The ultrastructure of small blood vessels of the posterior pituitary gland in relation to neurosecretion.
Explore the source record for details and available documents.
SEARCH · PubMed Health
Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
This study was designed to determine the relative contribution of vasopressin-secreting nerve terminals in the median eminence compared to those in posterior pituitary to the high concentrations of the hormone in hypophysial portal blood. Vasopressin was measured by radioimmunoassay in plasma obtained by microcannulation of individual long portal veins of 8 intact male Long-Evans rats (2.0 +/- 0.44 ng/ml SEM), and in 8 in which the posterior pituitary was removed just prior to collection (1.5 +/- 0.3 ng/ml SEM). Since there was no significant difference /p = 0.23, NS) in the concentration of vasopressin in portal plasma after removal of the posterior pituitary gland, these results suggest that the direct vasopressin pathway to the median eminence is the major source of vasopressin in portal blood of the rat.
The present experiments were performed to examine the effects of a new muscarinic M1-receptor agonist, (-)-YM796 ((-)-S-2,8-dimethyl-3-methylene-1-oxa-8-azaspiro[4.5]decane L-tartrate monohydrate), on yawning and oxytocin secretion from the posterior pituitary gland in rats YM796, at doses of 2.5-50 mg/kg (SC), elicited yawning. The yawning response was markedly increased by pretreatment with a beta-adrenoceptor antagonist, pindolol (20 mg/kg, IP), which per se did not elicit yawning. The yawning induced by YM796 (10 mg/kg, SC) in combination with pindolol (20 mg/kg, IP) was inhibited by scopolamine (0.5 mg/kg, SC), a muscarinic receptor antagonist, and pirenzcpine (300 micrograms/ rat, ICV) and EEDQ (N-ethoxycarbonyl-2-ethoxy-1,2-dihydroquinoline) (5 mg/kg, IP), muscarinic M1-receptor antagonists, but not by spiperone (0.5 mg/kg, SC), a dopamine D2-receptor antagonist, 4-DAMP (4-diphenylacetoxy-N-methylpiperidine methiodide) (100 micrograms/rat, ICV), a muscarinic M3-receptor antagonist, and [d(CH2)5, Tyr(Mc)2, Orn8]-vasotocin (100 ng/rat, ICV), an oxytocin receptor antagonist. YM796 at 2.5-50 mg/kg (SC) did not exert an action on prolactin levels but increased oxytocin secretion from the posterior pituitary gland in rats. This augmentation of oxytocin secretion by YM796 was inhibited by scopolamine (0.5 mg/kg, SC) and pirenzepine (3 mg/kg, SC), but not by mecamylamine (1 mg/kg, IP), a nicotinic receptor antagonist. The present findings obtained with YM796 suggest that the muscarinic M2-receptor stimulation participates in causing yawning behavior and oxytocin secretion in rats.
We describe three cases of central diabetes insipidus, each with a different pathogenesis, in which unexpected hyperintensity of the posterior pituitary gland was seen on T1-weighted MR images obtained at the time of presentation. In the first case (idiopathic), the posterior pituitary signal persisted more than 10 years; in the second case (Langerhans cell histiocytosis), the signal disappeared within 3 months, despite early specific chemotherapy with etoposide; and in the third case (transient), the posterior signal disappeared within 1 year, but it was documented at the time of spontaneous reversal of polyuria and polydipsia.
Magnetic resonance imaging in two children with idiopathic hypopituitarism demonstrated a signal of high intensity near the optic tract that was consistent with the signal produced by posterior pituitary tissue. Patient 1 was a 15-year-old girl with panhypopituitarism but intact posterior pituitary function. Computed tomography disclosed widening of the superior aspect of the pituitary stalk and a partially empty sella. Magnetic resonance imaging disclosed a 3-mm high-intensity signal abutting the optic tract in the midline just above the sella. The pituitary stalk was not clearly defined, the pituitary gland was small, and the sella was filled with cerebrospinal fluid. Patient 2 was a 12-year-old boy with isolated deficiency of growth hormone secretion. Findings from magnetic resonance imaging and computed tomography were similar to those in patient 1. These data suggest that the high-intensity magnetic resonance imaging findings represent a displaced or "ectopic" posterior pituitary gland, and that the hypopituitary state is due to an insult to the pituitary stalk.
Neurons comprising the endocrine hypothalamus are disposed in several nuclei that develop in tandem with their ultimate target the pituitary gland, and arise from a primordium in which three related class III POU domain factors, Brn-2, Brn-4, and Brn-1, are initially coexpressed. Subsequently, these factors exhibit stratified patterns of ontogenic expression, correlating with the appearance of distinct neuropeptides that define three major endocrine hypothalamic cell types. Strikingly, deletion of the Brn-2 genomic locus results in loss of endocrine hypothalamic nuclei and the posterior pituitary gland. Lack of Brn-2 does not affect initial hypothalamic developmental events, but instead results in a failure of differentiation to mature neurosecretory neurons of the paraventricular and supraoptic nuclei, characterized by an inability to activate genes encoding regulatory neuropeptides or to make correct axonal projections, with subsequent loss of these neurons. Thus, both neuronal and endocrine components of the hypothalamic-pituitary axis are critically dependent on the action of specific POU domain factors at a penultimate step in the sequential events that underlie the appearance of mature cellular phenotypes.
A 78-year-old man had extensive necrosis of the posterior lobe of the pituitary at autopsy. The anterior lobe was normal. This pattern of damage to the posterior lobe has not been described to date.
