Dynamism of chemoarchitecture in the hypothalamic paraventricular nucleus

Kiss, József Zoltán

doi:10.1016/0361-9230(88)90080-9

Cited by 103 publications

(38 citation statements)

References 70 publications

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“…In the same vein, it is also noteworthy that the TRH, vasoactive intestinal peptide, dopamine, and somatostatin neurons, which are known as the stimulatory or inhibitory neurons of PRL release, are also localized in the paraventricular hypothalamic nucleus (21,22). This close proximity of PrRP fibers to TRH fibers is especially pronounced in the bed nucleus of the stria terminalis (10).…”

Section: Discussionmentioning

confidence: 87%

Immunocytochemical Localization of Prolactin-Releasing Peptide in the Rat Brain

Maruyama

1999

Endocrinology

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A hypothalamic peptide that stimulates PRL release has recently been found as a ligand of an orphan receptor and named PRL-releasing peptide (PrRP). PrRP and its receptor were mainly detected in the hypothalamus and pituitary gland, respectively. Its characteristics suggested PrRP to be a novel hypophysiotropic peptide that stimulates the anterior pituitary PRL cell; however, this remained to be confirmed morphologically. We therefore performed an immunocytochemical study to locate PrRP in the rat brain using the regionspecific monoclonal antibodies, P2L-1C and P2L-1T, which recognize the C-terminal and the internal sequence of PrRP, respectively. Our results clearly show that dense immunoreactive nerve fiber networks are present in the paraventricular hypothalamic nucleus, supraoptic nucleus, paratenial thalamic nucleus, basolateral amygdaloid nucleus, and bed nucleus of the stria terminalis. A small number of PrRP nerve fibers was also observed in the neural lobe of the hypophysis. However, no immunopositive fiber was observed in the external region of the median eminence, which is known to be the release site of the classical hypophysiotropic hormones. Also, the distribution of PrRP was not changed during the estrous cycle. We therefore concluded that PrRP probably differs from classical hypothalamic releasing hormones. We found the immunoreactive cell bodies to be mainly in the caudal portion of the dorsomedial hypothalamic nucleus and solitary nucleus. A double immunocytochemical procedure revealed that some PrRP-positive neurons showed synaptic contact with oxytocin-positive cell bodies in the paraventricular hypothalamic nucleus, which suggests that PrRP regulates the function of oxytocin neurons. This is the first report to demonstrate the localization of the novel hypothalamic peptide, PrRP, and we therefore suggest that it takes part in a variety of brain functions. However, itis not yet known how PrRP is transported to the pituitary gland, which is the site that contains the greatest concentration of receptors to this new peptide. Therefore, additional work will be required to resolve this discrepancy between ligand and receptor site location. (Endocrinology 140: 2326 -2333, 1999) T HE DISCOVERY of the hypophysiotropic peptides and their delivery to the pituitary via the hypophyseal portal system was the most dramatic event in endocrinology during this century. Regulation of most of these pituitary hormones has been explained through the action of these hypothalamic hormones. PRL, which is included as one of the major anterior pituitary hormones, is known to have its secretion controlled by a variety of hypothalamic factors. Factors inhibiting its secretion are dopamine and somatostatin (1), whereas TRH, vasoactive intestinal polypeptide, serotonin (1), oxytocin (2), substance P, neurotensin (3), arginine vasopressin (4), pituitary adenylate cyclase-activating peptide, and galanin (5) all act to stimulate its secretion. However, the above secretagogues are all multifunctional peptides and a...

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Section: Discussionmentioning

confidence: 87%

Immunocytochemical Localization of Prolactin-Releasing Peptide in the Rat Brain

Maruyama

1999

Endocrinology

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“…The paraventricular nucleus (PVN) and supraoptic nucleus (SON) are associated with a variety of functions, which include regulation of metabolism and body temperature, control of water and food intake, and cardiovascular and gastrointestinal functioning (Lechan and Jackson, 1982;Crawley and Kiss, 1985;Leibowitz, 1978;Sawchenko et al, 1981;Porter and Brody, 1985). The PVN contains neurosecretory magnocellular cells, which produce oxytocin (OT) and vasopressin (AVP), and parvocellular cells, which synthesize corticotropin releasing factor (CRF), vasoactive intestinal peptide (VIP), thyroid releasing hormone (TRH), and other neuropeptides (Bloom et al, 1982;Kiss, 1988;Lechan and Jackson, 1982;Merchenthaler et al, 1982;Mezey and Kiss, 1985). The magnocellular OT and AVP cells project to the posterior lobe of the pituitary, while the parvocellular division projects to the AP via the median eminence.…”

