Neuroendocrinology (Neuroendocrinology)

Publisher: Karger

Journal description

ëNeuroendocrinologyí publishes papers reporting original research in basic and clinical neuroendocrinology. The journal explores the complex interactions between neuronal networks and endocrine glands (in some instances also immune cells) in both central and peripheral nervous systems. Original contributions cover all aspects of the field, from molecular and cellular neuroendocrinology, physiology, pharmacology, and the neuroanatomy of neuroendocrine systems to neuroendocrine correlates of coping behavior or clinical neuroendocrinology. Readers will also benefit from occasional, well-referenced reviews by noted experts which highlight especially active areas of current research.

Current impact factor: 4.37

Impact Factor Rankings

2015 Impact Factor Available summer 2016
2014 Impact Factor 4.373
2013 Impact Factor 4.934
2012 Impact Factor 3.537
2011 Impact Factor 2.376
2010 Impact Factor 3.272
2009 Impact Factor 3.074
2008 Impact Factor 2.913
2007 Impact Factor 2.295
2006 Impact Factor 2.68
2005 Impact Factor 2.65
2004 Impact Factor 2.509
2003 Impact Factor 2.844
2002 Impact Factor 2.511
2001 Impact Factor 2.144
2000 Impact Factor 2.744
1999 Impact Factor 3.214
1998 Impact Factor 3
1997 Impact Factor 2.441
1996 Impact Factor 2.445
1995 Impact Factor 2.684
1994 Impact Factor 2.422
1993 Impact Factor 2.702
1992 Impact Factor 2.841

Impact factor over time

Impact factor

Additional details

5-year impact 3.62
Cited half-life >10.0
Immediacy index 0.26
Eigenfactor 0.01
Article influence 1.07
Website Neuroendocrinology website
Other titles Neuroendocrinology (Online)
ISSN 1423-0194
OCLC 44647673
Material type Document, Periodical, Internet resource
Document type Internet Resource, Computer File, Journal / Magazine / Newspaper

Publisher details


  • Pre-print
    • Author can archive a pre-print version
  • Post-print
    • Author can archive a post-print version
  • Conditions
    • On author's server or institutional server
    • Server must be non-commercial
    • Publisher's version/PDF cannot be used
    • Publisher copyright and source must be acknowledged
    • Must link to publisher version
  • Classification
    ​ green

