Neuroendocrinology (NEUROENDOCRINOLOGY)

Publisher: International Society of Neuroendocrinology, 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: 4.93

Impact Factor Rankings

2015 Impact Factor Available summer 2015
2013 / 2014 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 3.63
Cited half-life 0.00
Immediacy index 1.33
Eigenfactor 0.01
Article influence 1.01
Website Neuroendocrinology website
Other titles Neuroendocrinology
ISSN 0028-3835
OCLC 1759699
Material type Periodical, Internet resource
Document type Journal / Magazine / Newspaper, Internet Resource

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

  • [Show abstract] [Hide abstract]
    ABSTRACT: Chromogranin A (CgA) has been considered to be valuable not only in the diagnosis but also in monitoring the disease response to treatment. However, only a few studies have been published on this issue. We purposed to evaluate whether biochemical response using plasma CgA level is reliable in concordance with the clinical response of grade 1-3 nonfunctiong gastroenteropancreatic neuroendocrine tumors (GEP-NETs). Between March 2011 and September 2013, a total of 27 cases in 18 patients were analysed, clinically and radiologically while serial CgA tests were also conducted during treatment. Tumor responses were defined by both RECIST criteria 1.1 and biochemical criteria based on the CgA level. Among the 27 cases analysed, no difference in the basal CgA level was observed with regard to gender, primary tumor site, tumor grade (WHO classification), liver metastasis, number of metastatic site, and line of chemotherapy. The overall response rate (RR) by RECIST criteria 1.1 was 6 out of the 27 cases (22.2%) and 8 out of the 27 cases (29.6%) for biochemical RR. The overall concordance rates of the response based on RECIST and biochemical criteria were 74%. In grades 1 and 2 GEP-NETs (n=17), the concordance rate of the disease control was 94.1%. There was a significant difference for progression free survival (PFS) between responders and non-responder in accordance to biochemical criteria (35.73 months vs. 5.93 months, p=0.05). s This study revealed that changes of the plasma CgA levels were associated with tumour response. Additionally, biochemical response based on serial CgA may be a predictive marker for PFS in GEP-NETs.
    Neuroendocrinology 03/2015; DOI:10.4143/crt.2014.183
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    ABSTRACT: Merkel cell carcinoma (MCC) is a rare neuroendocrine carcinoma with poorly understood molecular etiology. We implemented a comprehensive deep sequencing approach to identify mutations in the tumor DNA from a cohort of patients treated at our institution over the past 15 years. Our results indicate mutations that may constitute therapeutic targets in MCC. Methods: Five patients were treated for MCC within the study interval. Patients with adequate tissue (n = 4), positive neuroendocrine differentiation (Chromogranin, Synaptophysin, and CK20), and histopathological confirmation of MCC were included in the study. DNA was extracted from archival tumor tissue samples and analyzed by massively parallel sequencing using a targeted, multiplex PCR approach followed by semiconductor sequencing. Results: We demonstrate high penetrance nonsense mutations in PDE4DIP (n = 4) as well as various missense mutations in the DNA Damage Response (PRKDC, AURKB, ERCC5, ATR, and ATRX) and epigenetic modulating enzymes (MLL3). Conclusion: We describe several mutations in potential disease-relevant genes and pathways. These targets should be evaluated in a larger cohort to determine their role in the molecular pathogenesis of MCC. © 2015 S. Karger AG, Basel.
    Neuroendocrinology 12/2014; DOI:10.1159/000370310
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    ABSTRACT: Menopause is caused by changes in the function of the hypothalamic-pituitary-gonadal (HPG) axis that controls reproduction. Hypophysiotropic gonadotropin-releasing hormone (GnRH) neurons in the hypothalamus orchestrate the activity of this axis and are regulated by hormonal feedback loops. The mechanisms by which GnRH responses to the primary regulatory sex-steroid hormone, estradiol (E2) are still poorly understood in the context of menopause. Our goal was to determine whether the G protein-coupled estrogen receptor (GPER) is co-expressed in adult primate GnRH neurons, and whether this changes with aging and/or E2 treatment. We used immunofluorescence double labeling to characterize the co-expression of GPER in GnRH perikarya and terminals in the hypothalamus. Young and aged rhesus macaques were ovariectomized and given long-term (∼2 year) hormone treatments (E2, E2 + progesterone, or vehicle) selected to mimic currently prescribed hormone replacement therapies used for the alleviation of menopausal symptoms in women. We found that about half of GnRH perikarya co-expressed GPER, while only about 12% of GnRH processes and terminals in the median eminence (ME) were double labeled. Additionally, many GPER labeled processes were in direct contact with GnRH neurons, often wrapped around the perikarya and processes and in close proximity in the ME. These results extend prior work by showing robust colocalization of GPER in GnRH in a clinically relevant model, and support the possibility that GPER-mediated E2 regulation of GnRH occurs both in the soma and terminals in nonhuman primates. © 2015 S. Karger AG, Basel.
