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PubMed2006

Luteinization of porcine preovulatory follicles leads to systematic changes in follicular gene expression.

The LH surge initiates the luteinization of preovulatory follicles and causes hormonal and structural changes that ultimately lead to ovulation and the formation of corpora lutea. The objective of the study was to examine gene expression in ovarian follicles (n = 11) collected from pigs (Sus scrofa domestica) approaching estrus (estrogenic preovulatory follicle; n = 6 follicles from two sows) and in ovarian follicles collected from pigs on the second day of estrus (preovulatory follicles that were luteinized but had not ovulated; n = 5 follicles from two sows). The follicular status within each follicle was confirmed by follicular fluid analyses of estradiol and progesterone ratios. Microarrays were made from expressed sequence tags that were isolated from cDNA libraries of porcine ovary. Gene expression was measured by hybridization of fluorescently labeled cDNA (preovulatory estrogenic or -luteinized) to the microarray. Microarray analyses detected 107 and 43 genes whose expression was decreased or increased (respectively) during the transition from preovulatory estrogenic to -luteinized (P<0.01). Cells within preovulatory estrogenic follicles had a gene-expression profile of proliferative and metabolically active cells that were responding to oxidative stress. Cells within preovulatory luteinized follicles had a gene-expression profile of nonproliferative and migratory cells with angiogenic properties. Approximately, 40% of the discovered genes had unknown function.

Animals↗

PubMed2007

Molecular control of ovulation and luteinization in the primate follicle.

In recent years, significant progress was made, particularly through the use of the macaque monkey, in identifying three types of local factors that are induced by the midcycle LH surge and play a critical role in ovulation and/or luteinization of the primate follicle. The ovulatory gonadotropin surge increases prostaglandin (PTG, typically abbreviated PG) levels in follicles prior to rupture; although considerable attention has focused on LH stimulation of the "inducible" form of PG G/H synthase (PTGS2), other aspects of PG synthesis (notably a phospholipase A2, cPLA2, and a PGE synthase, PTGES) and metabolism (15-hydroxy PG dehydrogenase, HPGD) also appear LH-regulated and may control the timing of the PG rise in the ovulatory follicle. Local (intrafollicular) ablation and replacement of PGs suggests that PGE2 is essential for release of the oocyte; but not necessarily for follicle rupture, and not for luteinization. Novel PGE-regulated genes are being identified in macaque granulosa cells, including adipose differentiation-related protein (ADFP). Similar types of studies indicate that the rise in progesterone (P) synthesis, as well as the induction of the genomic P receptor in granulosa cells, is essential for both ovulation and luteinization of the primate follicle. Limited data suggest that P action controls cell cycle activity (via cyclin B1 and cyclin-dependent kinase inhibitor p27), cholesterol uptake and utilization (e.g., low density lipoprotein or LDL receptor), proteases and their inhibitors (matrix metalloproteinase or MMP1; tissue inhibitor of MMP or TIMP1) and cell health in the granulosa cell layer. Finally, members of two classes of angiogenic factors, originally proposed as important for embryonic and pathologic (tumorigenic) vasculogenesis, appear induced in the granulosa layer of the preovulatory follicle, i.e., vascular endothelial growth factor (VEGF) and angiopoietin (ANGPT). Local injection of antagonists to VEGF (soluble VEGF receptor) and ANGPT (the natural antagonist ANGPT2) into the preovulatory follicle suppressed ovulation and luteinization in monkeys, possibly by disrupting the structure-function of existing vessels or preventing angiogenesis in the avascular granulosa layer. Further studies using high-throughput genomic and proteomic analysis, particularly on specific cell types (e.g., granulosa, theca and microvascular cells) and distinct follicular regions (apex, base and cumulus-oocyte complex) of the dominant follicle in natural menstrual cycles, are needed. Such information is essential to advance our understanding of the cascade of events leading to ovulation and luteinization of the primate follicle, to unravel the causes of ovary-based infertility and to consider novel ovary-selective approaches to contraception.

Angiogenic Proteins↗

PubMed2000

Impaired insulin action on granulosa-lutein cells in women with polycystic ovary syndrome and insulin resistance.