Publications in this journal

  • Neuroendocrinology 09/2015; 102(3):181-183. DOI:10.1159/000441115
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    ABSTRACT: Background: Preclinical evidence suggests that progesterone improves recovery after intracerebral hemorrhage (ICH); however, gonadal hormones have sex-specific effects. Therefore, an experimental model of ICH was used to assess recovery after progesterone administration in male and female rats. Methods: ICH was induced in male and female Wistar rats via stereotactic intrastriatal injection of clostridal collagenase (0.5 U). Animals were randomized to receive vehicle or 8 mg/kg progesterone intraperitoneally at 2 h, then subcutaneously at 5, 24, 48, and 72 h post-injury. Outcomes included relevant physiology during the first 3 h, hemorrhage and edema evolution over the first 24 h, pro-inflammatory transcription factor and cytokine regulation at 24 h, rotarod latency and neuroseverity score over the first 7 days, and microglial activation/macrophage recruitment at 7 days after injury. Results: Rotarod latency (p = 0.001) and neuroseverity score (p = 0.01) were improved in progesterone-treated males, but worsened in progesterone-treated females (p = 0.028 and p = 0.008, respectively). Progesterone decreased cerebral edema (p = 0.04), microglial activation/macrophage recruitment (p < 0.001), and pro-inflammatory transcription factor phosphorylated nuclear factor-kappaB p65 expression (p = 0.0038) in males but not females, independent of tumor necrosis factor-α, interleukin-6, and toll-like receptor-4 expression. Cerebral perfusion was increased in progesterone-treated males at 4 h (p = 0.043) but not 24 h after injury. Hemorrhage volume, arterial blood gases, glucose, and systolic blood pressure were not affected. Conclusions: Progesterone administration improved early neurobehavioral recovery and decreased secondary neuroinflammation after ICH in male rats. Paradoxically, progesterone worsened neurobehavioral recovery and did not modify neuroinflammation in female rats. Future work should isolate mechanisms of sex-specific progesterone effects after ICH.
    Neuroendocrinology 09/2015; DOI:10.1159/000440883
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    ABSTRACT: Background: Appendix goblet cell carcinoids (GCCs) are known to share histological features of adenocarcinoma and neuroendocrine tumours. Due to their low incidence, quality evidence is lacking for management of these patients. Methods: We performed a single-centre retrospective study of patients with confirmed diagnosis of appendiceal GCC (1996-2014). Patients were divided into curative intent (CI) and palliative intent (PI) cohorts. Our primary end-point was overall survival (OS). Results: Seventy-four patients were eligible; 76% were treated with CI (surgery only (36%), Cytoreductive Surgery (CRS) and Hyperthermic Intra-peritoneal Chemotherapy (HIPEC) (36%), adjuvant chemotherapy (20%) and combination of CRS and HIPEC followed by adjuvant chemotherapy (9%)); 23% had advanced stage-disease amenable to palliative treatment (chemotherapy or supportive care) only. Completion right hemicolectomy, performed in 64% of the CI cohort, did not impact on relapse rate or disease-free survival. FOLFOX chemotherapy was used in both adjuvant and palliative settings; safety was as expected and we observed a high rate (60%) of disease control in the palliative cohort. The estimated median OS (all patients), disease-free (CI patients) and progression-free survivals (PI patients) were 52.1 (95% CI 29.4-90.3), 75.9 (26.6-not reached) and 5.3 (0.6-5.7) months, respectively. Age and stage were independent factors associated with OS in the multivariable analysis. Tang classification showed a trend for impact on OS. No benefit from specific adjuvant approach was identified; however selection bias for treatment approach was observed. Conclusion: Prospective trials are needed to define optimal approaches in GCC. All GCC patients should be managed by specialized centres due to their esoteric behaviour; we provide management considerations based on our experience and conclusions.
    Neuroendocrinology 09/2015; DOI:10.1159/000440725
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    ABSTRACT: The effects of gonadal steroids on neurological well-being and disease constitute a rich and rapidly expanding area of basic and clinical neuroscience. Gonadal hormones exert potent effects on monoaminergic, cholinergic and peptidergic pathways as well as neurosteroidogenesis which, in turn, impact normal brain organization and function. A spectrum of human neurological conditions are influenced by hormonal fluctuations associated with the menstrual cycle, pregnancy, the menopause and use of oral contraceptives. An appreciation of these relationships may facilitate the development of specific hormonal and anti-hormonal therapies for neurological disorders as disparate as catamenial epilepsy and acute intermittent porphyria. © 2015 S. Karger AG, Basel.