    Neuroendocrinology 11/2014; DOI:10.1159/000369820
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    ABSTRACT: The hypothalamic-pituitary system is essential to maintain life and control systemic homeostasis, but it is negatively affected by various diseases, leading to serious symptoms. Embryonic stem (ES) cells differentiate into neuroectodermal progenitors when cultured as floating aggregates under serum-free conditions. Recently, our colleagues showed that strict removal of exogenous patterning factors during early differentiation steps induced efficient generation of rostral hypothalamic-like progenitors from mouse ES cell-derived neuroectodermal cells. The use of growth factor-free chemically defined medium was critical for this induction. The ES cell-derived hypothalamic-like progenitors generated rostral-dorsal hypothalamic neurons, especially magnocellular vasopressinergic neurons that release the hormone upon stimulation. Subsequently, we reported efficient self-formation of three-dimensional adenohypophysis tissues in aggregate cultures of mouse ES cells. The ES cells were stimulated to differentiate into non-neural head ectoderm and hypothalamic neuroectoderm in adjacent layers within the aggregate, and then treated with Hedgehog. Self-organization of Rathke's pouch-like structures occurred at the interface of the two epithelia, as observed in vivo, and various endocrine cells including corticotrophs and somatotrophs were subsequently produced. The corticotrophs efficiently secreted adrenocorticotropic hormone in response to corticotropin-releasing hormone. Furthermore, when engrafted in vivo, these cells rescued the systemic glucocorticoid level in hypopituitary mice. Our present research aims are to prepare hypothalamic and pituitary tissues from human-induced pluripotent stem cells and establish effective transplantation techniques with clinical applications. To replicate the complex and precise control of the hypothalamic-pituitary system, regenerative medicine using pluripotent cells may be a hopeful option. © 2015 S. Karger AG, Basel.
    Neuroendocrinology 11/2014; 101(1). DOI:10.1159/000369821
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    ABSTRACT: Continuous activation of the kisspeptin receptor by its agonists causes abrogation of kisspeptin signaling, leading to decreased pulsatile luteinizing hormone (LH) secretion. Employing this phenomenon as a tool for probing kisspeptin action, this study aimed to clarify the role of kisspeptin in gonadotropin-releasing hormone (GnRH) pulse generation in goats. We examined the effects of chronic administration of TAK-683, an investigational kisspeptin analog, on LH secretion, GnRH immunostaining, pituitary responses to exogenous GnRH, and GnRH pulse generator activity, reflected by a characteristic increase in multiple-unit activity (MUA volley). An osmotic pump containing TAK-683 was subcutaneously implanted on Day 0. TAK-683 treatment dose-dependently suppressed pulsatile LH secretion on Day 1. Higher doses of chronic TAK-683 profoundly suppressed pulsatile LH secretion but had little effect on GnRH immunostaining patterns and pituitary responses to GnRH on Day 5. In ovariectomized goats, MUA volleys occurred at approximately every 30 min on Day -1. On Day 5 of chronic TAK-683 administration, pulsatile LH secretion was markedly suppressed, whereas MUA volleys were similar to those observed on Day -1. Male pheromones and senktide (neurokinin B receptor agonist) induced an MUA volley but had no effect on LH secretion during chronic TAK-683 administration. The results indicate that chronic administration of a kisspeptin analog profoundly suppresses pulsatile LH secretion without affecting GnRH content, pituitary function, or GnRH pulse generator activity, and suggest an indispensable role for kisspeptin signaling in the cascade driving GnRH/LH pulses by the GnRH pulse generator. © 2015 S. Karger AG, Basel.
