Neuroendocrine Function (neuroendocrine + function)

Distribution by Scientific Domains


Selected Abstracts


Neuroendocrine Function and Chronic Inflammatory Stress

EXPERIMENTAL PHYSIOLOGY, Issue 5 2002
Michael Harbuz
The factors regulating susceptibility and severity of autoimmune diseases are poorly understood. That neuroendocrine factors are critical modulators in this regard is self-evident. For example, there are major gender differences in susceptibility with women at greater risk than men of, for example, rheumatoid arthritis (RA) and multiple sclerosis (MS). The hypothalamo-pituitary-adrenal (HPA) axis has rightly attracted a considerable amount of attention. Of particular interest has been the hypothesis that susceptibility to autoimmune disease may be related to an impaired responsiveness of the HPA axis; that is, an inability to mount an appropriate cortisol response with which to down-regulate the immune system might allow the immune system to rampage unchecked and attack self. This hypothesis links regulation of the release from the adrenal gland of the potent anti-inflammatory glucocorticoids to the disease process. Endogenous glucocorticoids are crucial for the regulation of the severity of the disease process. The hypothesis proposing a link between a hyporesponsive HPA axis and susceptibility to disease is compelling. However, evidence from a number of sources has suggested that this may not be the entire story and alterations in the activity of the HPA axis have not been consistently observed in patients with RA. This review will concentrate on recent findings concerning the HPA axis in determining susceptibility to, and in regulating the severity of, inflammatory processes in autoimmune disease. These studies have revealed that a single exposure to endotoxin can confer protection to subsequent development of inflammation in an arthritis model in both neonatal and adult rats. Behavioural differences within a single population of rats are associated with differences in the plasma corticosterone responses to stress. However, relative hyporesponsiveness is not reflected by an increase in the severity of inflammation. In humans with RA the dexamethasone-corticotrophin-releasing factor (CRF) test has revealed two distinct sub-populations of patients. Studies in patients with MS have shown that this is not related to depression but rather to the severity of the disease. A better understanding of these complex neuroendocrine interactions may lead to novel clinical interventions. [source]


Neurokinin 3 Receptor Immunoreactivity in the Septal Region, Preoptic Area and Hypothalamus of the Female Sheep: Colocalisation in Neurokinin B Cells of the Arcuate Nucleus but not in Gonadotrophin-Releasing Hormone Neurones

JOURNAL OF NEUROENDOCRINOLOGY, Issue 1 2010
M. Amstalden
Recent evidence has implicated neurokinin B (NKB) in the complex neuronal network mediating the effects of gonadal steroids on the regulation of gonadotrophin-releasing hormone (GnRH) secretion. Because the neurokinin 3 receptor (NK3R) is considered to mediate the effects of NKB at the cellular level, we determined the distribution of immunoreactive NK3R in the septal region, preoptic area (POA) and hypothalamus of the ewe. NK3R cells and/or fibres were found in areas including the bed nucleus of the stria terminalis, POA, anterior hypothalamic and perifornical areas, dopaminergic A15 region, dorsomedial and lateral hypothalamus, arcuate nucleus (ARC) and the ventral premammillary nucleus. We also used dual-label immunocytochemistry to determine whether a neuroanatomical basis for direct modulation of GnRH neurones by NKB was evident. No GnRH neurones at any rostral-caudal level were observed to contain NK3R immunoreactivity, although GnRH neurones and fibres were in proximity to NK3R-containing fibres. Because NKB fibres formed close contacts with NKB neurones in the ARC, we determined whether these NKB neurones also contained immunoreactive NK3R. In luteal-phase ewes, 64% 11 of NKB neurones colocalised NK3R. In summary, NK3R is distributed in areas of the sheep POA and hypothalamus known to be involved in the control of reproductive neuroendocrine function. Colocalisation of NK3R in NKB neurones of the ARC suggests a potential mechanism for the autoregulation of this subpopulation; however, the lack of NK3R in GnRH neurones suggests that the actions of NKB on GnRH neurosecretory activity in the ewe are mediated indirectly via other neurones and/or neuropeptides. [source]


Central GABAA but not GABAB Receptors Mediate Suppressive Effects of Caudal Hindbrain Glucoprivation on the Luteinizing Hormone Surge in Steroid-Primed, Ovariectomized Female Rats