    Neuroendocrinology 09/2015; DOI:10.1159/000440620
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    ABSTRACT: The hepatocyte growth factor (HGF)/transmembrane tyrosine kinase receptor c-Met has been defined as a potential target in antitumoural treatment of various carcinomas. We aimed to investigate the direct effect of c-Met inhibition on neuroendocrine tumour cells in vitro. The effects of the multi-tyrosine-kinase inhibitors cabozantinib and tivantinib and of the highly specific c-Met inhibitor INC280 were investigated in human pancreatic neuroendocrine BON1, bronchopulmonary NCI-H727 and midgut GOT1 cells in vitro. INC280, cabozantinib and tivantinib inhibited c-Met phosphorylation, respectively. However, while equimolar concentrations (10 uM) of cabozantinib and tivantinib inhibited cell viability and cell migration, INC280 had no inhibitory effect. Knockdown experiments with c-Met siRNA also did not demonstrate effects on cell viability. Cabozantinib and tivantinib caused a G2 arrest in neuroendocrine tumor cells. Our in vitro data suggest that c-Met inhibition alone is not sufficient to exert direct antitumoural or antimigratory effects in neuroendocrine tumour cells. The multi-tyrosine-kinase inhibitors cabozantinib and tivantinib show promising antitumoural and antimigratory effects in neuroendocrine tumour cells, which are most probably 'off-target' effects, not mediated by c-Met. © 2015 S. Karger AG, Basel.
    Neuroendocrinology 08/2015; DOI:10.1159/000439431
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    ABSTRACT: CNS ischemia results in locally confined and rapid tissue damage accompanied by a loss of neurons and their circuits. Early and time-delayed inflammatory responses are critical variables determining the extent of neural disintegration and regeneration. Inflammasomes are vital effectors in innate immunity. Their activation in brain-intrinsic immune cells contributes to ischemia-related brain damage. The steroids 17ß-estradiol (E2) and progesterone (P) are neuroprotective and anti-inflammatory. Using a transient focal rat ischemic model, we have evaluated the time response of different inflammasomes in the peri-infarct zone from the early to late phase after ischemia post stroke. We show that the different inflammasome complexes reveal a specific time-oriented sequential expression pattern with a maximum at approx. 24 h after the infarct. Within the limits of antibody availability, immunofluorescence labeling demonstrated that microglia and neurons are major sources of the locally activated inflammasomes NLRP3 and ASC, respectively. E2 and P given for 24 h immediately after ischemia onset reduced hypoxia-induced mRNA expression of the inflammasomes NLRC4, AIM2 and ASC, and decreased the protein levels of ASC and NLRP3. In addition, mRNA protein levels of the cytokines IL1ß, IL18 and TNFα were reduced by the steroids. The findings provide for the first time a detailed flow chart of hypoxia-driven inflammasome regulation in the peri-infarct cerebral cortex. Further, we demonstrate that E2 and P alleviate the expression of certain inflammasome components sometimes in a hormone-specific way. Besides directly regulating other cellular neuroprotective pathways, the control of inflammasomes by these steroids might contribute to its neuroprotective potency. © 2015 S. Karger AG, Basel.
    Neuroendocrinology 08/2015; DOI:10.1159/000439435
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    ABSTRACT: Leptin replacement in patients with leptin gene mutations improves hypogonadotropic hypogonadism. The effects of leptin replacement on LH secretion in patients with lipodystrophy are unknown. We examined nocturnal LH secretory dynamics on and off exogenous leptin therapy using a 2 period, non-randomized study that included leptin-naïve and -treated subjects with lipodystrophy. In period 1 (5 days) the leptin-treated group (n = 4) continued leptin; leptin was withdrawn for the next 14 days (period 2). Leptin-naïve subjects (n = 8) were studied without leptin in period 1, and with leptin replacement in period 2. LH secretory dynamics were assessed [23:00-7:00, q10 min sampling, analyzed by multiparameter deconvolution algorithm] at the end of each period. Mean (on vs. off: 5.0 ± 3.1 U/l vs. 3.2 ± 1.3, p = 0.04) and integrated LH concentrations (2,403 ± 1,495 U × L(-a) × min(-a) vs. 1,534 ± 642, p = 0.04) were higher on leptin therapy. Leptin treatment increased burst mass (9.7± 15.4 