Stimuli and consequences of dendritic release of oxytocin within the brain

2007 ◽  
Vol 35 (5) ◽  
pp. 1252-1257 ◽  
Author(s):  
I.D. Neumann
Keyword(s):  
Paraventricular Nucleus ◽  
Stress Responses ◽  
Supraoptic Nucleus ◽  
Brain Regions ◽  
Model System ◽  
Intracerebral Microdialysis ◽  
Psychotherapeutic Intervention ◽  
Psychiatric Illnesses ◽  
Oxytocin Release ◽  
The Brain

The brain oxytocin system has served as a distinguished model system in neuroendocrinology to study detailed mechanisms of intracerebral release, in particular of somatodendritic release, and its behavioural and neuroendocrine consequences. It has been shown that oxytocin is released within various brain regions, but evidence for dendritic release is limited to the main sites of oxytocin synthesis, i.e. the hypothalamic SON (supraoptic nucleus) and PVN (paraventricular nucleus). In the present paper, stimuli of dendritic release of oxytocin and the related neuropeptide vasopressin are discussed, including parturition and suckling, i.e. the period of a highly activated brain oxytocin system. Also, exposure to various pharmacological, psychological or physical stressors triggers dendritic oxytocin release, as monitored by intracerebral microdialysis within the SON and PVN during ongoing behavioural testing. So far, dendritic release of the neuropeptide has only been demonstrated within the hypothalamus, but intracerebral oxytocin release has also been found within the central amygdala and the septum in response to various stimuli including stressor exposure. Such a locally released oxytocin modulates physiological and behavioural reproductive functions, emotionality and hormonal stress responses, as it exerts, for example, pro-social, anxiolytic and antistress actions within restricted brain regions. These discoveries make oxytocin a promising neuromodulator of the brain for psychotherapeutic intervention and treatment of numerous psychiatric illnesses, for example, anxiety-related diseases, social phobia, autism and postpartum depression.

Insights into the molecular basis of host behaviour manipulation by Toxoplasma gondii infection

2017 ◽  
Vol 1 (6) ◽  
pp. 563-572 ◽  
Author(s):  
Pierre-Mehdi Hammoudi ◽  
Dominique Soldati-Favre
Keyword(s):  
Toxoplasma Gondii ◽  
Stress Responses ◽  
Molecular Mechanisms ◽  
Brain Regions ◽  
Intermediate Hosts ◽  
Toxoplasma Gondii Infection ◽  
Host Parasite ◽  
Host Behaviour ◽  
The Brain ◽  
Brain Homeostasis

Typically illustrating the ‘manipulation hypothesis’, Toxoplasma gondii is widely known to trigger sustainable behavioural changes during chronic infection of intermediate hosts to enhance transmission to its feline definitive hosts, ensuring survival and dissemination. During the chronic stage of infection in rodents, a variety of neurological dysfunctions have been unravelled and correlated with the loss of cat fear, among other phenotypic impacts. However, the underlying neurological alteration(s) driving these behavioural modifications is only partially understood, which makes it difficult to draw more than a correlation between T. gondii infection and changes in brain homeostasis. Moreover, it is barely known which among the brain regions governing fear and stress responses are preferentially affected during T. gondii infection. Studies aiming at an in-depth dissection of underlying molecular mechanisms occurring at the host and parasite levels will be discussed in this review. Addressing this reminiscent topic in the light of recent technical progress and new discoveries regarding fear response, olfaction and neuromodulator mechanisms could contribute to a better understanding of this complex host–parasite interaction.

scholarly journals Environment and Behavior: Neurochemical Effects of Different Diets in the Calf Brain

Animals ◽  
2019 ◽  
Vol 9 (6) ◽  
pp. 358 ◽  
Author(s):  
Angelo Peli ◽  
Annamaria Grandis ◽  
Marco Tassinari ◽  
Paolo Famigli Bergamini ◽  
Claudio Tagliavia ◽  
...  
Keyword(s):  
Prefrontal Cortex ◽  
Paraventricular Nucleus ◽  
Stress Responses ◽  
Control Diet ◽  
Brain Regions ◽  
Diet Group ◽  
Stressful Events ◽  
Solitary Tract ◽  
Milk Diet ◽  
Housing Systems

