the capillaries of neurohypophysis.

Focal ischemia in the cerebral cortex has an effect on the neurohypophysis. II. Angiogenesis in the neurohypophysis is a consequence of the focal ischemia in the cerebral cortex.

OBJECTIVES: Focal ischemia in the cerebral cortex has an effect on neurohypophysis. The morphological changes of microvessels of neurohypophysis were evaluated in a model of the cerebral infarction initiated by a photochemical reaction in the cerebral cortex. After photochemically induced platelet aggregation, we observed the morphological features of angiogenesis. METHOD: The model of photochemically-induced cerebral ischemia was used. Seven days after intravenous injection of rose bengal and irradiation from a halogen lamp source through an intact cranium, the sampled material from neurohypophysis is processed for transmission electron microscopy using standard procedures. RESULTS: We observed morphological features of the new vessel formation: the alterations in the endothelium and extracellular matrix during separation of the endothelial cell from each other in a "mother" vessel, the migration of the endothelial cells in the extracellular matrix, the communication of the lumen of the new and the "mother" vessels. CONCLUSION: We observed development of the angiogenic phenotype in the neurohypophysis after focal ischemia in the cerebral cortex. The endothelium, basement membrane and extracellular matrix undergo morphological alterations which lead to new blood vessel formation.

Alterations in rat's brain capillaries in a model of focal cerebral necrosis.

Focal brain compression causes cerebral tissue damage. In this study we followed alterations in capillary ultrastructure in the rat cortex and neurohypophysis caused by 40 mm Hg compression for 15 minutes. One day after experiment we observed clogging of capillaries, accumulation of collagen fibrills under the basement membrane and necrosis or apoptosis of endothelial cells. Four days after it the basement membrane was multiplicated, blurred and thickened. In the neurohypophysis the formation of vessels lined with the atypical continuous endothelium was seen. There was also evidence for the migration of pericytes through the blurred basement membrane and the differentiation of pericytes into endothelial cells. Thus, vascular injury in the compressed brain is followed by a highly ordered sequence of processes in the basement membrane and perivascular cells leading to capillary repair.

NO contributes to neurohypophysial but not other regional cerebral fluorocarbon-induced hyperemia in cats.

The large increase in cerebral blood flow (CBF) after fluorocarbon (FC)-exchange transfusion is thought to be caused by low oxygen content, decreased viscosity, or direct vasodilatory effect of the FC perfusate. The aim of this study was to determine whether nitric oxide (NO)-mediated vasorelaxation is increased in FC-perfused hemoglobin (Hb)-free cats because NO is not scavenged by Hb. We measured regional CBF with radiolabeled microspheres in three groups of anesthetized mechanically ventilated cats. The first group [FC + N(omega)-nitro-L-arginine methyl ester (L-NAME), n = 7] underwent a complete FC-exchange transfusion with FC-43 and subsequent nitric oxide synthase (NOS) inhibition with L-NAME (10 mg/kg i.v.) followed by L-arginine (100 mg/kg i.v.). A second group (FC + saline; n = 6) underwent an identical protocol, but NOS was not antagonized (saline i.v.). In a third group (blood + L-NAME; n = 7), cats were not FC exchanged but NOS was inhibited. In a separate cohort of four FC-perfused cats, NOS activity in brain tissue samples was reduced to 26% of control after NOS inhibition. FC-exchange transfusion nearly doubled hemispheric blood flow in both FC-exchanged groups, whereas it was constant in the blood + L-NAME group. These increases in regional CBF (hemispheres, brain stem, cerebellum, thalamus, and white matter) were not reversed by inhibition of NOS, except in the neurohypophysis, where L-NAME reduced blood flow to levels comparable to values in the blood + L-NAME group. In summary, increases in regional CBF after total FC-exchange transfusion are not caused by a lack of NO scavenging, with the exception of neurohypophysis. These findings suggest an increased vasorelaxation in neurohypophysis of FC-perfused and Hb-free cats caused by unscavenged NO, but this mechanism does not play a major role in FC-related CBF increases in the rest of the cerebral circulation.

Dynamic MRI in the congenital agenesis of the neural pituitary stalk syndrome: the role of the vascular pituitary stalk in predicting residual anterior pituitary function.

