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Biomedical subjects

J D Glass

Publications and source records attributed to J D Glass.

At least 127 records · Page 7Linked to original sources

Boron neutron capture therapy of a murine melanoma.

Boron neutron capture therapy has been carried out on BALB/c mice carrying the Harding-Passey melanoma s.c. on the thigh. p-Boronophenylalanine (BPA), a boronated analogue of natural melanin precursors, was used to target boron selectively to melanoma. BPA was administered to the mice either via i.p. injection or p.o. by intubation. 10B concentrations in tumor ranged from 15 to 40 ppm depending on the route and timing of administration. Irradiations with a predominantly thermal neutron beam were performed at the Brookhaven Medical Research Reactor. In the absence of BPA, only transient tumor growth delays were observed at low neutron fluences. At 5 x 10(16) n/m2, 4 of 22 tumors irradiated in the absence of BPA underwent long-term tumor growth control; after p.o. administration of BPA (40 ppm 10B in the tumor), the fraction of tumors controlled increased to 11 of 19. The average dose to the tumor in the latter group was 17.8 Gy, of which 14.8 Gy were due to the 10B neutron capture reaction. The biological effectiveness of the absorbed dose from the neutron capture reaction, at the 50% tumor control level, was found to be twice that of 100 kVp X-rays.

Animals↗

Expression and characterization of a truncated murine Fc gamma receptor.

We have isolated a recombinant secreted Fc gamma R beta molecule by deletion of the transmembrane and cytoplasmic domains encoding sequence from a Fc gamma R beta 1 cDNA clone, and insertion of the truncated cDNA into a eukaryotic expression vector, pcEXV-3. To express and amplify the production of the truncated Fc gamma R beta molecule, we transfected the truncated cDNA plasmid into a dihydrofolate reductase-minus CHO cell line along with a dhfr minigene, and amplified the gene products with methotrexate. The resulting cell line secretes 2-3 micrograms/ml/24 h of truncated Fc gamma R beta, which can be readily purified by affinity chromatography on IgG-Sepharose. The truncated Fc gamma R beta has a Mr of 31-33,000 on SDS-PAGE and is glycosylated. N-glycosidase F cleavage reduces the Mr to 19,000, consistent with the size of the truncated product, 176 amino acid residues. There are two disulfide bonds in the protein. Binding of immune complexes formed between DNP20BSA and anti-DNP mAbs reveals better binding of IgG1 aggregates than that of IgG2b and IgG2a aggregates. The binding of the immune complexes was somewhat better at more acidic pH, in contrast to previous experiments with binding of purified Fc gamma R to immune complex-coated beads. We were surprised to observe that the truncated Fc gamma R beta did not react with the anti-Fc gamma R mAb 6B7C. Previous work had shown that 6B7C reacts with Fc gamma R on immunoblots, fails to bind to the surface of resting B cells and peritoneal macrophages, but does bind to macrophage cell lines and LPS-stimulated B cells. We show, by binding of mAb 6B7C to a peptide conjugate, that the 6B7C epitope lies within residues 169-183 of the intact Fc gamma R beta, which is just outside the plasma membrane. The availability of the truncated Fc gamma R beta in microgram quantities should facilitate further analysis of structure and function of these receptors.

Amino Acid Sequence↗

Effects of estradiol on secretion of LH, hypothalamic function and testicular development in bull calves.

Two experiments were conducted in order to determine the effects of estradiol (E2) on the development of the hypothalamic-pituitary-testicular axis in bull calves. In experiment 1, calves were assigned randomly to one of the following groups: 1) intact, 2) intact E2-treated, 3) castrated, or 4) castrated E2-treated. Treatments began when the calves were 7.5 wk of age and continued for 16.5 wk. Samples of blood were collected once a week from 3 to 14 wk of age and every 10 min for 6 hr at 8, 12 and 16 wk of age. Concentrations of E2 in plasma decreased between 3 and 4 wk of age and were further reduced by castration. Maximum concentrations of E2 (24.3 pg/ml) were observed 72 hr after insertion of E2 implants, however, plasma E2 stabilized at 5.9 pg/ml by 2 wk after insertion of E2 implants. Treatment with E2 eliminated the pulsatile secretion of LH in intact and castrated calves and retarded testicular growth. In experiment 2, calves were assigned to a control (n = 4) or E2-treated (n = 6) group. Implants of E2 were inserted at 7.5 wk of age. At 24 wk of age, calves were bled and then sacrificed to collect hypothalamic and pituitary tissues. Age-related changes in testicular weight and secretion of LH were blocked by E2. Neither the morphology nor the intensity of immunostaining of GnRH nerve cell bodies in the preoptic area (POA) were affected by E2. However, the density of GnRH fibers and beads in the stalk median eminence (SME), and concentrations of pituitary GnRH receptors were greater (P less than .01) in E2-treated compared to control calves. In addition, concentrations of norepinephrine (NE) in the SME were lower in E2-treated calves when compared to controls. Based on these observations, it is concluded that administration of E2 at 7.5 wk of age causes profound alterations in hypothalamic function including, changes in metabolism of NE and suppression of GnRH release.