We studied the in vitro response to insulin of granulosa-lutein cells derived from patients with polycystic ovary syndrome (PCOS) and clinically defined insulin resistance. Insulin sensitivity was assessed by continuous infusion of glucose with model assessment test (CIGMA). Insulin resistant (PCOS-IR; n = 8), noninsulin resistant (PCOS-NIR; n = 9) patients with PCOS, and women with tubal factor infertility (TF; n = 8) underwent controlled ovarian stimulation with long-term gonadotropin-releasing hormone (GnRH) agonist, recombinant follicle stimulating hormone (FSH), and in vitro fertilization. Primary cultures of granulosa-lutein cells were incubated with insulin (10, 100, 500 ng/ml) and/or luteinizing hormone (LH) (10, 100 ng/ml) in the presence of low density lipoprotein (100 micrograms/ml). The progesterone and lactate accumulation were measured in the culture medium. LH potently stimulated the progesterone secretion in all groups. Insulin alone had no effect on progesterone release in any of the groups, but stimulated lactate formation in the PCOS-NIR and TF groups. Insulin augmented the effect of LH on progesterone secretion selectively in the PCOS-NIR group. The expression of the insulin receptor was determined by Western blotting in separate cultures of granulosa-lutein cells, and showed receptor down-regulation in the PCOS-IR patients. We infer that the in vitro effect of insulin on progesterone and lactate release by granulosa-lutein cells is impaired in insulin resistant PCOS patients.

Androstenedione↗

PubMed1977

Luteinizing hormone and testosterone concentrations in plasma of bull calves treated with gonadotropin releasing hormone.

Twelve bull calves, 2 to 24 days of age, were assigned to two groups of six calves and administered a single 50 microng intramuscular injection of gonadotropin releasing hormone. Bull calves in group 1 were 2 to 5 days of age (mean 3.0 days), and bull calves in group 2 were 10 to 24 days of age (mean 17.1 days). Blood plasma for radioimmunoassay of luteinizing hormone and testosterone was collected at .5-h intervals for 3-h and at 4- and 6-h following treatment. With increasing age, preinjection luteinizing hormone concentrations in plasma decreased while preinjection testosterone concentrations increased. Mean preinjection luteinizing hormone concentrations for group 1 (1.01 +/- .07 ng/ml; mean +/- standard error) were higher than for group 2 (.61 +/- .12 ng/ml). Preinjection luteinizing hormone and testosterone concentrations were correlated--.63. Following treatment, luteinizing hormone increased with mean peak concentrations of 7.28 +/- .74 and 6.95 +/- 1.79 ng/ml for groups 1 and 2. Peak testosterone response following gonadotropin releasing hormone was higher for group 2 than 1 (1077 +/- 253 versus 436 +/- 116 pg/ml).

Animals↗

PubMed1980

Effect of carrier and administration on luteinizing hormone release by gonadotropin releasing hormone.

Ovariectomized ewes in groups of four were administered either saline (I) or 50 micrograms of gonadotropin releasing hormone (II to VII). Methods of administration and carriers were : II, intramuscular saline; III, intravenous saline; IV, subcutaneous saline; V, subcutaneous gelatin; VI, subcutaneous carboxymethylcellulose; and VII, subcutaneous gelatin capsule. Only subcutaneous administration of gonadotropin releasing hormone in the gelatin capsule (VII) prolonged the interval from treatment to luteinizing hormone peak; however, there were fewer ewes with peak luteinizing hormone concentrations equal to or greater than 100 ng/ml in VII than II, IV, V, and VI. Ewes in V, VI, and VII had luteinizing hormone surges of longer duration than II and III. Ewes in VII had the longest luteinizing hormone surge, which was 7.5 h, even though luteinizing hormone concentrations did not return to pretreatment concentrations by 8 h posttreatment in three of the four ewes.

Animals↗

PubMed1984

Secretion of luteinizing hormone and follicle-stimulating hormone from overfeeding dairy heifers.

