Neuroendocrinology (NEUROENDOCRINOLOGY )

Publisher: International Society of Neuroendocrinology, Blackwell Publishing

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.

  • Impact factor
    3.54
    Show impact factor history
     
    Impact factor
  • 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

Blackwell Publishing

  • Pre-print
    • Author can archive a pre-print version
  • Post-print
    • Author cannot archive a post-print version
  • Restrictions
    • Some journals impose embargoes typically of 6 or 12 months, occasionally of 24 months
    • no listing of affected journals available as yet
  • Conditions
    • See Wiley-Blackwell entry for articles after February 2007
    • Publisher's version/PDF cannot be used
    • On author's server, institutional server or subject-based server
    • Server must be non-commercial
    • Publisher copyright and source must be acknowledged with set statement ("The definitive version is available at www.blackwell-synergy.com")
    • Articles in some journals can be made Open Access on payment of additional charge
    • 'Blackwell Publishing' is an imprint of 'Wiley'
  • Classification
    ​ yellow

Publications in this journal

  • [Show abstract] [Hide abstract]
    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;
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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;
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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;
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    ABSTRACT: 3,4-Methylenedioxymethamphetamine (MDMA, 'ecstasy') and methylphenidate are widely used psychoactive substances. MDMA primarily enhances serotonergic neurotransmission, and methylphenidate increases dopamine but has no serotonergic effects. Both drugs also increase norepinephrine, resulting in sympathomimetic properties. Here we studied the effects of MDMA and methylphenidate on 24-h plasma steroid profiles. Sixteen healthy subjects (eight men, eight women) were treated with single doses of MDMA (125 mg), methylphenidate (60 mg), MDMA + methylphenidate, and placebo on four separate days using a cross-over study design. Cortisol, cortisone, corticosterone, 11-dehydrocorticosterone, aldosterone, 11-deoxycorticosterone, dehydroepiandrosterone (DHEA), dehydroepiandrosterone sulfate (DHEAS), androstendione, and testosterone were repeatedly measured up to 24-h using liquid-chromatography tandem mass-spectroscopy. MDMA significantly increased the plasma concentrations of cortisol, corticosterone, 11-dehydrocorticosterone, and 11-deoxycorticosterone and also tended to moderately increase aldosterone levels compared with placebo. MDMA also increased the sum of cortisol + cortisone and the cortisol/cortisone ratio, consistent with an increase in glucocorticoid production. MDMA did not alter the levels of cortisone, DHEA, DHEAS, androstendione, or testosterone. Methylphenidate did not affect any of the steroid concentrations, and it did not change the effects of MDMA on circulating steroids. In summary, the serotonin releaser MDMA has acute effects on circulating steroids. These effects are not observed after stimulation of the dopamine and norepinephrine systems with methylphenidate. The present findings support the view that serotonin rather than dopamine and norepinephrine mediates the acute pharmacologically-induced stimulation of the hypothalamic-pituitary-adrenal axis in the absence of other stressors. © 2014 S. Karger AG, Basel.
    Neuroendocrinology 06/2014;
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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;
  • 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.
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    ABSTRACT: Recently we showed that 24 h after copulation to satiety, there is a reduction in androgen receptor density (ARd) in the medial preoptic area (MPOA) and in the ventromedial hypothalamic nucleus (VMH), but not in the bed nucleus of the stria terminalis (BST). The present study was designed to analyze whether the ARd changes in these and other brain areas, such as the medial amygdala (MeA) and lateral septum, ventral part (LSV), were associated with changes in sexual behavior following sexual satiety. Males rats were sacrificed 48 h, 72 h or 7 days after sexual satiety (4 h ad libitum copulation) to determine ARd by immunocytochemistry; additionally, testosterone serum levels were measured in independent groups sacrificed at the same intervals. In another experiment, males were tested for recovery of sexual behavior 48 h, 72 h or 7 days after sexual satiety. The results showed that 48 h after sexual satiety 30% of the males displayed a single ejaculation and the remaining 70% showed a complete inhibition of sexual behavior. This reduction in sexual behavior was accompanied by an ARd decrease exclusively in the MPOA-medial part (MPOM). Seventy-two hours after sexual satiety there was a recovery of sexual activity accompanied by an increase in ARd to control levels in the MPOM and an overexpression of ARd in the LSV, BST, VMH and MeA. Serum testosterone levels were unmodified during the post-satiety period. The results are discussed on the basis of the similarities and discrepancies between ARd in specific brain areas and male sexual behavior.
