Facilitation of 5-HT2A/2C-mediated neurotransmission in the ventromedial hypothalamic nucleus decreases anxiety in the elevated T-maze

Silva, E.S. da; Poltronieri, S. C.; Nascimento, Juliana O.G.; Zangrossi, Hélio; Viana, Milena de Barros

doi:10.1016/j.bbr.2010.09.016

Cited by 17 publications

(17 citation statements)

References 52 publications

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“…In conclusion, the result obtained in studies with SF‐1 KO mice models are in agreement with those obtained from previous studies showing a role of VMH neurones in energy homeostasis (138–140), female sexual behaviour (141–143), anxiety (31, 140, 144) and female reproduction (145). Specific molecular roles of SF‐1 in the regulation of these processes await further elucidation.…”

Section: Brain Sexual Differentiation and Behaviour In Sf‐1 Ko Micesupporting

confidence: 91%

Steroidogenic Factor 1 and the Central Nervous System

Büdefeld

Tobet

Majdič

2011

J Neuroendocrinology

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Steroidogenic factor 1 (SF‐1; officially designated NR5a1) is a member of a nuclear receptor superfamily with important roles in the development of endocrine systems. Studies with global and tissue‐specific (i.e. central nervous system) knockout mice have revealed several roles of SF‐1 in brain. These include morphological effects on the development of the ventromedial nucleus of the hypothalamus and functional effects on body weight regulation through modulation of physical activity, anxiety‐like behaviours and female sexual behaviours. Although such defects are almost certainly a result of the absence of SF‐1 acting as a transcription factor in the hypothalamus, global SF‐1 knockout mice also represent a model for studying the sex differences in the brain that develop in the absence of exposure to foetal sex steroid hormones as a result of the absence of gonads. In the present review, current knowledge of the roles of SF‐1 protein in the central nervous system is discussed.

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Section: Brain Sexual Differentiation and Behaviour In Sf‐1 Ko Micesupporting

confidence: 91%

Steroidogenic Factor 1 and the Central Nervous System

Büdefeld

Tobet

Majdič

2011

J Neuroendocrinology

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“…Ablation of SF1 neurons in the VMHdm attenuate both innate and learned defensive behaviors (38), and activation of SF1 neurons in the VMHdm can induce defensive-like motor and autonomic responses (23). Serotonin receptors on VMH neurons not only contribute to the regulation of bone metabolism (15), but also in generalized anxiety (39). In addition to these findings, we further show that the link between stress-induced anxiety and bone regulation occur at the level of the VMHdm.…”

Section: The Vmh An Important Hypothalamic Region Regulates Both Besupporting

confidence: 59%

Identification of a Central Neural Circuit that Regulates Anxiety-induced Bone Loss

Yang

Liu

Chen

et al. 2019

Preprint

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# These authors contributed equally to this work. One Sentence Summary: Identification of a new GABAergic neural circuit from forebrain to hypothalamus used for regulation of anxiety-induced bone loss. Abstract:The homeostasis of bone metabolism is finely regulated by the central nervous system and recent studies have suggested that mood disorders, such as anxiety, are closely related to bone metabolic abnormalities; however, our understanding of central neural circuits regulating bone metabolism is still largely limited. In this study, we first demonstrate that confined isolation of human participants under normal gravity resulted in decreased bone density and elevated anxiety levels. We then used an established mouse model to dissect the neural circuitry regulating anxiety-induced bone loss. Combining electrophysiological, optogenetic and chemogenetic approaches, we demonstrate that GABAergic neural circuitry in ventromedial hypothalamus (VMH) modulates anxiety-induced bone loss; importantly, the GABAergic input in VMHdm arose from a specific group of somatostatin neurons in the bed nucleus of the stria terminalis (BNST), which is both indispensable for anxiety-induced bone loss and able to trigger bone loss in the absence of stressors. VGLUT2 neurons in Nucleus tractus solitaries (NTS) and peripheral sympathetic system were employed by this BNST-VMH neural circuit to regulate anxiety-induced bone loss. Overall, we uncovered new GABAergic neural circuitry from the forebrain to hypothalamus, used in the regulation of anxiety-induced bone loss, and revealed a population of somatostatin neurons in BNST not previously implicated in bone mass regulation.These findings thus identify the underlying central neural mechanism of psychiatric disorders, such as anxiety, that influences bone metabolism at the circuit level.