Secretory effects of gonadotropins and various ovarian and uterine measurements were investigated in 22 prepubertal or postpubertal dairy heifers fed a concentrate to forage ration (60:40) in restricted or ad libitum amounts until they gained 125 kg. Average daily gain of heifers on restricted feeding was 613 g compared with 1218 g for heifers fed for ad libitum intake. During three stages of the experiment blood was collected either at 30-min intervals for two 4-h periods (Stage I and III) or at frequent intervals before and after an injection of luteinizing hormone-releasing hormone (Stage II). At the end of Stage III, all heifers were slaughtered, and ovaries and uteri were collected. Of the variables measured in ovaries and uteri, nutrition affected only number of uterine caruncles (76.5 in ad libitum versus 59.7 in restricted-fed heifers). Excess feeding increased frequency of luteinizing hormone pulses during Stage I but not during Stage II. However, amplitude baseline and overall concentrations of luteinizing hormone were unaffected. Release of luteinizing hormone induced by luteinizing hormone-releasing hormone was reduced in heifers with ad libitum intake. Secretion of follicle-stimulating hormone was not affected by overfeeding.

Animals↗

PubMed2000

Influence of lutein supplementation on macular pigment, assessed with two objective techniques.

PURPOSE: Macular pigment (MP) may protect against age-related macular degeneration. This study was conducted to determine the extent of changes in the macular pigment density as a consequence of oral supplementation with lutein. A second purpose was to compare two objective measurement techniques. METHODS: In the first technique, reflectance maps were made with a scanning laser ophthalmoscope. Digital subtraction of log reflectance maps and comparison between the foveal area and a 14 degrees temporal site provided MP density estimates. In the second technique, spectral fundus reflectance of the fovea was measured with a fundus reflectometer and analyzed with a detailed optical model, to arrive at MP density values. Eight subjects participated in this study. They took 10 mg lutein per day for 12 weeks. Plasma lutein concentration was measured at 4-week intervals. RESULTS: After 4 weeks, mean blood level of lutein had increased from 0.18 to 0.90 microM. It stayed at this level throughout the intake period and declined to 0.28 microM 4 weeks after termination. Measurement of the density of MP showed a within-subject variation of 10% with MP maps and 17% with spectral reflectance analysis. MP density showed a mean linear 4-week increase of 5.3% (P: < 0.001) and 4.1% (P: = 0. 022), respectively. CONCLUSIONS: Supplementation with lutein significantly increased the density of the MP. Analyzing reflectance maps with a scanning laser ophthalmoscope provided very reliable estimates of MP.

Adolescent↗

PubMed2001

Macular pigment and lutein supplementation in retinitis pigmentosa and Usher syndrome.

PURPOSE: To determine macular pigment (MP) in patients with inherited retinal degeneration and the response of MP and vision to supplementation of lutein. METHODS: Patients with retinitis pigmentosa (RP) or Usher syndrome and normal subjects had MP optical density profiles measured with heterochromatic flicker photometry. Serum carotenoids, visual acuity, foveal sensitivity, and retinal thickness (by optical coherence tomography [OCT]) were quantified. The effects on MP and central vision of 6 months of lutein supplementation at 20 mg/d were determined. RESULTS: MP density in the patients as a group did not differ from normal. Among patients with lower MP, there was a higher percentage of females, smokers, and light-colored irides. Disease expression tended to be more severe in patients with lower MP. Inner retinal thickness by OCT correlated positively with MP density in the patients. After supplementation, all participants showed an increase in serum lutein. Only approximately half the patients showed a statistically significant increase in MP. Retinal nonresponders had slightly greater disease severity but were otherwise not distinguishable from responders. Central vision was unchanged after supplementation. CONCLUSIONS: Factors previously associated with lower or higher MP density in normal subjects showed similar associations in RP and Usher syndrome. In addition, MP in patients may be affected by stage of retinal disease, especially that leading to abnormal foveal architecture. MP could be augmented by supplemental lutein in many but not all patients. There was no change in central vision after 6 months of lutein supplementation, but long-term influences on the natural history of these retinal degenerations require further study.

Adolescent↗

PubMed2006

The retinal carotenoids zeaxanthin and lutein scavenge superoxide and hydroxyl radicals: a chemiluminescence and ESR study.