Animals↗

Effects of photoperiod, beta-endorphin, and naloxone on in vitro secretion of testosterone in white-footed mouse (Peromyscus leucopus) testes.

The effects of the pro-opiomelanocortin-derived beta-endorphin (B-EP) and the opioid antagonist naloxone on in vitro secretion (accumulation of testosterone (T) in the medium) of T by testicular cells were assessed in adult white-footed mice (Peromyscus leucopus). Animals were housed under long days (16L:8D) to maintain testicular function or under short days (8L:16D) to induce gonadal regression. In vitro treatment with B-EP or naloxone did not affect basal secretion of T in dispersed cells from active or regressed testes. However, B-EP caused a dose-dependent reduction in secretion of T from cells stimulated maximally with human chorionic gonadotropin (hCG) or dibutyryl cyclic adenosine 3', 5'-monophosphate (dbcAMP). Conversely, naloxone enhanced maximal hCG- and dbcAMP-stimulated secretion of T in testicular incubates from both long- (1.5-fold) and short-day (3.5-fold)-exposed mice. The finding that the addition of naloxone to maximally stimulated cells increased further the secretion of T is evidence that B-EP may act to inhibit gonadotropin-stimulated secretion of T. Also, the stimulatory effect of naloxone on cells from regressed testes indicates that B-EP may be involved in suppressing production of T during the gonadally regressed state. Testicular B-EP-like immunostaining is present within the cytoplasm of interstitial cells and is not apparent in the seminiferous tubules. Together, these results support the idea that in P. leucopus endogenous opioid peptides in the testes may aid in the regulation of testicular function throughout the yearly breeding cycle.

Animals↗

Melatonin does not affect in vitro secretion of testosterone in white-footed mouse testis.

There is evidence that melatonin may exert its antigonadal effect by acting in the gonad to inhibit steroidogenesis. To explore this possibility a hormonally sensitive in vitro system of dispersed Peromyscus leucopus testis was used to assess the effects of melatonin on human chorionic gonadotropin (hCG)- and dibutyryl-cAMP (dbcAMP)-stimulated secretion of testosterone (T). At near-maximally stimulating doses of hCG and dbcAMP, melatonin in concentrations of 2 x 10(-12) M to 2 x 10(-7) M did not affect the rate of secretion of T in cells from active or regressed testes. These results do not support the idea that melatonin helps to regulate seasonal reproduction by acting in the testes to inhibit steroidogenesis.

Animals↗

Photoperiodic adjustments in hypothalamic amines, gonadotropin-releasing hormone, and beta-endorphin in the white-footed mouse.

This study was undertaken to examine short photoperiod (SD; 8 h of light, 16 h of darkness)-induced alterations in reproductive endocrine and neuroendocrine parameters in the male white-footed mouse, Peromyscus leucopus. Exposure to SD for 8 weeks caused dramatic reductions in testis and seminal vesicle weights, decreased circulating LH and testosterone levels, and lowered the content of LH in the pituitary gland relative to those in mice under long photoperiod (LD; 16 h of light, 8 h of darkness). These changes were associated with significant increases in content of radioimmunoassayable GnRH in the mediobasal hypothalamus (MBH) and anterior hypothalamus at two time points in the light/dark cycle: 2100 h (dark phase) and 0900 h (light phase), respectively. Exposure to SD also caused an increase in radioimmunoassayable beta-endorphin in the MBH and preoptic area of the hypothalamus (POA) at 2100 h, but not at 0900 h. Mice exposed to SD also had a significantly higher metabolism of serotonin in the MBH at 0900 and 2100 h compared to mice under LD. The concentration of noradrenaline in the hypothalamus was unaffected by exposure to SD. However, the metabolism of dopamine (DA) in the POA at 0900 h was significantly increased relative to that in mice maintained under LD at this time. This increase in DA metabolism was associated with enhanced immunocytochemical staining for tyrosine hydroxylase in nerve fibers of the POA. Conversely, staining for tyrosine hydroxylase in tuberoinfundibular DA cell bodies of the arcuate nucleus was less intense under SD exposure. From these data it is concluded that exposure to SD caused regional and time-dependent alterations in the activities of hypothalamic amines (serotonin and DA) and neuropeptides (beta-endorphin and GnRH). These changes may be part of the neuroendocrine mechanism for SD-induced seasonal adaptations.