Calves reared for the production of white veal are subjected to stressful events due to the type of liquid diet they receive. Stress responses are mediated by three main stress-responsive cerebral regions: the prefrontal cortex, the paraventricular nucleus of the hypothalamus, and the nucleus of the solitary tract of the brainstem. In the present study, we have investigated the effects of different diets on these brain regions of ruminants using immunohistochemical methods. In this study, 15 calves were used and kept in group housing systems of five calves each. They were fed with three different diets: a control diet, a milk diet, and a weaned diet. Brain sections were immunostained to evaluate the distribution of neuronal nitric oxide synthase and myelin oligodendrocyte glycoprotein immunoreactivity in the prefrontal cortex; the expression of oxytocin in the paraventricular nucleus; and the presence of c-Fos in the A2 group of the nucleus of the solitary tract. The main results obtained indicate that in weaned diet group the oxytocin activity is lower than in control diet and milk diet groups. In addition, weaning appears to stimulate myelination in the prefrontal cortex. In summary, this study supports the importance of maintaining a nutritional lifestyle similar to that occurring in natural conditions.

scholarly journals Molecular Characterization and Biological Function of Neuroendocrine Regulatory Peptide-3 in the Rat

Endocrinology ◽  
2012 ◽  
Vol 153 (3) ◽  
pp. 1377-1386 ◽  
Author(s):  
Hiroaki Fujihara ◽  
Kazuki Sasaki ◽  
Emi Mishiro-Sato ◽  
Toyoaki Ohbuchi ◽  
Govindan Dayanithi ◽  
...  
Keyword(s):  
Paraventricular Nucleus ◽  
Supraoptic Nucleus ◽  
Biologically Active ◽  
Regulatory Peptide ◽  
Salt Loading ◽  
Peptidomic Analysis ◽  
Biologically Active Peptide ◽  
Body Fluid Balance ◽  
The Brain

Neuroendocrine regulatory peptide (NERP)-3, derived from the neurosecretory protein VGF (non-aconymic), is a new biologically active peptide identified through peptidomic analysis of the peptides secreted by an endocrine cell line. Using a specific antibody recognizing the C-terminal region of NERP-3, immunoreactive (ir)-NERP-3 was identified in acid extracts of rat brain and gut as a 30-residue NERP-3 with N-terminal pyroglutamylation. Assessed by radioimmunoassay, ir-NERP-3 was more abundant in the brain, including the posterior pituitary (PP), than in the gut. Immunohistochemistry demonstrated that ir-NERP-3 was significantly increased in the suprachiasmatic nucleus, the magnocellular division of the paraventricular nucleus, and the external layer of the median eminence, but not in the supraoptic nucleus, after dehydration. The immunoreactivity was, however, markedly decreased in all of these locations after chronic salt loading. Intracerebroventricular administration of NERP-3 in conscious rats induced Fos expression in a subset of arginine vasopressin (AVP)-containing neurons in the supraoptic nucleus and the magnocellular division of the paraventricular nucleus. On in vitro isolated rat PP preparations, NERP-3 caused a significant AVP release in a dose-related manner, suggesting that NERP-3 in the PP could be an autocrine activator of AVP release. Taken together, the present results suggest that NERP-3 in the hypothalamo-neurohypophyseal system may be involved in the regulation of body fluid balance.

scholarly journals Network Dysfunction in Comorbid Psychiatric Illnesses and Epilepsy

2020 ◽  
Vol 20 (4) ◽  
pp. 205-210
Author(s):  
Phillip L. W. Colmers ◽  
Jamie Maguire
Keyword(s):  
Cognitive Impairments ◽  
Brain Regions ◽  
Network Activity ◽  
Hypothalamic Pituitary Adrenal ◽  
Psychiatric Illnesses ◽  
Ictal Activity ◽  
Episodic Nature ◽  
Network States ◽  
The Brain ◽  
Pituitary Adrenal Axis