Opioid receptor binding was measured in cryostat sections of supraoptic nucleus (SON) and posterior pituitary of virgin and pregnant rats by quantitative receptor autoradiography after in vitro incubation with [3H]etorphine or [3H](-)-bremazocine in the presence of unlabelled sub-type-selective agonists. Mu-selective [3H]etorphine-binding in the SON was reduced on the last day (21) of pregnancy vs. virgin controls (9.9 +/- 2.2 vs. 31.7 +/- 6.5 fmol/mg). Kappa-selective [3H](-)-bremazocine binding to the SON was not altered by pregnancy. Kappa-selective [3H](-)-bremazocine-binding to the posterior pituitary was less on day 16 of pregnancy vs. virgin females (19.1 +2- 5.2 vs. 74.4 +/- 16.2 fmol/mg). The results suggest mechanisms for the changes in actions of opioids on oxytocin neurones in pregnancy.
The characteristics of atropine-sensitive binding of l-[3H]-quinuclidinyl benzilate ([3H]-QNB) to membrane suspensions of sheep posterior pituitary indicate that the binding sites represent muscarinic cholinergic receptors. Scatchard plots of 6 saturation experiments showed a single class of binding sites, with an equilibrium dissociation constant of 16 +/- 2 pM and a density equivalent to 1.8 +/- 0.2 pmol/g wet weight of tissue. Kinetic analysis of 2 association and 3 dissociation curves yielded mean association and dissociation rate constants of 3.9 x 10(8) M-1 min-1 and 4.3 x 10(-3) min-1, respectively. The binding had a detailed pharmacology for 12 drugs consistent with muscarinic receptor identification. In rat neurointermediate lobes, superior cervical ganglionectomy had no demonstrable effect on [3H]-QNB binding. The location(s) and functional role(s) of neurohypophyseal muscarinic receptors remain to be elucidated.
Tuberohypophysial dopamine (DA) neurons terminate in the intermediate and neural lobes of the posterior pituitary. The objective of this study was to determine if concentrations of 3,4-dihydroxyphenylacetic acid (DOPAC), a major metabolite of DA in these regions, reflect the activity of tuberohypophysial DA neurons. The concentrations of DOPAC and DA in the intermediate lobe were approximately twice those in the neural lobe, so that the ratios of DOPAC/DA were similar between lobes. The administration of a monoamine oxidase inhibitor pargyline produced a rapid decline (by 5 min) of DOPAC concentrations in both the intermediate and neural lobes. The administration of nomifensine, an inhibitor of DA uptake at the nerve terminal, produced a modest 33% decline in DOPAC concentrations in the intermediate lobe, but was without effect in the neural lobe. Activation of tuberohypophysial DA neurons by electrical stimulation of the pituitary stalk increased both the rate of DA synthesis (accumulation of dihydroxyphenylalanine (DOPA) after administration of the decarboxylase inhibitor NSD 1015) and the concentrations of DOPAC in the intermediate and neural lobes. Administration of the DA antagonist haloperidol increased, and the DA agonist apomorphine decreased both the rate of DOPA accumulation and DOPAC concentrations in the intermediate lobe but not the neural lobe. The results of the present study demonstrate that: (1) elimination of DOPAC from the intermediate lobe and neural lobe is rapid and alterations in DOPAC concentrations reflect dynamic changes in metabolism of DA; (2) DA which is released and recaptured is a minor contributor to DOPAC concentrations; and (3) alterations in the activity of tuberohypophysial DA neurons are accompanied by corresponding changes in DOPAC concentrations.(ABSTRACT TRUNCATED AT 250 WORDS)
A galanin-like peptide (GALP) was recently isolated as a ligand of GalR2, a galanin receptor subtype. The GALP mRNA is expressed in the arcuate nucleus of the hypothalamus and the posterior pituitary (PP). In this study, we demonstrated the localization of GALP-immunoreactive (-ir) cells in the rat PP. In normal conditions, a few GALP-ir cells were detected in the PP, and these cells increased on dehydration for 4 days. The GALP-immunopositive reaction was dramatically enhanced by the intraperitoneal injection of colchicine. For the identification of GALP-ir cells in the PP, we performed electron microscopic observation, and also double immunocytochemical staining for GALP and S-100 protein. Both studies clearly indicated that the GALP-ir cells in the PP are pituicytes.
Galanin-like peptide (GALP) was recently isolated from the porcine hypothalamus. The GALP mRNA is restricted in the hypothalamic arcuate nucleus and pituicytes in the posterior pituitary grand (PP) of the rat. The physiological function of the GALP is not clear in both areas. We focused on the regulation of the GALP gene expression to determine the role of GALP in the PP. We examined the effects of potent stressors to modulate a pituitary function, nociceptive stimuli and acute and chronic inflammatory stresses on the expression of the GALP gene in the PP using in situ hybridization histochemistry. Subcutaneous (s.c.) injection of 5% formalin in the bilateral hind paws caused a moderate increase of GALP gene expression in the PP. Intraperitoneal (i.p.) injection of lipopolysaccharide (LPS) also caused a marked increase of GALP gene expression in the PP. Effects of i.p. injection of LPS on the expression of the GALP gene in the PP were attenuated by pretreatment with i.p. injection of indomethacin. The levels of GALP mRNA in the PP were markedly increased by two peaks at 24 h and 15 days after s.c. injection of heat-inactivated M. butyricum that induced adjuvant arthritis. These results suggested that inflammatory stresses may be a potent stimulant to induce the expression of the GALP gene in the PP.