U/l vs. 7.0 ± 11.2, p = 0.03) and tended to non-significantly increase LH burst frequency (0.77 ± 0.26 h(-a) vs. 0.67 ± 0.24, p = 0.08). Consequently, leptin therapy increased pulsatile production rate (64 ± 101 U × L(-a) × 8 h(-a) vs. 57 ± 73, p = 0.01). On leptin, testosterone (507 ± 286 ng/dl vs. 360 ± 174, p = 0.09) and estradiol levels (74 ± 36 pg/ml vs. 29 ± 24, p = 0.01) were higher, in males and females, respectively. Leptin increases spontaneous nocturnal LH secretion in patients with lipodystrophy. This is consistent with rodent and in vitro studies showing a direct stimulatory effect (hypothalamic, pituitary or both) of leptin on LH secretion. These novel findings may explicate some of the salutary effects of leptin therapy on the hypothalamic-pituitary-gonadal axis in lipodystrophy. © 2015 S. Karger AG, Basel.
    Neuroendocrinology 08/2015; DOI:10.1159/000439432
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    ABSTRACT: Apolipoprotein A-IV (apoA-IV) in the brain potently suppresses food intake. However the mechanisms underlying its anorexigenic effects remain to be identified. We first examined the effects of apoA-IV on cellular activities in hypothalamic neurons that co-express agouti-related peptide (AgRP) and neuropeptide Y (NPY) and in neurons that express pro-opiomelanocortin (POMC). We then compared anorexigenic effects of apoA-IV in wild type mice and in mutant mice lacking melanocortin 4 receptors (MC4Rs, the receptors of AgRP and the POMC gene product). Finally, we examined expression of apoA-IV in mouse hypothalamus and quantified its protein levels at fed vs. fasted states. We demonstrate that apoA-IV inhibited the firing rate of AgRP/NPY neurons. The decreased firing was associated with hyperpolarized membrane potential and decreased miniature excitatory postsynaptic current. We further used c-fos immunoreactivity to show that intracerebroventricular (i.c.v.) injections of apoA-IV abolished the fasting-induced activation of AgRP/NPY neurons in mice. Further, we found that apoA-IV depolarized POMC neurons and increased their firing rate. In addition, genetic deletion of MC4Rs blocked anorexigenic effects of i.c.v. apoA-IV. Finally, we detected endogenous apoA-IV in multiple neural populations in mouse hypothalamus, including AgRP/NPY neurons, and food deprivation suppresses hypothalamic apoA-IV protein levels. Our findings support a model where central apoA-IV inhibits AgRP/NPY neurons and activates POMC neurons to activate MC4Rs, which in turn suppresses food intake. © 2015 S. Karger AG, Basel.
    Neuroendocrinology 08/2015; DOI:10.1159/000439436
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    ABSTRACT: Neuropeptides of the hypothalamic arcuate nucleus (ARC) regulate important homeostatic and endocrine functions and also play critical roles in pubertal development. Altered peptidergic and amino acidergic neurotransmission accompanying pubertal maturation of the ARC are not fully understood. Here we studied the developmental shift in the gene expression profile of the ARC of male mice. RNA samples for quantitative RT-PCR studies were isolated from the ARC of day-14 infantile and day-60 adult male mice with laser-capture microdissection. The expression of 18 neuropeptide-, 15 neuropeptide receptor-, 4 sex steroid receptor and 6 classic neurotransmitter marker mRNAs were compared between the two timepoints. Adult animals showed increased mRNA levels encoding cocaine- and amphetamine-regulated transcript, galanin-like peptide, dynorphin, kisspeptin, proopiomelanocortin, proenkephalin and galanin and reduced expression of mRNAs for pituitary adenylate cyclase activating peptide, calcitonin gene-related peptide, neuropeptide Y, substance P, agouti-related protein, neurotensin and growth hormone-releasing hormone. From the neuropeptide receptors tested, melanocortin receptor-4 showed the most striking (5-fold) increase. Melanocortin receptor-3 and the Y1 and Y5 neuropeptide Y receptors increased 1.5-1.8-fold, whereas δ-opioid receptor and neurotensin receptor-1 transcripts were reduced by 27 and 21%, respectively. Androgen-, progesterone- and α-estrogen receptor transcripts increased by 54-72%. The mRNAs of glutamic acid decarboxylase 65, and 67, vesicular GABA transporter and choline acetyltransferase remained unchanged. Tyrosine hydroxylase mRNA increased by 44%, whereas type-2 vesicular glutamate transporter mRNA decreased by 43% by adulthood. Many of the developmental changes we revealed in this study suggest reduced inhibitory and/or enhanced excitatory neuropeptidergic drive on fertility in adult animals. © 2015 S. Karger AG, Basel.
    Neuroendocrinology 08/2015; DOI:10.1159/000439430