PURPOSE: Carotenoids are present in many biological systems, often decreasing the formation of products of oxidative damage to biological molecules. In the macula their concentration is so high that it has been believed that the yellow color filters out damaging blue light. Recent reports that dietary lutein reduces the risk of cataract in the eye lens suggested that the antioxidant action of carotenoids, which has been inferred from decreased oxidative damage, warranted further direct investigation. METHODS: Superoxide and hydroxyl radical scavenging by lutein and zeaxanthin (retinal carotenoids), beta-carotene, lycopene, lutein esters (from marigolds), and a commercial mixture of soy carotenoids were compared to scavenging by ascorbate and ascorbyl palmitate. Radical scavenging was measured with a chemiluminescent assay (luminol) and by electron spin resonance, ESR. Inhibitory concentrations, IC(50), were determined with the luminescent assay. RESULTS: All of the carotenoids scavenged both superoxide (in ESR 30-50% at 16.7 microM) and hydroxyl radicals (in ESR 50-70% at 16.7 microM, in a luminescent assay 90-99%). CONCLUSIONS: While crocin may be unable to scavenge superoxide, some of the other carotenoids do so quite effectively. The mixtures of 15,15'-cis and all-trans-carotenoids studied by ESR and luminescent assay scavenge both superoxide and hydroxyl radicals. Lycopene and beta-carotene both scavenge superoxide more effectively than the xanthophylls of the retina, zeaxanthin and lutein. All of the carotenoids examined scavenged the hydroxyl radicals more effectively than superoxide radicals. The predominant carotenoid in the fovea of the retina, zeaxanthin, scavenged hydroxyl radicals more effectively than the other retinal carotenoid, lutein. Possible mechanisms of radical scavenging by the carotenoids are discussed.

Electron Spin Resonance Spectroscopy↗

PubMed1986

Effect of cortisol on luteinizing hormone release during sexual behavior in the boar.

The effect of inhibiting the rise in cortisol concentrations that occurs at copulation upon luteinizing hormone release was studied in seven adult boars. Plasma samples were collected for assay of luteinizing hormone, testosterone and cortisol on a control day and before, during and after exposure to an estrous sow. The area under the curve was used to evaluate hormone production and treatment effects were evaluated by a paired Student's t-test. The 11 beta-hydroxylase inhibitor, metyrapone, was used to suppress glucocorticoid hormone production. Cortisol concentrations increased significantly (p less than 0.05) after breeding compared to values on the control day while treatment with metyrapone prior to breeding prevented the cortisol increase (p greater than 0.05). Although luteinizing hormone production increased significantly after copulation in both breeding experiments, metyrapone pretreatment resulted in a reduction of luteinizing hormone secretion (p less than 0.05). Testosterone production was also reduced in boars pretreated with metyrapone. The results suggest that the increased levels of cortisol occurring at copulation may enhance luteinizing hormone release in boars.

Animals↗

PubMed1984

Effect of estrogens on luteinizing hormone release in testicular feminization syndrome before and after gonadectomy.

The effect of exogenous estrogens on luteinizing hormone release was studied in three siblings with complete testicular feminization syndrome. Two subjects, 21 and 20 years old, were postpubertal. The third, 15 years old, was in the early pubertal stage. An estrogen provocation test was performed in which 20 mg of conjugated estrogens were administered intravenously and serum follicle-stimulating hormone and luteinizing hormone levels were assessed every 12 hours for 96 hours under basal conditions, on day 5 of an eight-day treatment with 0.2 mg/day ethinyl estradiol orally, and on day 5 of a subsequent eight-day treatment with 0.2 mg/day ethinyl estradiol and 120 mg/day cyproterone acetate orally. The first two tests were repeated one month after gonadectomy. During pregonadectomy treatments there was an overall luteinizing hormone fall. After gonadectomy, the two postpubertal subjects exhibited luteinizing hormone surges during ethinyl estradiol treatment -in one as a single peak and in the other as multiple peaks. A positive feedback effect was not induced in the youngest patient either before or after gonadectomy as in normal prepubertal and early pubertal females. The data suggest that testosterone or some other testicular factor inhibits estrogen induced positive feedback for luteinizing hormone. This inhibition mechanism acts independently of the testosterone cytosol receptor.

Adolescent↗

PubMed1982

A priming effect of gonadotrophin releasing hormone on luteinizing hormone secretion in the boar.

The possibility that gonadotrophin releasing hormone (GnRH) can prime the anterior pituitary to a second dose of GnRH resulting in a greatly enhanced secretion of luteinizing hormone was examined in three adult boars. Four experiments were conducted: saline injection followed one hour later by a second saline injection (control); 1 microgram of synthetic GnRH injection followed one hour later by saline injection; saline injection followed one hour later by GnRH injection; GnRH injection followed one hour later by a second GnRH injection. Immunoassayable levels of plasma luteinizing hormone resulting from GnRH plus GnRH treatment were significantly greater than the sum obtained when values from GnRH plus saline and saline plus GnRH were added. Testosterone values in plasma reached maximal concentrations about 60 minutes after peak values of luteinizing hormone were achieved. The results suggest that the first dose of GnRH, in addition to stimulating release of luteinizing hormone can also sensitize the gonadotrophs to a second dose of GnRH causing a significantly greater release of luteinizing hormone.