    Neuroendocrinology 02/2007; 85(1):16-26.
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    ABSTRACT: In recent years the demonstration that human pituitary adenomas are monoclonal in origin provides further evidence that pituitary neoplasia arise from the replication of a single mutated cell in which growth advantage results from either activation of proto-oncogenes or inactivation of tumor suppressor genes. Mutations in common oncogenes and tumor suppressor genes are only exceptionally involved in pituitary tumors. Since pituicytes may proliferate in response to hypothalamic neurohormones, locally produced growth factors and peripheral hormones, it has been speculated that dysregulation of the signaling molecules that constitute these pathways may confer growth advantage to the target cell, finally resulting in tumor formation. The only mutational change so far recognized to be unequivocally associated with pituitary tumors occur in the Gs alpha gene (GNAS1) and cause constitutive activation of the cAMP-dependent pathway. However, other components of pituitary-specific pathways are frequently altered in their expression and activity. This review will focus on the possible impact of G proteins and other components of hormone signaling on pituitary tumorigenesis.
    Neuroendocrinology 02/2007; 85(2):101-9.
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    ABSTRACT: Tissue-specific stem cells are uncovered in a growing number of organs by their molecular expression profile and their potential for self-renewal, multipotent differentiation and tissue regeneration. Whether the pituitary gland also contains a pool of versatile 'master' cells that drive homeostatic, plastic and regenerative cell ontogenesis is at present unknown. Here, I will give an overview of data that may lend support to the existence of stem cells in the postnatal pituitary. During the many decades of pituitary research, various approaches have been used to hunt for the pituitary stem cells. Transplantation and regeneration studies advanced chromophobes as possible source of new hormonal cells. Clonogenicity approaches identified pituitary cells that clonally expand to floating spheres, or to colonies in adherent cell cultures. Behavioural characteristics and changes of marginal, follicular and folliculostellate cells during defined developmental and (patho-)physiological conditions have been interpreted as indicative of a stem cell role. Expression of potential stem cell markers like nestin, as well as topographical localization in the marginal zone around the cleft has also been considered to designate pituitary stem cells. Finally, a 'side population' was recently identified in the postnatal pituitary which in many other tissues represents a stem cell-enriched fraction. Taken together, in the course of the long-standing study of the pituitary, several arguments have been presented to support the existence of stem cells, and multiple cell types have been placed in the spotlight as possible candidates. However, none of these cells has until now unequivocally been shown to meet all quintessential characteristics of stem cells.
    Neuroendocrinology 02/2007; 85(2):110-30.
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    ABSTRACT: Critical interactions between genetic and environmental factors -- among which stress is one of the most potent non-genomic factors -- are involved in the development of mood disorders. Intensive work during the past decade has led to the proposal of the network hypothesis of depression [Castren E: Nat Rev Neurosci 2005;6:241-246]. In contrast to the earlier chemical hypothesis of depression that emphasized neurochemical imbalance as the cause of depression, the network hypothesis proposes that problems in information processing within relevant neural networks might underlie mood disorders. Clinical and preclinical evidence supporting this hypothesis are mainly based on observations from depressed patients and animal stress models indicating atrophy (with basic research pointing at structural remodeling and decreased neurogenesis as underlying mechanisms) and malfunctioning of the hippocampus and prefrontal cortex, as well as the ability of antidepressant treatments to have the opposite effects. A great research effort is devoted to identify the molecular mechanisms that are responsible for the network effects of depression and antidepressant actions, with a great deal of evidence pointing at a key role of neurotrophins (notably the brain-derived neurotrophic factor) and other growth factors. In this review, we present evidence that implicates alterations in the levels of the neural cell adhesion molecules of the immunoglobulin superfamily, NCAM and L1, among the mechanisms contributing to stress-related mood disorders and, potentially, in antidepressant action.