The episodic nature of both epilepsy and psychiatric illnesses suggests that the brain switches between healthy and pathological states. The most obvious example of transitions between network states related to epilepsy is the manifestation of ictal events. In addition to seizures, there are more subtle changes in network communication within and between brain regions, which we propose may contribute to psychiatric illnesses associated with the epilepsies. This review will highlight evidence supporting aberrant network activity associated with epilepsy and the contribution to cognitive impairments and comorbid psychiatric illnesses. Further, we discuss potential mechanisms mediating the network dysfunction associated with comorbidities in epilepsy, including interneuron loss and hypothalamic–pituitary–adrenal axis dysfunction. Conceptually, it is necessary to think beyond ictal activity to appreciate the breadth of network dysfunction contributing to the spectrum of symptoms associated with epilepsy, including psychiatric comorbidities.

scholarly journals Dynamic Changes in Oxytocin Receptor Expression and Activation at Parturition in the Rat Brain

Endocrinology ◽  
2007 ◽  
Vol 148 (10) ◽  
pp. 5095-5104 ◽  
Author(s):  
Simone L. Meddle ◽  
Valerie R. Bishop ◽  
Effimia Gkoumassi ◽  
Fred W. van Leeuwen ◽  
Alison J. Douglas
Keyword(s):  
Mrna Expression ◽  
Paraventricular Nucleus ◽  
Maternal Behavior ◽  
Brain Regions ◽  
Oxytocin Receptor ◽  
Lateral Septum ◽  
Receptor Expression ◽  
Olfactory Bulbs ◽  
Bed Nucleus ◽  
The Brain

Oxytocin plays a pivotal role in rat parturition, acting within the brain to facilitate its own release in the supraoptic nucleus (SON) and paraventricular nucleus, and to stimulate maternal behavior. We investigated oxytocin receptor (OTR) expression and activation perinatally. Using a 35S-labeled riboprobe complementary to OTR mRNA, OTR expression was quantified in proestrus virgin, 21- and 22-day pregnant, parturient (90 min. from pup 1 birth), and postpartum (4–12 h from parturition) rats. Peak OTR mRNA expression was observed at parturition in the SON, brainstem regions, medial preoptic area (mPOA), bed nucleus of the stria terminalis (BnST), and olfactory bulbs, but there was no change in the paraventricular nucleus and lateral septum. OTR mRNA expression was increased on the day of expected parturition in the SON and brainstem, suggesting that oxytocin controls the pathway mediating input from uterine signals. Likewise, OTR mRNA expression was increased in the mPOA and BnST during labor/birth. In the olfactory bulbs and medial amygdala, parturition induced increased OTR mRNA expression compared with pre-parturition, reflecting their immediate response to new stimuli at birth. Postpartum OTR expression in all brain regions returned to levels observed in virgin rats. Parturition significantly increased the number of double-immunolabeled cells for Fos and OTR within the SON, brainstem, BnST, and mPOA regions compared with virgin rats. Thus, there are dynamic region-dependent changes in OTR-expressing cells at parturition. This altered OTR distribution pattern in the brain perinatally reflects the crucial role oxytocin plays in orchestrating both birth and maternal behavior.

Effects of central sodium on epithelial sodium channels in rat brain

2010 ◽  
Vol 299 (1) ◽  
pp. R222-R233 ◽  
Author(s):  
Hong-Wei Wang ◽  
Md Shahrier Amin ◽  
Esraa El-Shahat ◽  
Bing S. Huang ◽  
Balwant S. Tuana ◽  
...  
Keyword(s):  
Choroid Plexus ◽  
Supraoptic Nucleus ◽  
Third Ventricle ◽  
Brain Regions ◽  
Neural Precursor Cells ◽  
Epithelial Sodium Channels ◽  
Artificial Cerebrospinal Fluid ◽  
Hypothalamic Nuclei ◽  
Hypothalamic Tissue ◽  
The Brain

