Distribution and Coexistence of Corticotropin-Releasing Factor-, Neurotensin-, Enkephalin-, Cholecystokinin-, Galanin- and Vasoactive Intestinal Polypeptide/Peptide Histidine Isoleucine-Like Peptides in the Parvocellular Part of the Paraventricular Nucleus

Ceccatelli, Sandra; Eriksson, Maud; Hökfelt, Tomas

doi:10.1159/000125133

Cited by 169 publications

(94 citation statements)

References 35 publications

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“…Other hypothalamically abundant neuropeptides such as corticotrophin-releasing factor (52) and arginine vasopressin (53) have also been implicated in mood regulation. Double immunolabeling studies have showed that whereas the coexistence between corticotrophin-releasing factor and galanin is very low (54), the coexistence between arginine vasopressin and galanin is very common in the paraventricular nucleus (55), and it has been shown that the arginine vasopressin release can be regulated by galanin (56). On the other hand, a recent study showed that REM sleep deprivation selectively up-regulates galanin expression without affecting the mRNA levels of either corticotrophin-releasing factor or arginine vasopressin (51), suggesting that a galaninergic antidepressant-like effect might be achieved without the influence of these additional neuropeptide systems.…”

Section: Discussionmentioning

confidence: 99%

A role for galanin in antidepressant actions with a focus on the dorsal raphe nucleus

Lü

Barr²,

Kinney³

et al. 2005

Proc. Natl. Acad. Sci. U.S.A.

121

131

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Selective serotonin reuptake inhibitors, such as fluoxetine (FLX), are the most commonly used drugs in the treatment of major depression. However, there is a limited understanding of their molecular mechanism of action. Although the acute effect of selective serotonin reuptake inhibitors in elevating synaptic serotonin concentrations is well known, the clinical amelioration of depressive symptoms requires 14 -21 days of treatment, suggesting that numerous other rearrangements of function in the CNS must take place. In the present study, we demonstrated that 14 days of FLX treatment up-regulated galanin mRNA levels by 100% and GalR2-binding sites by 50%, in the rat dorsal raphe nucleus, where galanin coexists with serotonin. Furthermore, a galanin receptor antagonist, M40, attenuated the antidepressant-like effect of FLX in the forced swim test, a rodent preclinical screen commonly used to evaluate antidepressant-like efficacy. Direct activation of galanin receptors by a galanin receptor agonist, galnon, was found to produce an antidepressant-like effect in the same task. Two other antidepressant treatments also affected the galaninergic system in the monoaminergic nuclei: Electroconvulsive shock elevated galanin mRNA levels in dorsal raphe nucleus, whereas sleep deprivation increased galanin mRNA levels in the locus coeruleus, further underlining the connection between activation of the galaninergic system and antidepressant action of various clinically proven treatments. O ur understanding of the molecular mechanism of action of fluoxetine (FLX), beyond its effect of elevating synaptic serotonin [5-hydroxytryptamine (5-HT)] concentration, is limited. The delay in the onset of clinical antidepressant effect suggests that transcriptional and translational events, leading to functional changes in signaling within the major serotoninergic nucleus dorsal raphe nucleus (DRN) and in its projection areas, may be required for these therapeutic effects (1-3). One potential player in mediating the long-term effects of FLX, besides 5-HT, is the neuropeptide galanin. Galanin, through its three G-protein-coupled receptors, GalR1, GalR2, and GalR3 (4), regulates homeostatic and motivated behaviors including pain perception, sleep, food intake, sexual activity, learning, and memory (5). Galaninergic transmission modulates the activity of monoaminergic neurons in the ventral tegmental area, DRN, and locus coeruleus (LC) (6-10). Galanin receptor subtypes GalR1 (7) and GalR2 are expressed in DRN neurons (11) that can be activated by galanin dendritically released from the dorsal raphe 5-HT neurons (9, 12) or from surrounding galanin immunoreactive terminals (7). In the noradrenergic nucleus LC, an area that is closely connected both structurally and functionally to DRN (13,14), GalR1 expression is induced by morphine withdrawal (15), and the galanin receptor agonist, galnon, was shown to attenuate several withdrawal signs (16). It is worth noting that drug withdrawal often precipitates symptoms of depression, and depression is a ...