Amines↗

Melatonin acts in the brain to mediate seasonal steroid inhibition of luteinizing hormone secretion in the white-footed mouse (Peromyscus leucopus).

A melatonin-induced supersensitivity of the gonadotropin-secretory system to the negative feedback action of sex steroids is thought to be important to the timing of seasonal reproduction. However, little is known concerning this action of melatonin. In the present study the antigonadal action of melatonin in the anterior hypothalamus (AH) of the white-footed mouse, Peromyscus leucopus, was used to examine the neuroendocrine mechanism whereby melatonin enhances the sensitivity to sex steroid negative feedback. Mice received a melatonin-containing pellet in the AH for 14 weeks, at which time they were castrated and treated sc with a Silastic testosterone (T) capsule for 3 weeks. At the time of castration, weight of the testes and the concentration of T in the blood of mice with a melatonin pellet were greatly reduced compared to mice with a blank (melatonin-free) implant in the AH (P less than 0.01). In mice treated with melatonin the physiological dose of T significantly reduced the concentrations of LH in blood and pituitary (P less than 0.05). This dose of T, however, had little effect on LH in mice with a blank pellet in the AH. Melatonin in the AH markedly increased the content of gonadotropin-releasing hormone (GnRH) in the mediobasal hypothalamus (P less than 0.05) in mice treated with T; however, there was little effect of melatonin and/or T in any other region examined. Melatonin and T had little effect on the contents of immunoreactive beta-endorphin (B-EP) in the hypothalamus, but T alone increased the content of B-EP in the preoptic area. These results are evidence that melatonin and T act in concert to induce the reproductively-quiescent state by suppressing secretion of GnRH from the hypothalamus.

Animals↗

Selective targeting of boronophenylalanine to melanoma in BALB/c mice for neutron capture therapy.

Melanoma cells actively accumulate aromatic amino acids for use as precursors in the synthesis of the pigment melanin. Using the Harding-Passey melanoma carried s.c. in BALB/c mice, we have demonstrated that p-boronophenylalanine (BPA) is taken up by melanoma tissue to a much greater extent than by normal tissues. Following a single i.p. injection, or a series of injections given over 1 h, the accumulation of boron in melanoma was found to be transient, reaching a maximum approximately 6 h postinjection. The concentrations of boron achieved in tumor ranged from 9-33 micrograms/g, and are within the range estimated to be necessary for successful application of the nuclear reaction 10B(n,alpha)7Li for neutron capture therapy. Boron concentrations in tumor and tissues were determined using either a prompt-gamma spectroscopic technique or by quantitative neutron capture radiography using whole-body sections. Distribution studies with the resolved stereoisomers of BPA indicated that the L isomer is preferentially accumulated in the melanoma compared to the D isomer. The L isomer of BPA was shown to be targeted to actively dividing tumor cells by simultaneously comparing the boron and [3H]thymidine distribution in tumor. Under conditions which selectively deliver high concentrations of boron to Harding-Passey melanomas in BALB/c mice, BPA did not deliver useful concentrations of boron to a mammary adenocarcinoma in Hale-Stoner mice. These results, along with the selectivity of the Harding-Passey melanoma for the L isomer of BPA, are consistent with our working hypothesis that BPA is actively transported into the melanomas as an analogue of natural melanin precursors.

Animals↗

[1-Desamino, 7-lysine, 8-arginine]vasotocin: attachment of reporter groups and affinity ligands through the lysine side chain.