Animals↗

PubMed1975

Structural modifications of lutein cell gap junctions during pregnancy in the rat and the mouse.

By use of lanthanum tracer and freeze-fracture procedures it was found that granulosa-lutein cells of the pregnant mouse and rat ovaries are connected by gap junctions and septate-like zones of contact. Lutein cell gap junctions enlarge and become partially internalized by the end of the first week of gestation. Expansion of the gap junction domain appears to be due initially to intercalation of particles along borders of small gap junctions devoid of smaller non-junctional particles. The number of gap junction lined processes appearing at the cell border increases concomitantly with hypertrophy of the lutein cell during the second week of pregnancy. Strands of particulate or grooved membrane emanate from the margin of larger gap junctions undergoing interiorization. Most large gap junctions are intimately associated with elements of the smooth endoplasmic reticulum. Spherical gap junctional profiles assume a deeper location in the lutein cell and may form concentric arrays by term while true surface gap junctions appear to fragment in the post-partum corpus luteum. The modifications observed are interpreted with respect to biogenesis of the gap junction and the hormonal control of lutein cell function.

Animals↗

PubMed1996

Expression of follicle-stimulating hormone-receptor mRNA alternate transcripts in bovine granulosa cells during luteinization in vivo and in vitro.

In cattle, as in many other species, formation of the corpus luteum is associated with loss of sensitivity to FSH. To determine whether this is associated with changes in FSH-receptor mRNA levels or alternate splicing of the primary transcript, reverse transcription and the polymerase chain reaction (RT-PCR) were used to examine transcripts during granulosa cell luteinization in vivo and in vitro. Using RT-PCR and Southern blotting, three alternate transcripts of the FSH-receptor were found consistently in bovine granulosa cells. The largest transcript encoded the full-length receptor while the other transcripts lacked either exon 9 or exons 4, 5 and 9. One day after luteinization in vivo, full-length FSH-receptor mRNA was detectable at low levels in the newly-formed corpus luteum. By day 3, however, no full-length transcripts were detectable in the corpus luteum. In contrast, when primers were used which amplify only the extracellular domain, FSH-receptor transcripts were detectable in all corpora lutea tested up to mid-cycle. In granulosa cells, luteinized in vitro, there was a similar loss of full-length FSH-receptor transcripts after day 1 but continued expression of transcripts encoding the extracellular domain. Results show that granulosa cell luteinization in cattle is associated with a change in splicing of the FSH-receptor primary transcript such that after luteinization only shortened transcripts coding for the extracellular domain are detectable. This process resembles, in reverse, changes in FSH-receptor transcript splicing during development of the gonads.

Alternative Splicing↗

PubMed1988

Immunocytochemical identification of luteinizing hormone-releasing hormone-positive fibres and terminals in the olfactory system of the rat.

Luteinizing hormone-releasing hormone immunoreactivity was studied in the olfactory system of the rat in combination with acetylcholinesterase histochemistry. Neuronal perikarya containing luteinizing hormone-releasing hormone lie in the medial septal nucleus, the vertical limb of the diagonal band of Broca, the olfactory tubercule and the ganglionated plexus of the terminal nerve. Labelled fibres spread in the superficial layers of the main and accessory olfactory bulbs, some encompassing the strongly acetylcholinesterase-positive atypical glomeruli. Others are observed on the medial side of the bulb, running along the terminal nerve bundles and ganglia. These fibres join the vomeronasal nerve branches and proceed distally towards the nasal cavity. In the septal submucosa, immunoreactive fibres are partly associated with the terminal nerve network. Conspicuous endings filled with luteinizing hormone-releasing hormone are observed on blood vessels of the olfactory mucosa. Such well-differentiated terminals might be the neurosecretory afferents of a new neurohemal area. Immunoreactive terminals are also observed around the excretory ducts of the anterior medial glands. We have failed to observe any labelled fibres in the olfactory and vomeronasal epithelia. The results of the present study are discussed with respect to possible functional interpretations. It is suggested that significant amounts of luteinizing hormone-releasing hormone could be released in the submucosal capillaries in spite of the scarcity of immunoreactive fibres. Similar afferents could also modulate the secretory activity of some nasal glands. Synaptic events involving the neuropeptide might occur in the olfactory bulb, particularly in atypical glomerular areas previously characterized by their high acetylcholinesterase content. Finally, no anatomical support for a chemosensory function of fibres containing luteinizing hormone-releasing hormone has been brought out by our work.