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    ABSTRACT: Function of the central aspects of the hypothalamo-pituitary-gonadal axis has been assessed in a number of ways including direct measurements of hypothalamic output and indirect measures using gonadotropin release from the pituitary as a bioassay for reproductive neuroendocrine activity. Here, methods for monitoring these various parameters are briefly reviewed and then examples presented of both concordance and discrepancy between central and peripheral measurements, with a focus on situations in which elevated GnRH neurosecretion is not reflected accurately by pituitary luteinizing hormone release. Implications for interpretation of gonadotropin data are discussed. © 2015 S. Karger AG, Basel.
    Neuroendocrinology 08/2015; DOI:10.1159/000438790
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    ABSTRACT: Over the last ten years, kisspeptins - peptide products of varying lengths encoded by the KISS1 gene - have been found to be key regulators of normal reproductive function throughout life in animals and humans. By activating the kisspeptin receptor (previously known as orphan G protein-coupled receptor 54 (GPR54)) they elicit an effect on the central gonadotrophin releasing hormone (GnRH) neurons. Administration of kisspeptin by either the subcutaneous or intravenous route potently stimulates endogenous gonadotrophin hormone release in healthy men and women and animals. Kisspeptin also stimulates endogenous release of gonadotrophins in subfertile as well as healthy volunteers, and therefore kisspeptin has potential as a novel therapeutic agent in reproductive disorders. Further human studies have shown that chronic, high dose administration of kisspeptin causes desensitization with rapid subsequent suppression of the hypothalamic-pituitary-gonadal axis, and therefore high dose long-acting analogues may have a clinical role in treating sex-hormone dependent malignancies. By further elucidating the intricacies and mechanisms of the kisspeptin signalling system, and the tissues it acts on during different phases of the reproductive timeline (including during puberty, fertility, pregnancy and menopause), pharmacologic analogues could become clinically useful. © 2015 S. Karger AG, Basel.
    Neuroendocrinology 08/2015; DOI:10.1159/000439133
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    ABSTRACT: Treatment goals in acromegaly include symptom relief, tumour control and reversal of the excess morbidity and mortality associated with the disorder. Cardiovascular complications include concentric biventricular hypertrophy and cardiomyopathy, hypertension, valvular heart disease and arrhythmias, while metabolic disturbance (insulin resistance/diabetes mellitus, dyslipidaemia) further increases the risk of cardiovascular and cerebrovascular events. Sleep disordered breathing (in the form of sleep apnoea) is also common in patients with acromegaly and may exacerbate cardiovascular dysfunction, in addition to contributing to impaired quality of life. Accordingly, and in keeping with evidence that cardiorespiratory complications in acromegaly are not automatically reversed/ameliorated simply through the attainment of 'safe' growth hormone (GH) and insulin-like growth factor 1 (IGF-1) levels, recent guidelines have emphasised the need not only to achieve stringent biochemical control, but also to identify and independently treat these comorbidities. It is important therefore that patients with acromegaly are systematically screened at diagnosis, and periodically thereafter, for the common cardiovascular and respiratory manifestations, and that biochemical targets do not become the only treatment goal. © 2015 S. Karger AG, Basel.
    Neuroendocrinology 07/2015; DOI:10.1159/000438903
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    ABSTRACT: Neuroendocrine tumors (NETs) metastasize to the bone. However, incidence, clinical features, management and pathogenesis of bone involvement in NET patients have been poorly investigated. We reviewed all published reports of histologically-confirmed bone metastatic NETs and explored clinical, radiological, prognostic and therapeutic characteristics in a population of 152 patients. Then, we evaluated immunohistochemical expression of a panel of 8 epithelial-to-mesenchymal transition (EMT)-related factors including Snail, TGF-β1, CTGF, IL-11, PTHrP, EpCAM, CXCR4 and RANK in an independent cohort of 44 archival primary NETs. Biomarker expression was correlated with clinico-pathological variables including the skeletal involvement and tested for survival prediction. We found that 55% of NET patients with bone metastases were male, with a median age of 55 years at diagnosis. Metastases were restricted to the skeleton in the 34% of