The chemically reactive groups of [8-arginine]vasotocin (AVT) are the alpha-amino group in position 1, the phenolic hydroxyl group of the tyrosyl residue in position 2, and the side-chain functional group of the basic amino acid residue in position 8. Acylation or alkylation of any of these chemically reactive groups yields hormone analogues with sharply diminished biological activities in most assay systems. Since none of the chemically reactive groups in the native AVT (or other neurohypophyseal hormone) sequences is a suitable chemical port for acylation with affinity ligands and reporter groups, we have undertaken the rational design of AVT analogues in which a residue capable of being acylated has been incorporated into points of the AVT structure where structural modifications are expected to have as little effect as possible on biological activity. Empirical structure-activity relationships among neurohypophyseal hormone analogues as well as conformational models in solution and in the crystalline state suggest that positions 4 and 7 are likely points for the introduction of acylation ports. We have previously synthesized an analogue of [1-desamino]AVT (dAVT) with a lysyl residue in position 4 ([4-lysine]dAVT) and demonstrated that acylation of the side chain of this residue yields useful reporter and photoaffinity analogues. We now report the synthesis of the corresponding analogue with a lysyl residue in position 7 ([7-lysine]dAVT), which also yields potent acyl derivatives suitable for affinity ligands and photoaffinity ligands.

Animals↗

Covalent labeling of hydrosmotic toad bladder receptors with an antagonist of vasotocin.

A photoreactive analogue of vasotocin, [1-desamino,4-lysine(azidobenzoyl),8-arginine]vasotocin (4-N3-AVT), has been examined in the isolated toad urinary bladder for biological activity and binding to hormonal receptors. Although 4-N3-AVT induced only a small increase in bladder permeability to water, it behaved as a potent inhibitor of hydrosmotic action of [8-arginine]vasotocin (AVT) and [8-arginine]vasopressin (AVP). The inhibitory action of 4-N3-AVT was readily reversed on removal of the analogue from the serosal bathing solution. On the other hand, when bladders were exposed to 4-N3-AVT in the presence of long wavelength UV light (365 nm), the inhibition by 4-N3-AVT was not reversed on washout of the analogue. The dose of vasopressin required for a half-maximal response (ED50 value) was increased from 5 X 10(-9) to 1.3 X 10(-7) M in bladders photolabeled with 4-N3-AVT and the maximal response capacity of the tissue (intrinsic activity) was reduced to 79% of nonphotolabeled controls. A crude membrane preparation derived from bladders photolabeled with 4-N3-AVT contained 72 fmol of specific binding sites for tritium-labeled vasopressin per milligram protein, whereas nonphotolabeled controls had 136 fmol of specific binding sites per milligram protein. These observations suggest that 4-N3-AVT forms a covalent bond with hydrosmotic receptors in the presence of UV light. This is the first antagonistic photoaffinity analogue observed in the toad bladder and it may serve as a useful tool for analyzing the cellular mechanism of action of antidiuretic hormone.

Animals↗

A brain site for the antigonadal action of melatonin in the white-footed mouse (Peromyscus leucopus): involvement of the immunoreactive GnRH neuronal system.

Quantitative assessment of immunocytochemical staining for gonadotropin-releasing hormone (GnRH) was undertaken to determine the effects of an intracranial implant of melatonin on the GnRH neuronal system in the male white-footed mouse (Peromyscus leucopus). Melatonin-containing pellets stereotaxically placed in the anterior hypothalamic area (AH) caused a 60% reduction in testes weight relative to control mice with melatonin-free pellets in the AH (p less than 0.01). Subcutaneous melatonin-containing implants had little effect on reproductive state (p less than 0.8). Melatonin pellets in the AH increased significantly both the optical density (OD) for immunostaining of cell bodies in the medial preoptic area and AH (p less than 0.04), and the percentage of area covered by GnRH fibers and beads in the median eminence (p less than 0.01). The melatonin-induced increase in OD of the GnRH cell bodies was independent of the distance of the cells from the melatonin implant, and there was little apparent effect of melatonin on the size and morphology of the GnRH cell bodies, or the trajectories of their fiber pathways. These results support the hypothesis that the antigonadal action of melatonin in the brain involves suppression of the release, rather than the synthesis of GnRH. Also, this effect may not be mediated via a direct action of melatonin on GnRH neurons. The finding that the brain site and time course for melatonin's antigonadal action in male. P. leucopus is similar to that found previously in the female is evidence that melatonin may induce gonadal regression, in part, by helping to suppress the tonic secretion of gonadotropins.