Acetylcholinesterase↗

PubMed1989

Synaptology of luteinizing hormone-releasing hormone neurons in the preoptic area of the male rat: effects of gonadectomy.

Ultrastructural analysis of the synaptic input to luteinizing hormone-releasing hormone neurons has previously shown that in male rats these cells acquire an increased density of innervation with increasing age [Witkin J. W. (1987) Neuroscience 22, 1003-1013]. To determine if this aging phenomenon might be due to changes in the steroid environment, we examined luteinizing hormone-releasing hormone neurons, using methods identical to the earlier study, in sham operated and 1 day and 4 week castrated male rats. The density of synaptic input to luteinizing hormone-releasing hormone neurons did not vary among the three experimental groups. Furthermore, there were no differences in the relative numbers of various morphological categories of synaptic boutons (characterized by vesicle type: clear vs dense and round vs pleomorphic) among the groups. Long term castration did result in a slight decrease in immunocytochemically detectable luteinizing hormone-releasing hormone neuron numbers. These results suggest that gonadal steroid deprivation does not alter the total density or morphological characteristics of synaptic input to the luteinizing hormone-releasing hormone neuron in the male rat.

Animals↗

PubMed1989

Immunohistochemical colocalization of delta sleep-inducing peptide and luteinizing hormone-releasing hormone in rabbit brain neurons.

The anatomical distributions of luteinizing hormone-releasing hormone and delta sleep-inducing peptide immunoreactivity in the rabbit brain were studied by indirect immunofluorescence technique. The comparison of adjacent serial sections, one being immunolabeled with an antiserum to luteinizing hormone-releasing hormone, the other with an antiserum to delta sleep-inducing peptide, showed that the respective distribution patterns of immunoreactivity exhibited a remarkable overlap through the basal forebrain and hypothalamic regions. A sequential double-immunolabelling (elution-restaining method) clearly indicated that all the luteinizing hormone-releasing hormone-immunoreactive cell bodies displayed delta sleep-inducing peptide immunoreactivity. These cell bodies were sparse and mainly located throughout the septal-preoptico-suprachiasmatic region and the ventrolateral hypothalamus. The colocalization of luteinizing hormone-releasing hormone and delta sleep-inducing peptide immunoreactivity was also observed in many fibres supplying all these brain regions and terminal areas such as the organum vasculosum of the lamina terminalis, the subfornical organ, the median eminence and the pituitary stalk. These neuroanatomical findings are suggestive of interaction between delta sleep-inducing peptide and luteinizing hormone-releasing hormone in various brain areas including some circumventricular organs.

Brain↗

PubMed1990

Access of luteinizing hormone-releasing hormone neurons to the vasculature in the rat.

Luteinizing hormone-releasing hormone is secreted into the hypophysial portal vasculature through which it controls the release of the gonadotropins. The peptide also acts as a neurotransmitter in various loci within the central nervous system. It is not known whether these roles are performed by separate populations of luteinizing hormone-releasing hormone neurons. Some recent tracing experiments suggest that this is the case (Silverman et al., J. Neurosci. 7, 2312, 1987; Jennes and Stumpf, Neuroscience 18, 403, 1986). One aspect of this question was addressed in the current study by intraperitoneal introduction of Fluoro-Gold (a retrograde tracer) into male and female rats under various age and hormonal conditions. Brain sections from the anterior olfactory nuclei to the median eminence were treated for the immunocytochemical demonstration of luteinizing hormone-releasing hormone. In all cases, regardless of the age, sex or hormonal condition of the animal, the Fluoro-Gold tracer was found in more than 90% of the luteinizing hormone-releasing hormone neurons. We conclude that virtually all luteinizing hormone-releasing hormone neurons in the rat secrete outside the blood-brain barrier, including those which project to sites within the central nervous system.

Aging↗