    Neuroendocrinology 11/2014; 100(2-3). DOI:10.1159/000369819
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    ABSTRACT: Hyperactivity of the hypothalamic-pituitary-adrenal axis is a consistent biological characteristic of depression and response normalization coincides with clinical responsiveness to antidepressant medications. Desensitization of serotonin 1A receptor (5-HT1AR) signaling in the hypothalamic paraventricular nucleus (PVN) follows selective serotonin reuptake inhibitor (SSRI) antidepressant treatment and contributes to the antidepressant response. Estradiol alone produces a partial desensitization of 5-HT1AR signaling, and synergizes with SSRIs to result in a complete and more rapid desensitization than with SSRIs alone as measured by a decrease in the oxytocin and adrenocorticotrophic hormone(ACTH) responses to 5-HT1AR stimulation. G protein-coupled estrogen receptor1 (GPER1) is necessary for estradiol-induced desensitization of 5-HT1AR signaling, although the underlying mechanisms are still unclear. We now find that stimulation of GPER1 with the selective agonist G-1 and non-selective stimulation of estrogen receptors dramatically alter isoform expression of a key component of the 5-HT1AR signaling pathway, RGSz1, a GTPase activating protein selective for Gαz, the Gα subunit necessary for 5-HT1AR-mediated hormone release. RGSz1 isoforms are differentially glycosylated, SUMOylated, and phosphorylated, and differentially distributed in subcellular organelles. High molecular weight RGSz1 is SUMOylated and glycosylated, localized to the detergent-resistant microdomain (DRM) of the cell membrane, and increased by estradiol and G-1 treatment. Because activated Gαz also localizes to the DRM, increased DRM-localized RGSz1 by estradiol and G-1could reduce Gαz activity, functionally uncoupling 5-HT1AR signaling. Peripheral G-1 treatment produced partial reduction in oxytocin and ACTH responses to 5-HT1AR-stimulation similar to direct injections into the PVN. Together, these results identify GPER1 and RGSz1 as novel targets for the treatment of depression. © 2014 S. Karger AG, Basel.
    Neuroendocrinology 11/2014; 100(2-3). DOI:10.1159/000369467
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    ABSTRACT: New tools for mapping and manipulating molecularly defined neural circuits have improved understanding of how the central nervous system regulates appetite. Studies focused on AGRP neurons, a starvation-sensitive hypothalamic population, have identified multiple circuit elements that can elicit or suppress feeding behavior. Distinct axon projections of this neuron population point to different circuits that regulate long-term appetite, short-term feeding, or visceral malaise-mediated anorexia. Here, we review recent studies examining these neural circuits that control food intake. © 2014 S. Karger AG, Basel.
    Neuroendocrinology 11/2014; 100(2-3). DOI:10.1159/000369072
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    ABSTRACT: Objective: The onset of menstruation is the hallmark of female pubertal development. The present study determined whether pubertal girls experience adrenocortical and ovarian steroid secretions within their first waking hour before getting their period, similar to those observed in adult females with regular cycles. Methods: Cortisol, dehydroepiandrosterone (DHEA), and estradiol-17β concentrations were measured in saliva samples collected after awakening (0, 30, and 60 min after awakening) from 158 normal premenarcheal pubertal girls and 69 adult females with regular menstrual cycles. The girls were subgrouped according to self-reported Tanner breast (B) and pubic hair (PH) stages (B1PH1, B2PH1, B2PH2, B3PH1, and B3PH2). Results: All the subgroups showed a similar pattern of cortisol secretion. However, cortisol levels were higher in girls at B3PH1 and at B3PH2 than other subgroups. DHEA secretion showed a similar pattern across the groups examined. The largest increase in DHEA levels occurred between B1PH1 and B2PH1 stages, and further increased with pubertal progression. DHEA levels in girls at B3PH2 were approximately one-half of the adult value. Estraiol-17β profiles in girls at B3PH1 and B3PH2 differed from those of other subgroups of girl. A sharp increase in estraiol-17β levels after awakening which observed in adult females emerged in girls at B3PH1 and B3PH2. However, the estradiol-17β levels did not reach adult values until B3PH2 stage. Conclusions: The progression of female puberty includes an increase in the levels of adrenocortical and ovarian steroid secretions and a gain of adult female-like patterns of estradiol-17β secretion within their first waking hour. © 2014 S. Karger AG, Basel.