    Neuroendocrinology 02/2007; 85(3):158-76.
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    ABSTRACT: Molecular pathogenesis of digestive neuroendocrine tumors (dNETs) is largely unknown. Recently, the serine-threonine kinase B-Raf was identified as an oncogene in endocrine cancer such as thyroid carcinoma. In endocrine cells, the small G-protein Rap1 stimulates mitogen-activated protein kinase (MAPK) signaling by activating B-Raf. We examined the expression of Rap1 and B-Raf in dNETs and their contribution to MAPK signaling in neuroendocrine cell lines. In addition, we explored the effect of suppressing B-Raf kinase by the recently developed inhibitor BAY43-9006 (Sorafinib) on growth, apoptosis and MAPK activation neuroendocrine cell lines. Expression of Rap1 and B-Raf in dNETs (19 insulinomas, 15 carcinoid tumors and 10 gastrinomas) was examined by immunohistochemistry, which revealed that Rap1 and B-Raf were highly prevalent in the majority of dNETs. Overexpression of Rap1 and B-Raf activated MAPK extracellular dependent kinase (ERK) ERK-2 and ERK-dependent transcription factor Elk-1 in neuroendocrine cell lines Bon and INS-1. Suppression of B-Raf by BAY43-9006 inhibited growth and induced apoptosis in Bon and INS-1 cells. In addition, BAY43-9006 suppressed phosphorylation of MAPK ERK1/2 and its upstream kinase MEK1/2 in Bon and INS-1 cells. These results indicate that Rap1-B-Raf signaling may contribute to pathogenesis of dNETs and provides a molecular target for treatment of dNETs.
    Neuroendocrinology 02/2007; 85(1):45-53.
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    ABSTRACT: Atypical antipsychotics (SGA) have the propensity to induce weight gain. The aim was to evaluate early changes in hormones involved in neuroendocrine regulations (serum cortisol, growth hormone and prolactin) and positive energy balance (serum insulin, leptin and ghrelin) during SGA treatment in normal-weight patients with schizophrenia with the purpose of exploring the possibility to combat weight gain early through manipulation of circulating hormone levels. We conducted a randomized, partly cross-sectional and partly longitudinal, prospective study. Eighteen normal-weight in-patients with schizophrenia treated with FGA (first-generation antipsychotics) were referred to the Institute of Psychiatry. Twenty age-, gender- and BMI-matched healthy subjects were investigated at the Neuroendocrine Unit, Belgrade University. Oral glucose tolerance test (OGTT) was performed at baseline in all and then 13 patients were assigned to receive SGA (risperidone or clozapine) and OGTT was repeated after 1 and 3 months. At baseline, patients with schizophrenia had higher peak glucose levels (p < 0.05), glucose area under the curve (AUC; p < 0.05), peak insulin levels (p < 0.05), insulin AUC values during OGTT (p < 0.01) and the calculated homeostasis model assessment (HOMA-IR) value than control subjects (p < 0.05). Patients with schizophrenia showed higher morning cortisol (p < 0.05) levels than control subjects. After 1 and 3 months of SGA therapy patients with schizophrenia gained bodyweight by 3.5 and 8.6%, respectively. Leptin levels steadily increased while cortisol levels decreased in the first month and remained so. Serum glucose, insulin and ghrelin levels on SGA were similar as at baseline. Circulating ghrelin levels decreased after OGTT during SGA which is consistent with a role for ghrelin in the initiation of meals. Treatment with SGA was associated with continuous weight gain, with an early increase in serum leptin levels and decrease in cortisol levels. Elevated circulating leptin was ineffective in the control of fat deposition. Similar plasma ghrelin levels and similar decrease pattern of ghrelin after OGTT compared to healthy subjects signify intact meal-promoting effects of ghrelin during SGA therapy, which at the same time renders anorexigenic pathways ineffective. This may lead to weight gain and further studies with a ghrelin antagonist may provide support for this hypothesis.
    Neuroendocrinology 02/2007; 85(4):249-56.
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    ABSTRACT: Adipokines such as leptin, resistin, and fasting-induced adipose factor (FIAF) are secreted by adipocytes, but their expression is also detectable in the brain and pituitary. The role of central adipokines remains elusive, but we speculate that they may modulate those hypothalamic signaling pathways that control energy homeostasis. Here we describe experiments to test this in which we exploited a novel hypothalamic neuronal cell line (N-1) that expresses a variety of neuropeptides and receptors that are known to be implicated in appetite regulation. Using real-time RT-PCR, we confirmed that N-1 neurons express resistin (rstn) and fiaf, as well as suppressor of cytokine signaling-3 (socs-3), a feedback inhibitor of leptin signaling. Treating N-1 cells with recombinant resistin (200 ng/ml, 30 min) reduced