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Section: Discussionmentioning

confidence: 99%

A role for galanin in antidepressant actions with a focus on the dorsal raphe nucleus

Lü

Barr²,

Kinney³

et al. 2005

Proc. Natl. Acad. Sci. U.S.A.

121

131

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show abstract

“…In the central nervous system, Vip expression is found in the suprachiasmatic nucleus and the paraventricular nucleus of the hypothalamus, where it influences circadian clocks and pituitary adrenocorticotropic hormone secretion, respectively (Ceccatelli et al, 1989;Hökfelt et al, 1987;Nussdorfer and Malendowicz, 1998;Vosko et al, 2007). Although Vip immunoreactivity and Vip binding sites have been found in the mammillary nuclei (Saper, 2000;Sarrieau et al, 1994), VIP expression itself in the MA is not reported in the mouse expression atlas, suggesting that the expression of Vip in this region in zebrafish might not be an evolutionarily conserved feature.…”

Section: Evolutionary Conservation Of the Vip-and Uts1-positive Neuromentioning

confidence: 99%

Specification of posterior hypothalamic neurons requires coordinated activities of Fezf2, Otp, Sim1a and Foxb1.2

Wolf

Ryu

2013

Development

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SUMMARYThe hypothalamus is a key integrative center in the brain that consists of diverse cell types required for a variety of functions including homeostasis, reproduction, stress response, social and cognitive behavior. Despite our knowledge of several transcription factors crucial for hypothalamic development, it is not known how the wide diversity of neuron types in the hypothalamus is produced. In particular, almost nothing is known about the mechanisms that specify neurons in the posteriormost part of the hypothalamus, the mammillary area. Here, we investigated the specification of two distinct neuron types in the mammillary area that produce the hypothalamic hormones Vasoactive intestinal peptide (Vip) and Urotensin 1 (Uts1). We show that Vip-and Uts1-positive neurons develop in distinct domains in the mammillary area defined by the differential expression of the transcription factors Fezf2, Otp, Sim1a and Foxb1.2. Coordinated activities of these factors are crucial for the establishment of the mammillary area subdomains and the specification of Vip-and Uts1-positive neurons. In addition, Fezf2 is important for early development of the posterior hypothalamus. Thus, our study provides the first molecular anatomical map of the posterior hypothalamus in zebrafish and identifies, for the first time, molecular requirements underlying the specification of distinct posterior hypothalamic neuron types.

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“…It is specifically involved in the initiation of parturition and milk ejection, and is itself a stimulator of PRL secretion (see below) (Samson et al, 1986). VIP, also a major mediator of PRL secretion, is found in cells of the parvocellular PVN (see below) (Ceccatelli et al, 1989). The SON, which has developmental and cellular similarities to the PVN, contains OT-positive cells (Saper, 1990;Van de Kar et al, 1995).…”

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.

show abstract

Distribution and Coexistence of Corticotropin-Releasing Factor-, Neurotensin-, Enkephalin-, Cholecystokinin-, Galanin- and Vasoactive Intestinal Polypeptide/Peptide Histidine Isoleucine-Like Peptides in the Parvocellular Part of the Paraventricular Nucleus

Cited by 169 publications

References 35 publications

A role for galanin in antidepressant actions with a focus on the dorsal raphe nucleus

A role for galanin in antidepressant actions with a focus on the dorsal raphe nucleus

Specification of posterior hypothalamic neurons requires coordinated activities of Fezf2, Otp, Sim1a and Foxb1.2

From Galactorrhea to Osteopenia: Rethinking Serotonin–Prolactin Interactions

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