the NET population, and axial and osteoblastic lesions were prevalent. NETs differently expressed proteins involved in the EMT activation. High CXCR4 (p < 0.0001) and low TGF-β1 levels (p = 0.0015) were significantly associated with increased risk of skeletal metastases, suggesting that EMT is implicated in NET osteotropism. By applying an algorithm measuring distinct immunohistochemical predictors of osteotropism on primary tumors, we were able to identify NET patients with bone metastases with a sensitivity and specificity of 91 and 100% respectively (p < 0.0001). Patients whose primary tumors expressed CTGF (p = 0.0007) as well as the truncated form of EpCAM (p = 0.06) underwent shorter survival. Although underestimated, bone metastases are a prominent feature of NETs and the tumor expression of EMT markers at the diagnosis may predict concurrent or subsequent skeleton colonization. © 2015 S. Karger AG, Basel.
    Neuroendocrinology 07/2015; DOI:10.1159/000438902
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    ABSTRACT: Studies on 24-hour growth hormone (GH) secretion are rare. The influence of sex, age and adiposity are well recognized but generally derived from specific selected subject groups, not spanning sexes, many age decades, and a range of body weights. The goal was to investigate GH dynamics in a group of 130 healthy adult subjects, both men and women, across 5 age decades, and a 2.5 fold range of body mass index (BMI). GH was measured by a sensitive immunofluorometric assay. Secretion parameters were quantified by automated deconvolution and relative pattern randomness by approximate entropy (ApEn). Median age was 40, range 20-77 year. Median BMI was 26, range 18.3-49.8 kg/m(2). Pulsatile 24-hour GH secretion was negatively correlated with age (p = 0.002) and BMI (p < 0.0001). Basal GH secretion negatively correlated with BMI (p = 0.003) and not with age. The sex-dependent GH secretion (larger in women) was no longer detectable after 50 year. IGF-1 levels were lower in women after 50 year compared with men of similar age. ApEn showed age-related increase in both sexes and was higher in premenopausal and postmenopausal women than men of comparable age (p < 0.0001). A single fasting GH measurement is non-informative of 24-hour GH secretion. BMI dominates the negative regulation of 24-hour GH secretion across 5 decades of age in this till now largest cohort of healthy adults, who underwent 24-hour blood sampling. Sex also impacts GH secretion before age 50 year and its regularity at all ages. Serum IGF-I differences partly depend on pre- or postmenopausal state. Finally, a single GH measurement is not informative of 24-hour GH secretion. © 2015 S. Karger AG, Basel.
    Neuroendocrinology 07/2015; DOI:10.1159/000438904
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    ABSTRACT: Primary adrenal insufficiency (AI) requires hormone replacement therapy with fludrocortisone and hydrocortisone stimulating glucocorticoid (GR) and mineralocorticoid receptors (MR). Evidence from animal and human studies shows that MR function is crucial for cognitive function and mood. Regarding patients with AI very little is known about the role of MR in cognitive function and mood. Repeated measures within-subject design was used to determine whether cognitive function and mood are related to MR occupation in patients with AI. Intraindividually, patients were examined twice with one week apart: once with fludrocortisone (high MR occupation) and once without fludrocortisone (low MR occupation). All patients kept their stable regimen of hydrocortisone. Assessment of cognitive function included executive function, attention and verbal, visuospatial, and working memory. Additionally, mood and blood pressure were measured. Verbal memory improved significantly during high MR occupation (after fludrocortisone intake) compared to low MR occupation (without fludrocortisone, t(29) = -2.1, p = 0.046). There were trend level differences in the Number-Combination-Test (t(29) = -1.9, p = 0.074) and in the Stroop Interference Task (t(29) = -1.9, p = 0.068). No significant differences in visuospatial and working memory were found. Furthermore, current mood state was better during high MR occupation compared to low MR occupation (t(29) = -2.4, p = 0.023) as was diastolic blood pressure (F(2, 29) = 3.6, p = 0.07). Cognitive function and mood in patients with AI depend in part on MR occupation. Because the medium effect size indicates a potential clinical significance, further studies should systematically examine which dosages of fludrocortisone are associated with optimal cognitive function and mood in AI patients. © 2015 S. Karger AG, Basel.
    Neuroendocrinology 07/2015; DOI:10.1159/000438791