Section: Hypothalamusmentioning

confidence: 99%

From Galactorrhea to Osteopenia: Rethinking Serotonin–Prolactin Interactions

Emiliano

Fudge

2004

Neuropsychopharmacol

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The widespread use of the selective serotonin reuptake inhibitors (SSRIs) has been accompanied by numerous reports describing a potential association with hyperprolactinemia. Antipsychotics are commonly known to elevate serum prolactin (PRL) through blockade of dopamine receptors in the pituitary. However, there is little awareness of the mechanisms by which SSRIs stimulate PRL release. Hyperprolactinemia may result in overt symptoms such as galactorrhea, which may be accompanied by impaired fertility. Long-term clinical sequelae include decreased bone density and the possibility of an increased risk of breast cancer. Through literature review, we explore the possible pathways involved in serotonin-induced PRL release. While the classic mechanism of antipsychotic-induced hyperprolactinemia directly involves dopamine cells in the tuberoinfundibular pathway, SSRIs may act on this system indirectly through GABAergic neurons. Alternate pathways involve serotonin stimulation of vasoactive intestinal peptide (VIP) and oxytocin (OT) release. We conclude with a comprehensive review of clinical sequelae associated with hyperprolactinemia, and the potential role of SSRIs in this phenomenon.

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“…For objective evaluation, the images of at least three stions per animal were scanned by a computer-assisted image analyzer (Optimas-Bioscan) fitted with a Zeiss Axioplan microscope and a Sony CCD camera. The images were overlapped with predefined masks, which enclosed either the magnocellular or the parvocellular part of the PVN (according to Kiss 1988, Kiss et al 1991. Levels of mRNA expression (optical density) were determined by measuring the mean gray value on inverted (in situ hybridization signal: black), automatically thresholded images in the PVN, with the left and right hemispheres being analyzed separately.…”

Section: In Situ Hybridization Histochemistrymentioning

confidence: 99%

Vasopressin Mediates the Response of the Combined Dexamethasone/CRH Test in Hyper-anxious Rats Implications for Pathogenesis of Affective Disorders

Keck

Wigger

Welt

et al. 2002

Neuropsychopharmacology

156

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To investigate the neuroendocrine alterations linked to inborn emotionality in two Wistar rat lines selectively bred for either high (HAB) or low (LAB) anxiety-related behavior, we administered the combined dexamethasone (DEX)/corticotropin-releasing hormone (CRH)testNeuroendocrine studies provide strong indications that hyperactivity of central corticotropin-releasing hormone (CRH) circuits, resulting in a characteristic dysregulation of the hypothalamic-pituitary-adrenocortical (HPA) system, plays a causal role in the symptomatology of affective and anxiety disorders (review: Keck and Holsboer 2001). The effects of CRH are modulated by vasopressin (AVP), which, after prolonged stress and in senescence, is increasingly coexpressed and secreted from hypothalamic CRH neurons in both humans and rodents (Antoni 1993;Tilders et al. 1993;Hatzinger et al. 2000;Keck et al. 2000). Similarly, increased numbers of CRH neurons that coexpress AVP mRNA have been found in the hypothalamus of depressed patients (Raadsheer et al. 1993;Purba et al. 1996). The excessive release of CRH and AVP into hypophysial portal blood is thought to increase the secretion of corticotropin (ACTH) from pituitary corticotrope cells, and this in turn to increase the release of corticosteroids from the adrenal gland. In this context, a variety of changes in HPA system regulation have been demonstrated in psychiatric disorders such as major depression, among them defective negative feedback of the HPA system, basal hypercortisolemia, inappropriate HPA suppression by the synthetic corticosteroid dexamethasone (DEX) and a paradoxical stimulation of ACTH secretion by CRH after DEX pretreatment (review: Holsboer and Barden 1996;Holsboer 2000). In depression, the combined DEX/CRH test, in which DEX-pretreated subjects receive a single dose of CRH, has proven to be the most sensitive tool for the detection of altered HPA regulation. Depending on age and gender, up to 90% of patients with depression show this neuroendocrine phenomenon (Heuser et al. 1994). Moreover, studies using the DEX/CRH test not only agree that normalization of an initial aberrance is predictive of a favorable treatment response but also corroborate other evidence that a persistent HPA abnormality correlates with chronicity or relapse (Heuser et al. 1996;Zobel et al. 1999). Since activation of corticosteroid receptors suppresses the synthesis and release of CRH and AVP from the hypothalamic paraventricular nucleus (PVN) , these findings are consistent with the hypothesis of functionally impaired corticosteroid receptor signaling in both depressed patients (Modell et al. 1997) and healthy subjects at genetic risk for depression Modell et al. 1998).As the mechanisms underlying the abnormal HPA reactivity in patients with certain psychiatric disorders are not fully understood, animal models are needed to further investigate the hypothesized linkage between these disorders and changes in the regulation of the HPA system. After several generations of selective breeding, we could establish ...

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Dynamism of chemoarchitecture in the hypothalamic paraventricular nucleus

Cited by 103 publications

References 70 publications

Immunocytochemical Localization of Prolactin-Releasing Peptide in the Rat Brain

Immunocytochemical Localization of Prolactin-Releasing Peptide in the Rat Brain

From Galactorrhea to Osteopenia: Rethinking Serotonin–Prolactin Interactions

Vasopressin Mediates the Response of the Combined Dexamethasone/CRH Test in Hyper-anxious Rats Implications for Pathogenesis of Affective Disorders

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