OBJECTIVE: Magnetic resonance imaging (MRI) without contrast medium is unable to give detailed information on the hypothalamic-pituitary structures. MRI using gadopentetate dimeglumine (Gd-DTPA), and dynamic MRI, were performed in patients with hypopituitarism previously diagnosed as having anterior pituitary hypoplasia, ectopic posterior pituitary and unidentified pituitary stalk (1) to determine whether Gd-DTPA improves the delineation of hypothalamic-pituitary structures; (2) to verify whether, if so, such improvement can be correlated with residual pituitary function in patients subjected to long-term follow-up; and (3) to identify the hypothalamic-pituitary vascular network in such cases. PATIENTS: Eighteen patients (13 males, 5 females) aged 10-26.4 years with unidentified pituitary stalk at first MRI study were evaluated. Eight had isolated GH deficiency (IGHD), and 10 had multiple pituitary hormone defect (MPHD) with the progression to complete anterior pituitary deficits seen by the age of 15 years in 8 patients (1 had GH and FSH-LH deficiency and 1 had GH, TSH and FSH-LH deficiency). RESULTS: The MRI revealed a very thin pituitary stalk in 7 patients (38.8%), 6 with IGHD (75%) and 1 (10%) with MPHD (GH and FSH-LH deficiency), after Gd-DTPA administration. Reassessment of anterior pituitary function showed that the thyroid, adrenal and gonadal functions were intact in the 6 patients with IGHD and pituitary stalk identified by Gd-DTPA as well as in one IGHD patient with no evidence of pituitary stalk. In one 10-year-old with IGHD at the time of presentation (6 years) and no pituitary stalk seen after Gd-DTPA, subclinical hypothalamic hypothyroidism and suspected hypogonadotropic hypogonadism were documented. Partial ACTH deficiency was recorded in the patient with TSH and FSH-LH deficiency with no pituitary stalk. After Gd-DTPA, patients with absent pituitary stalk had a risk of developing MPHD 27 times greater than had those with an identified pituitary stalk (relative risk = 27, 95% confidence interval 1.9-368.4, Fisher's exact test P = 0.009). Dynamic MR images obtained every 4.6 s revealed rapid enhancement of hypothalamic-pituitary structures and allowed the determination of the times to initial enhancement of ectopic posterior pituitary and hypoplastic anterior pituitary which ranged between 9.2 and 18.4 s, and that of complete anterior pituitary (32.2-41.4 s). The time to maximum enhancement of anterior pituitary was significantly longer than in controls (35.5 +/- 3.8 s vs 25.2 +/- 1.6 s, P < 0.0001). CONCLUSIONS: MRI with Gd-DTPA proved more sensitive in identifying the vascular component of pituitary stalk and added new information about the partial preservation of hypothalamo-hypophyseal portal vessels. The vascular pituitary stalk is easily recognized after Gd-DTPA in most IGHD patients, but exceptionally in MPHD; this sheds light on the possible normal course of affected patients. The neural component of the pituitary stalk is lacking regardless of whether patients have IGHD or MPHD, indicating that the term congenital agenesis of the neural pituitary stalk is more appropriate than pituitary stalk interruption. The times to enhancement of ectopic posterior pituitary and residual anterior pituitary obtained by the fast-framing MRI technique disclose dynamic changes in regional blood supply which appear direct, arterial and mainly independent of the portal system.

Development of the neurogliohemal complex in the mouse neurohypophysis.

The mouse neurohypophysis was studied at different ages of development in order to analyse the ultrastructural changes that lead to the maturation of the neurogliohemal complex and to determine the existence of permeability between the blood capillaries and the neurohypophysial channels. In all the studies ages, two groups of 5 animals each were intravenously injected with different tracer solutions: to one group, 10 microliters of cationized ferritin were used and to the other, 10 microliters of ferrous fumarate were applied. For the ultrastructural studies the tissue samples were processed using the conventional techniques for electron microscopy. At day 17 of prenatal age, some hypothalamic axons (10 axonic profiles/20 microns2) were already seen within the neurohypophysis, increasing threefold (26 to 30 axonic profiles/20 microns2) at prenatal day 19. In these axons terminals, the first neurosecretory vesicles began to appear. At this early age, the glial cells formed few prolongations. Between postnatal days 1 and 9, numerous axon terminals containing dense neurosecretory vesicles composed the neuropile areas. After day 9, there was a broadening of the intercellular space, which we have termed as neurohypophysial channels; these were actually expansions of the existing extracellular space in the neurohypophysis. Between days 9 and 21, the population of axon terminals showing a higher density of neurosecretory vesicles continued to increase in number. Some of these axon terminals were separated by irregular neurohypophysial channels. The glial cells showed scarce cytoplasm and formed numerous lamellar prolongations, which became increasingly finer surrounding bundles of individual axons.(ABSTRACT TRUNCATED AT 250 WORDS)

Perivascular microglia in the rat neural lobe engulf magnocellular secretory terminals during osmotic stimulation.

The response of microglia in the rat neural lobe to osmotic stimulation has been studied. Microglia were identified by immunoreactivity for the macrophage markers OX-42 and F4/80. The numerical density of microglia did not change significantly with osmotic stimulation but microglia in the perivascular space partially or completely enclosed significantly greater numbers of neurosecretory terminals in osmotically stimulated animals.

The vascularization of the pituitary gland of the chicken (Gallus domesticus). A scanning electron microscope study of vascular corrosion casts.

Microvascular corrosion casts of the pituitary gland of one to nine-day-old chickens (Gallus domesticus, white leghorn hybrids) were analysed with the scanning electron microscope. Results show that the chicken median eminence is supplied by branches of the infundibular and the neural-lobe arteries. They form a flat two-dimensional primary capillary plexus, which lacks any capillary loops and is continuous with the plexus in the neural lobe. The capillaries occupy about 60% of the total area of the median eminence. A subependymal plexus is present, showing no contact with the plexus of the median eminence. The chicken neural lobe consists of many hollow buds. These buds are supplied by branches of the neural-lobe artery, which gives rise to a two-dimensional capillary meshwork similar to that of the median eminence. An anterior group of portal vessels, comprising 14-16 vessels with a mean diameter of 37 microns, and a posterior group of portal vessels, comprising 2-4 shorter and slightly thinner vessels, arise from the median eminence are the sole blood supply for the adenohypophysis (distal lobe). Anterior portal vessels supply the cephalic lobe and the most rostral area of the caudal lobe, and posterior portal vessels supply the caudal lobe of the distal lobe. There are no short portal vessels connecting the neural lobe with the distal lobe. The (sinusoidal) capillary bed of the distal lobe is laminated. The chicken hypophysis drains into the cavernous sinus, which empties into the cerebral carotid veins. Within the period studied (days 1-9 after hatching) no age-related changes were found.