    Neuroendocrinology 06/2014; 99(3-4). DOI:10.1159/000363368
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    ABSTRACT: Background: Female Cushing's disease (CD) patients with active disease present more frequently with depression compared to their male co-sufferers. This study investigated whether the gender difference prevails after remission and whether gender-specific factors contributing to mental health exist. Methods: Seventy-two biochemically cured CD patients (11 male, mean age 45.9 ± 13.7 years) who underwent transsphenoidal tumour removal filled out the Symptom Checklist-90-Revised inventory on average 42.1 ± 32.9 months after surgery. Regression analyses included the following independent factors: (i) age, (ii) presence of comorbidities, (iii) presence of hypocortisolism, (iv) presence of hypopituitarism, (v) disease duration until diagnosis, (vi) time elapsed since surgery and (vii) postoperative radiotherapy to predict postoperative psychopathology. Results: Regarding the Global Severity Index, 23.0% of the female and 27.3% of the male CD patients presented with abnormal scores. In all nine dimensions, psychopathological abnormalities were present in both female and male patients with the same frequency and intensity (each p > 0.05). Prolonged time to diagnosis was a strong predictive factor for worse psychopathological status only in male patients. Among female patients, merely the presence of comorbidities and to some extent pituitary deficiencies were related to psychopathological status. Conclusions: During the remissional phase of CD, female and male patients present with similar psychopathological profiles. In males, long-term biochemical effects of previous hypercortisolism seem to be salient for psychopathology. In contrast, in females, the presence of comorbidities/stressors they have to cope with is the predictive factor for psychopathology. The results underline gender differences in Cushing's disease and the need to separate them on various issues. © 2014 S. Karger AG, Basel.
    Neuroendocrinology 06/2014; 100(1). DOI:10.1159/000364878
  • European Neuroendocrine Tumour Society - NEUROENDOCRINOLOGY, Barcelona, Spain; 01/2014
  • European Neuroendocrine Tumour Society - NEUROENDOCRINOLOGY, Barcelona, Spain; 01/2014
  • Neuroendocrinology 01/2012;
  • Neuroendocrinology 01/2009; 90(1}, Meeting Abstract = {29):106.
  • Neuroendocrinology 01/2009;
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    ABSTRACT: Serotonin and its receptor agonists stimulate the release of arginine vasopressin (AVP) into peripheral blood under intraventricular injection. To test the hypothesis that brain serotonin can modulate the development of natural osmoregulatory responses, the effect of an increase in endogenous brain serotonin on the response to an intragastric hypo- or hyperosmotic loading was studied in Wistar and AVP-deficient Brattleboro rats. 5-Hydroxytryptophan (5-HTP), the rate-limiting serotonin biosynthesis precursor known to increase the brain level of serotonin, was injected intraperitoneally (5 mg/100 g body weight). The renal functional parameters (glomerular filtration rate [GFR], free water reabsorption, and urine flow rate) were monitored during the 4 h after intragastric infusion of water or a 2% NaCl solution (5% of body weight). Plasma AVP was measured by radioimmunoassay. In Wistar rats, intraperitoneal injection of 5-HTP at the same time as water loading prevented the development of the renal diuretic response: there was no increase in urine flow rate and GFR, and free water reabsorption remained at the high level. In AVP-deficient Brattleboro rats, unlike Wistar rats, 5-HTP treatment was without effect on the renal function parameters. In Wistar rats, injection of 5-HTP at the peak of water diuresis produced an abrogation of the diuretic response to water loading due to the increase in free water reabsorption. Plasma AVP increased from 1.2 +/- 0.4 to 4.2 +/- 1.6 pg/ml (n = 8 in each group, p < 0.01). Hyperosmotic treatment of Wistar rats with a 2% NaCl solution stimulated AVP secretion compared to baseline (from 3.2 +/- 0.1, n = 7 to 5.6 +/- 0.9, n = 7, p < 0.01), and the saluretic response developed on the background of high free water reabsorption. When injected concomitantly with NaCl solution, 5-HTP revealed no additive effect on plasma AVP and on free water reabsorption. We conclude that the 5-HTP-caused increase in brain serotonin contributed significantly to the dynamics of changes in the osmoregulatory response to the hypo-osmotic challenge due to stimulation of AVP secretion. 5-HTP had no additive effect on the osmoregulatory response to hyperosmotic loading. Peripherally injected 5-HTP had no effect on the renal function, being absent in AVP-deficient Brattleboro rats.
    Neuroendocrinology 02/2007; 85(4):242-8. DOI:10.1159/000103450