Animals↗

Synthesis and biological activities of a photoaffinity probe for vasotocin receptors.

This study reports the synthesis and biological activities of 1-desamino, 7-lysine-(4-azidobenzoyl), 8-arginine vasotocin (d7-N3-AVT). This compound was found to be biologically active in the rat antidiuretic assay (20 U/mg), to behave as an antagonist of vasopressin in the rat pressor assay (pA2 = 6.6), and to yield a half-maximal hydroosmotic response in the isolated toad urinary bladder at a bath concentration of 2.4 X 10(-8) M. When toad bladders were exposed to d7-N3-AVT in the presence of long wavelength UV light, the hydroosmotic response persisted in spite of prolonged and repeated periods of washout. By contrast, the hydroosmotic response in control bladders after stimulation with d7-N3-AVT in the absence of UV irradiation was fully reversed within 15 min of washout. A membrane preparation derived from bladders that had been photolabeled with d7-N3-AVT and washed for 1 h specifically bound 325 fmol [3H]vasopressin/mg protein. Matched bladders exposed to the analog in the absence of UV irradiation and washed for 1 h specifically bound 591 fmol [3H]vasopressin per mg of protein. These studies indicate that d7-N3-AVT binds covalently to hydroosmotic receptors of toad urinary bladder and forms a complex that is functional in triggering an increase in the permeability to water of the epithelium. This analog may prove useful in the isolation and purification of vasotocin receptors in lower vertebrates.

Affinity Labels↗

Effects of estradiol and progesterone on the gonadotropin-releasing hormone (GnRH)-immunoreactive neuronal system of the anestrous ewe.

The effects of treatment with estradiol-17 beta (E2) and progesterone (P4) on the neuronal system for gonadotropin-releasing hormone (GnRH) of the ovariectomized ewe during the non-breeding season were examined using immunocytochemical and radioimmunoassay analyses. The majority of GnRH-immunoreactive cell bodies are located in the medial preoptic area (POA). Clusters of labelled cell bodies also are found in the septum and anterior hypothalamus. GnRH fibers projected from the medial POA to a dense fiber plexus in the median eminence (ME). For ewes treated with E2, the percentage of GnRH cell bodies that were multipolar was approximately twice that for ewes not treated with E2 (P less than 0.05). The intensity of immunocytochemical staining in the GnRH cell body, and the incidence of fiber branching close to the cell body also were significantly greater for ewes treated with E2 (P less than 0.01 and P less than 0.05, respectively). The intensity for staining of GnRH in the ME appeared to be greater for ewes not treated with steroid, and this was reflected by a greater density of GnRH fibers in ewes not treated with steroid (P less than 0.05). The mass of GnRH in the ME of the ewes not treated with E2 was approximately twice that for E2-treated ewes; however, there was little difference in the total contents of GnRH in the hypothalamus and POA between E2 and non-E2-treated ewes.(ABSTRACT TRUNCATED AT 250 WORDS)

Anestrus↗

Prepubertal changes in the hypothalamic-pituitary axis of Holstein bulls.

We investigated the nature and sites of changes in the hypothalamic-pituitary axis associated with the onset of high-frequency, high-amplitude discharges of luteinizing hormone (LH) in young bulls during the transition from the infantile to the prepubertal phase of development. Blood serum and neuroendocrine tissues from bulls killed at 1, 6, 10, 14, or 18 wk of age were evaluated. Concentrations of LH in serum from bulls 1 or 6 wk old averaged less than 0.25 ng/ml and only one episodic discharge of LH was detected for 10 bulls. At 10, 14, or 18 wk, 14 of 15 bulls had episodic discharges of LH. Concentrations of testosterone in serum were progressively higher at 10, 14, and 18 wk, but the concentration of estradiol was maximal at 6 wk. The concentrations of gonadotropin-releasing hormone (GnRH) in the anterior hypothalamus, posterior hypothalamus, or median eminence were not influenced by age. However, concentration of GnRH receptors in the anterior pituitary gland increased 314% between 6 and 10 wk and the concentration of LH increased 67%. Between 6 and 10 wk, concentrations of estradiol receptors in the anterior and posterior hypothalamus declined by 68% and 46%, but the concentration of estradiol receptors in the anterior pituitary gland increased by 103%. For most characteristics, there was no major change between 10 and 18 wk. We postulate that between 6 and 10 wk of age, there is 1) removal of an estradiol-mediated block of GnRH secretion and 2) an estradiol-mediated, and possibly GnRH-mediated, increase in pituitary GnRH receptors. Together, these changes result in greatly increased stimulation of the anterior pituitary gland by GnRH between 6 and 10 wk of age and stimulation of the discharges of LH characteristic of bulls in the early prepubertal phase of development.