We evaluated the effects of intracerebroventricular (icv) infusion of Na+-rich artificial cerebrospinal fluid (aCSF), with or without the mineralocorticoid receptor (MR) blocker spironolactone, on epithelial Na+ channel (ENaC) subunits and regulators, such as MR, serum/glucocorticoid-inducible kinase 1, neural precursor cells expressed developmentally downregulated 4-like gene, 11β-hydroxylase, and aldosterone synthase, in brain regions of Wistar rats. The effects of icv infusion of the amiloride analog benzamil on brain tissue and CSF Na+ concentration ([Na+]) were also assessed. In the choroid plexus and ependyma of the anteroventral third ventricle, ENaC subunits are present in apical and basal membranes. Na+-rich aCSF increased β-ENaC mRNA and immunoreactivity in the choroid plexus and increased α- and β-ENaC immunoreactivities in the ependyma. Na+-rich aCSF increased α- and β-ENaC-gold-labeled particles in the microvilli of the choroid plexus and in basolateral membranes of the ependyma. Spironolactone only prevented the increase in β-ENaC immunoreactivity in the choroid plexus and ependyma. In the supraoptic nucleus, paraventricular nucleus, and subfornical organ, Na+-rich aCSF did not affect mRNA expression levels of the studied genes. Benzamil significantly increased CSF [Na+] in the control, but not Na+-rich, aCSF group. In contrast, benzamil prevented the increase in hypothalamic tissue [Na+] by Na+-rich aCSF. These results suggest that CSF Na+ upregulates ENaC expression in the brain epithelia, but not in the neurons of hypothalamic nuclei. ENaC in the choroid plexus and ependyma appear to contribute to regulation of Na+ homeostasis in the brain.

Stimulation of oxytocin release within the supraoptic nucleus and into blood by CCK-8

1994 ◽  
Vol 267 (6) ◽  
pp. R1626-R1631 ◽  
Author(s):  
I. Neumann ◽  
R. Landgraf ◽  
Y. Takahashi ◽  
Q. J. Pittman ◽  
J. A. Russell
Keyword(s):  
Supraoptic Nucleus ◽  
Jugular Vein ◽  
Female Rats ◽  
Reproductive Behaviors ◽  
Vasopressin Release ◽  
Hypothalamic Nuclei ◽  
Oxytocin Release ◽  
Left And Right ◽  
Complex Regulation ◽  
The Brain

Simultaneous microdialysis in brain and blood was used to monitor the effects of systemic and central cholecystokinin octapeptide (CCK-8) on the release of oxytocin and vasopressin within the hypothalamic supraoptic nucleus (SON) as well as into blood of urethan-anesthetized female rats. Administration of CCK-8 (20 micrograms/kg iv) increased oxytocin contents in 30-min microdialysates sampled simultaneously within the SON (1.8-fold) and blood (2.4-fold, both P < 0.05) compared with prestimulation levels. In another experiment, after bilateral administration of CCK-8 directly into the SON (10 ng/0.5 microliter) via a microdialysis/infusion probe, oxytocin contents in dialysates sampled from the left and right SON were increased 2.3- and 1.7-fold (P < 0.05), respectively. In simultaneously sampled dialysates from the jugular vein, oxytocin content increased 2.3-fold (P < 0.05). In contrast, oxytocin in dialysates sampled outside the hypothalamic nuclei was not altered by systemic or central CCK-8. The direct infusion of CCK-8 into both SON increased the release of vasopressin within the SON 1.7-fold (P < 0.05) but failed to significantly change vasopressin release into blood. The present findings show a coordinated regulation of intranuclear and systemic release of oxytocin in response to systemic and central CCK-8 and provide further evidence for a possible involvement of endogenous oxytocin in the complex regulation of ingestive and reproductive behaviors induced by CCK-8 at the brain level.