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“…Doses were chosen based on their ability to influence anxiety or other behaviors when injected intraperitoneal or site-specifically into the rodent brain (Bertrand, Lehmann, Lazarus, Jeltsch & Cassel, 2000; Carli, Tatarczynska, Cervo & Samanin, 1993; Clark, 1991; De Almeida, Giovenardi, Charchat & Lucion, 1998; Da Silva, Poltronieri, Nascimento, Zangrossi & Viana, 2011; Dodge & Badura, 2002; Fendt et al, 2005; Gulia, Kumar & Mallick, 2002; Guo et al, 1996; Schweimer et al, 2005; Solderpalm & Engel, 1988; Toufexis et al, 1999). The intra-BSTv infusions were done slowly over the course of 1 min through a 16-mm-long bilateral 28-gauge injector connected by polyethylene tubing to a 0.5 μl Hamilton syringe (Hamilton, Reno, NV).…”

Section: Methodsmentioning

confidence: 99%

Noradrenergic alpha-2 receptor modulators in the ventral bed nucleus of the stria terminalis: Effects on anxiety behavior in postpartum and virgin female rats.

Smith

Piasecki

Weera

et al. 2013

Behavioral Neuroscience

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Emotional hyper-reactivity can inhibit maternal responsiveness in female rats and other animals. Maternal behavior in postpartum rats is disrupted by increasing norepinephrine release in the ventral bed nucleus of the stria terminalis (BSTv) with the α2-autoreceptor antagonist, yohimbine, or the more selective α2-autoreceptor antagonist, idazoxan (Smith et al., 2012). Because high noradrenergic activity in the BSTv can also increase anxiety-related behaviors, increased anxiety may underlie the disrupted mothering of dams given yohimbine or idazoxan. To assess this possibility, anxiety-related behaviors in an elevated plus maze were assessed in postpartum rats after administration of yohimbine or idazoxan. It was further assessed if the α2-autoreceptor agonist clonidine (which decreases norepinephrine release) would, conversely, reduce dams’ anxiety. Groups of diestrous virgins were also examined. It was found that peripheral or intra-BSTv yohimbine did increase anxiety-related behavior in postpartum females. However, BSTv infusion of idazoxan did not reproduce yohimbine’s anxiogenic effects and anxiety was not reduced by peripheral or intra-BSTv clonidine. Because yohimbine is a weak 5HT1A receptor agonist, other groups of females received BSTv infusion of the 5HT1A receptor agonist 8OH-DPAT, but it did not alter their anxiety-related behavior. Lastly, levels of norepinephrine and serotonin in tissue punches from the BSTv did not differ between postpartum and diestrous rats, but serotonin turnover was lower in mothers. These results suggest that the impaired maternal behavior after BSTv infusion of yohimbine or idazoxan cannot both be readily explained by an increase in dams’ anxiety, and that BSTv α2-autoreceptor modulation alone has little influence anxiety-related behaviors in postpartum or diestrous rats.

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Facilitation of 5-HT2A/2C-mediated neurotransmission in the ventromedial hypothalamic nucleus decreases anxiety in the elevated T-maze

Cited by 17 publications

References 52 publications

Steroidogenic Factor 1 and the Central Nervous System

Steroidogenic Factor 1 and the Central Nervous System

Identification of a Central Neural Circuit that Regulates Anxiety-induced Bone Loss

Noradrenergic alpha-2 receptor modulators in the ventral bed nucleus of the stria terminalis: Effects on anxiety behavior in postpartum and virgin female rats.

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