Animals↗

Short photoperiod-induced gonadal regression: effects on the gonadotropin-releasing hormone (GnRH) neuronal system of the white-footed mouse, Peromyscus leucopus.

The peroxidase-antiperoxidase method was used to determine quantitatively the effect of short photoperiod-induced gonadal regression on the immunoreactive gonadotropin-releasing hormone (GnRH) neuronal system of female Peromyscus leucopus. In mice exposed to either long (16L:8D) or short (8L:16D) photoperiod, immunoreactive cell bodies were loosely organized into six groups: olfactory peduncle, diagonal band of Broca, septum, preoptic area (POA), anterior hypothalamus (AH), and basal hypothalamus. The POA and AH contain the largest number of cell bodies, which supply the major GnRH innervation to the median eminence (ME) and several extrahypothalamic brain sites. Exposure to short photoperiod increased the number of immunoreactive cell bodies within the anterior hypothalamus and preoptic area (AHPOA) and also increased the optical density for staining of immunoreactive cell bodies in the AHPOA and olfactory peduncle. The ME of mice exposed to short photoperiod had a higher density of GnRH fibers relative to that of mice exposed to long photoperiod, and the content of GnRH fibers in the rostral ME was correlated with the optical content for immunostaining of cell bodies in the AHPOA. These results are evidence that gonadal regression induced by short photoperiod (mediated by the pineal gland) involves alterations of GnRH neuronal activity. Notably, data from this study are consistent with the hypothesis that suppressed release of GnRH from neurovascular terminals in the ME, rather than lack of availability of the decapeptide, promotes gonadal regression.

Animals↗

Desaminopenicillamine tocinoic acid derivatives--inhibitors of oxytocin.

Tocinoic acid analogs with penicillamine in place of one or both of the cysteine residues have been studied and [1-beta-mercaptopropionic acid, 6-penicillamine] tocinoic acid (dPen6TA) and [1-beta,beta-dimethyl-beta-mercaptopropionic acid, 6-penicillamine] tocinoic acid (dPen1Pen6TA) have been synthesized in solution. Biological activities of these 2 compounds and those of the previously synthesized [1-beta,beta-dimethyl-beta-mercaptopropionic acid] tocinoic acid (dPen1TA) have been assayed. It was found that dPen1TA and dPen1Pen6TA, both of which have a beta,beta-dimethyl-beta-mercaptopropionic acid in position 1, are strong inhibitors of the uterine activity of oxytocin in vitro (without Mg2+) with pA2 values of 7.1 and 7.8, respectively, whereas dPen6TA with penicillamine in position 6 is a mild agonist.

Amino Acid Sequence↗

Gonadotropin-releasing hormone neuronal system of the white-footed mouse, Peromyscus leucopus.

The cytoarchitecture of the gonadotropin-releasing hormone (GnRH) neuronal system of the female white-footed mouse (Peromyscus leucopus) was characterized using immunocytochemical procedures on thick vibratome sections. Most of the labelled cell bodies are organized loosely into three groups associated with the periventricular region of the medial preoptic area, the diagonal band of Broca, and the olfactory peduncle. A small number of cells are scattered throughout the medial septum, retrochiasmatic area, and in the posterior hypothalamus, lateral from the median eminence (ME). Labelled fibers are distributed widely throughout the brain, with heavy concentrations within the ME and the organum vasculosum of the lamina terminalis (OVLT). A subchiasmatic pathway for GnRH fibers, which courses from the OVLT to the ME, was identified. Fiber plexuses are present in the olfactory bulbs, accessory olfactory bulbs, triangular nucleus of the septum, medial habenular nucleus, and the amygdala. The ependymal layer of the third ventricle that is associated with the ME and OVLT contains large numbers of GnRH fibers, some of which appear to extend into the ventricular lumen. The wide dispersion of the GnRH neuronal system throughout the brain of P. leucopus is evidence that, in addition to its role as a gonadotropin-releasing hormone, GnRH may have a neurophysiologic function in the central nervous system of this species.

Animals↗