JOURNAL OF NEUROENDOCRINOLOGY, Issue 7 2005
S. R. Singh
Abstract The neurochemical mechanisms that link caudal hindbrain glucoprivic-,sensitive' neurones with the forebrain gonadotrophin-releasing hormone (GnRH)-pituitary luteinizing hormone (LH) axis remain unclear. Available studies indicate that the amino acid neurotransmitter, ,-aminobutyric acid (GABA), inhibits reproductive neuroendocrine function, and that caudal fourth ventricular administration of the glucose antimetabolite, 5-thioglucose (5TG), enhances GABA turnover within discrete septopreoptic structures that regulate LH secretion. The current experiments utilized the selective GABAA and GABAB receptor antagonists, bicuculline and phaclofen, as pharmacological tools to investigate whether one or both receptor subtypes function within neural pathways that suppress GnRH neuronal transcriptional activation and LH release during central glucose deficiency. During the ascending phase of the afternoon LH surge, groups of steroid-primed, ovariectomized female Sprague-Dawley rats were pretreated by lateral ventricular administration of bicuculline, phaclofen, or vehicle only, before fourth ventricular injection of 5TG or vehicle. The data indicate that, 2 h after 5TG treatment, Fos immunoexpression by rostral preoptic GnRH neurones and plasma LH levels were diminished relative to the vehicle-treated controls, and that inhibitory effects of 5TG on these parameters were attenuated by pretreatment with bicuculline, but not phaclofen. These results demonstrate that central GABAA, but not GABAB receptor stimulation during hindbrain glucoprivation, is required for maximal inhibition of reproductive neuroendocrine function by this metabolic challenge. The current studies thus reinforce the view that central GABAergic neurotransmission mediates regulatory effects of central glucoprivic signalling on the GnRH-pituitary LH axis. [source]


Effects of 4-piperidinomethyl-2-isopropyl-5-methylphenol on oxidative stress and calcium current

JOURNAL OF PHARMACY AND PHARMACOLOGY: AN INTERNATI ONAL JOURNAL OF PHARMACEUTICAL SCIENCE, Issue 9 2005
Mei-Han Huang
4-Piperidinomethyl-2-isopropyl-5-methylphenol (THPI) was synthesized by reaction of thymol with piperidine and formaldehyde. The biological effect of THPI on superoxide anion scavenging activity, antiplatelet activity and calcium current inhibition were investigated. THPI (50 ,m) was shown to be a scavenger of superoxide radicals in human neutrophils stimulated with N -formyl-Met-Leu-Phe (66% inhibition). Since superoxide anions are essential for platelet aggregation and L-type Ca2+ -channel activity, we further found that THPI inhibited platelet aggregation induced by arachidonic acid (IC50 46.80 6.88 ,m). The effect of THPI on Ca2+ current in NG108,15 cells was investigated using the whole-cell voltage-clamp technique. THPI inhibited voltage-dependent L-type Ca2+ current (ICa,L). The IC50 value of THPI-induced inhibition of ICa,L was 3.60 0.81 ,m. THPI caused no change in the overall shape of the current-voltage relationship of ICa,L. This indicates that THPI is an inhibitor of ICa,L in NG108,15 cells. Therefore, the channel-blocking properties of THPI may contribute to the underlying mechanism by which it affects neuronal or neuroendocrine function. Furthermore, no significant cytotoxic effects of THPI (0.3,50 ,m) were observed in NG108,15 cells. The results indicate that THPI is a potential reactive oxygen species scavenger and may prevent platelet aggregation or inhibit L-type Ca2+ -channel activity, possibly by scavenging reactive oxygen species. [source]


Alcohol Consumption and the Body's Biological Clock

ALCOHOLISM, Issue 8 2005
Rainer Spanagel
This review summarizes new findings on the bidirectional interactions between alcohol and the clock genes, underlying the generation of circadian rhythmicity. At the behavioral level, both adult and perinatal ethanol treatments alter the free-running period and light response of the circadian clock in rodents; genetic ethanol preference in alcohol-preferring rat lines is also associated with alterations in circadian pacemaker function. At the neuronal level, it has been shown that ethanol consumption alters the circadian expression patterns of period (per) genes in various brain regions, including the suprachiasmatic nucleus. Notably, circadian functions of ,-endorphin,containing neurons that participate in the control of alcohol reinforcement become disturbed after chronic alcohol intake. In turn, per2 gene activity regulates alcohol intake through its effects on the glutamatergic system through glutamate reuptake mechanisms and thereby may affect a variety of physiological processes that are governed by our internal clock. In summary, a new pathologic chain has been identified that contributes to the negative health consequences of chronic alcohol intake. Thus, chronic alcohol intake alters the expression of per genes, and, as a consequence, a variety of neurochemical and neuroendocrine functions become disturbed. Further steps in this pathologic chain are alterations in physiological and immune functions that are under circadian control, and, as a final consequence, addictive behavior might be triggered or sustained by this cascade. [source]