Brain activation following peripheral administration of the GLP-1 receptor agonist exendin-4

2011 ◽  
Vol 301 (4) ◽  
pp. R1011-R1024 ◽  
Author(s):  
Elena-Dana Baraboi ◽  
David H. St-Pierre ◽  
Julie Shooner ◽  
Elena Timofeeva ◽  
Denis Richard
Keyword(s):  
Vagus Nerve ◽  
Mrna Expression ◽  
Supraoptic Nucleus ◽  
Brain Activation ◽  
Brain Regions ◽  
Nodose Ganglion ◽  
Central Regions ◽  
The Brain ◽  
Pituitary Adrenal Axis

The aim of our study was to investigate the anorectic and brain stimulatory effects of various doses of exendin-4 (Ex-4) and to investigate the role of the vagus nerve in Ex-4-induced brain activation. A dose-related increase in c- fos mRNA expression was observed following Ex-4 administration (0.155–15.5 μg/kg). Doses of Ex-4 that caused anorexia without aversive effects (0.155, 0.775 μg/kg) induced c- fos expression in the hypothalamic arcuate and paraventricular (PVH; parvocellular) nuclei as well as in the limbic and brainstem structures. Doses of Ex-4 that caused aversion (1.55, 15.5 μg/kg) stimulated the same regions (in a more intense way) and additionally activated the magnocellular hypothalamic structures (supraoptic nucleus and PVH magnocellular). The brain c- fos pattern induced by Ex-4 showed both similarities and differences with that induced by refeeding. Subdiaphragmatic vagotomy significantly blunted the stimulation of c- fos mRNA expression induced by Ex-4 in the nodose ganglion, the medial part of nucleus of the solitary tract, and the parvocellular division of the PVH. Pretreatment with Ex-9-39 (330 μg/kg ip) impaired the neuronal activation evoked by Ex-4 in all brain regions and in the nodose ganglion. Effects of Ex-4 on hypothalamic-pituitary-adrenal axis activity were not altered by vagotomy. Results of this study demonstrate and relate the anorectic and brain stimulatory effects of aversive and nonaversive doses of Ex-4 and indicate that the activation of specific central regions induced by the peripheral administration of Ex-4 is, at least in part, dependent on the integrity of the vagus nerve.

Selective contributions of the medial preoptic nucleus to testosterone-dependant regulation of the paraventricular nucleus of the hypothalamus and the HPA axis

2008 ◽  
Vol 295 (4) ◽  
pp. R1020-R1030 ◽  
Author(s):  
Martin Williamson ◽  
Victor Viau
Keyword(s):  
Hpa Axis ◽  
Paraventricular Nucleus ◽  
Stress Responses ◽  
Brain Regions ◽  
Inhibitory Effect ◽  
Mrna Levels ◽  
Preoptic Nucleus ◽  
External Zone ◽  
Medial Preoptic Nucleus ◽  
Medial Nucleus

Previous data have consistently demonstrated an inhibitory effect of androgens on stress-induced hypothalamic-pituitary-adrenal (HPA) responses. Several brain regions may influence androgen-mediated inhibition of the HPA axis, including the medial preoptic area. To test the role of the medial preoptic nucleus (MPN) specifically, we examined in high- and low-testosterone-replaced gonadectomized rats bearing discrete bilateral lesions of the MPN basal and stress-induced indexes of HPA function, and the relative levels of corticotropin-releasing hormone (CRH) and arginine vasopressin (AVP) mRNA in the amygdala. High testosterone replacement decreased plasma adrenocorticotropin hormone (ACTH) and paraventricular nucleus (PVN) Fos responses to restraint exposure in sham- but not in MPN-lesioned animals. AVP-, but not CRH-immunoreactivity staining in the external zone of the median eminence was increased by testosterone in sham animals, and MPN lesions blocked this increment in AVP. A similar interaction between MPN lesions and testosterone occurred on AVP mRNA levels in the medial nucleus of the amygdala. These findings support an involvement of MPN projections in mediating the AVP response to testosterone in both the medial parvocellular PVN and medial amygdala. We conclude that the MPN forms part of an integral circuit that mediates the central effects of gonadal status on neuroendocrine and central stress responses.

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