both fiaf (25%, p < 0.005) and socs-3 (29%, p < 0.005) mRNA levels, and similar reductions in fiaf (40%, p < 0.001) and socs-3 (25%, p < 0.001) resulted following the overexpression of resistin. Conversely, when RNA interference (RNAi) was used to reduce endogenous rstn levels (-60%, p < 0.005), fiaf and socs-3 expression was increased (46 and 65% respectively, p < 0.005). A similar reduction in rstn mRNA was achieved using RNAi in differentiated 3T3-L1 adipocytes, and this manipulation also reduced fiaf and socs-3 expression (-53, -21 and -20% respectively, p < 0.005). In contrast, although RNAi successfully reduced fiaf mRNA by 50% (p < 0.001) in N-1 cells and 40% (p < 0.001) in 3T3-L1 cells, there was no effect on rstn or socs-3 mRNA. These data suggest that resistin exerts a novel autocrine/paracrine control over fiaf and socs-3 expression in both 3T3-L1 adipocytes and N-1 neurons. Such a mechanism could be part of the central feedback system that modulates the effects of adipokines, and other adiposity signals, implicated in hypothalamic energy homeostasis. However, it remains to be determined whether these in vitro results can be translated to the control of adipokine expression in brain and adipose tissue.
    Neuroendocrinology 02/2007; 85(4):232-41.
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    ABSTRACT: A new retrograde neuron-tracing technique with microspheres was used to explore the possible innervation of calcitonin gene-related peptide (CGRP)-immunolabeled vestibular afferent neurons in the vestibular efferent immunolabeled nucleus in the brainstem. 0.1 microl of 5% microfluorospheres was injected into the area of the vestibular efferent nucleus, which is located lateral to the genu of the facial nerve. CGRP immunohistochemistry was processed in serial sections of the brainstem at the facial nerve genu level. Double-labeled neurons with both CGRP immunoreactivity and microfluorospheres were examined with fluorescence and confocal laser microscopy. Three types of labeled neurons were observed: (1) neurons only retrogradely microfluorosphere-labeled that were mainly located in the medial vestibular nucleus, lateral vestibular nucleus, superior vestibular nucleus and parvicellular reticular nucleus on the ipsilateral side of the injection; (2) neurons that were both immunolabeled with CGRP and also retrogradedly labeled with microfluorospheres, indicating that they are CGRP cells projecting to the area of vestibular efferent nucleus, these cells were mainly distributed in the superior vestibular nucleus and dorsal vestibular nucleus, and (3) cells only immunolabeled for CGRP that were scattered extensively in the brainstem. The presented methodical contribution demonstrates the suitability of fluorescein-labeled microspheres for retrograde neuronal tracing. The vestibular nuclei contain numerous afferent neurons that send projections to the vestibular efferent nucleus, some of which are CGRP cells. This afferent innervation provides morphological evidence that the vestibular efferent neurons receive input from the vestibular afferent neurons including CGRP cells. These vestibular primary CGRP afferent neurons may have an influence on vestibular efferent neurons. CGRP acts as an important co-transmitter or modulator in the afferent-mediated activity of vestibular efferent neurons, which in turn affect afferents in the vestibular end organs.
    Neuroendocrinology 02/2007; 85(3):131-8.
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    ABSTRACT: Reproductive experience (i.e., pregnancy and lactation) alters anxiety-like behavior. One neurotransmitter system that may mediate the effects of reproductive experience on anxiety-like behavior is gamma-aminobutyric acid (GABA). The purpose of the current study was to determine whether reproductive experience alters the mRNA expression of selective GABA(A) receptor subunits in brain regions associated with anxiety-like behaviors. Brains were collected from age-matched nulliparous and primiparous female rats in either diestrus or proestrus, and the subunit mRNA expression was determined using real-time reverse transcription-polymerase chain reaction with Taqman. Increased alpha1 mRNA expression was found in proestrus within both medial preoptic area (MPOA) and medial amygdala (MeA) in nulliparous and primiparous females. The expression of alpha2 mRNA was also increased within the MPOA in proestrus in both nulliparous and primiparous females; however, within the MeA, an increased alpha2 mRNA expression in proestrus was only observed in nulliparous females, with primiparous females having a significantly reduced expression when compared to nulliparous controls. In addition, a significant increase in the expression of alpha2 mRNA expression was observed within the periaqueductal gray of reproductively experienced female rats. These results indicate that reproductive experience results in significant shifts in the expression of GABA(A) alpha2 mRNA expression in the MeA.
    Neuroendocrinology 02/2007; 85(3):148-56.