Hormonal-Neural Integration in the Female Rat Ventromedial Hypothalamus: Triple Labeling for Estrogen Receptor-α, Retrograde Tract Tracing from the Periaqueductal Gray, and Mating-Induced Fos Expression

Calizo, Lyngine H.; Flanagan‐Cato, Loretta M.

doi:10.1210/en.2003-0331

Cited by 43 publications

(26 citation statements)

References 54 publications

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“…Subsequently, estradiol induces necessary gene transcription and translation for the expression of lordosis behavior (reviewed in Micevych and Sinchak, 2007). The integrated response of the entire limbic-hypothalamic circuit is funneled through the VMH to descending projections that activate spinal motoneurons innervating muscles responsible for lordosis behavior (Calizo and Flanagan-Cato, 2003; Sinchak et al, 2010; reviewed in Pfaff et al, 2008). …”

Section: Hormonal Priming Of Sexual Behaviormentioning

confidence: 99%

Membrane-Initiated Estradiol Signaling Regulating Sexual Receptivity

Micevych¹,

Dewing²

2011

Front. Endocrin.

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Estradiol has profound actions on the structure and function of the nervous system. In addition to nuclear actions that directly modulate gene expression, the idea that estradiol can rapidly activate cell signaling by binding to membrane estrogen receptors (mERs) has emerged. Even the regulation of sexual receptivity, an action previously thought to be completely regulated by nuclear ERs, has been shown to have a membrane-initiated estradiol signaling (MIES) component. This highlighted the question of the nature of mERs. Several candidates have been proposed, ERα, ERβ, ER-X, GPR30 (G protein coupled estrogen receptor), and a receptor activated by a diphenylacrylamide compound, STX. Although each of these receptors has been shown to be active in specific assays, we present evidence for and against their participation in sexual receptivity by acting in the lordosis-regulating circuit. The initial MIES that activates the circuit is in the arcuate nucleus of the hypothalamus (ARH). Using both activation of μ-opioid receptors (MOR) in the medial preoptic nucleus and lordosis behavior, we document that both ERα and the STX-receptor participate in the required MIES. ERα and the STX-receptor activation of cell signaling are dependent on the transactivation of type 1 metabotropic glutamate receptors (mGluR1a) that augment progesterone synthesis in astrocytes and protein kinase C (PKC) in ARH neurons. While estradiol-induced sexual receptivity does not depend on neuroprogesterone, proceptive behaviors do. Moreover, the ERα and the STX-receptor activation of medial preoptic MORs and augmentation of lordosis were sensitive to mGluR1a blockade. These observations suggest a common mechanism through which mERs are coupled to intracellular signaling cascades, not just in regulating reproduction, but in actions throughout the neuraxis including the cortex, hippocampus, striatum, and dorsal root ganglias.

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Section: Hormonal Priming Of Sexual Behaviormentioning

confidence: 99%

Membrane-Initiated Estradiol Signaling Regulating Sexual Receptivity

Micevych¹,

Dewing²

2011

Front. Endocrin.

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“…The VMH is a sexually dimorphic group of intensely ERa expressing neurones that has extensive projections to areas of the brain involved in autonomic regulation, such as the CeA, PAG, PBN, NTS and RVLM as well as other hypothalamic nuclei (Canteras et al, 1994;Calizo and Flanagan-Cato, 2003). Rapid membrane effects on excitability and effects on gene transcription have been demonstrated in VMH neurones in hypothalamic slice preparations (Kelly and Ronnekleiv, 2008).…”

Section: Oestrogen Actions In Hypothalamic Nucleimentioning

confidence: 99%

Oestrogen receptors in the central nervous system and evidence for their role in the control of cardiovascular function

Spary

Maqbool

Batten

2009

Journal of Chemical Neuroanatomy

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“…Originally, because of the abundant expression of ORL-1 in the VMH, we concluded that OFQ/N was acting on descending motor output pathways to facilitate lordosis (Calizo and Flanagan-Cato, 2002, 2003; Cottingham et al, 1987; Pfeifle et al, 1980; Sinchak et al, 1997). However, preliminary experiments showed that similar OFQ/N infusions into the VMH deactivated MPN MOP suggesting that OFQ/N activates ORL-1 circuits that inhibit ARH β-END neurons that project to the MPN to facilitate lordosis (Sinchak et al, 2006a; Sinchak et al, 2006b).…”

Section: Introductionmentioning

confidence: 99%

Orphanin FQ in the mediobasal hypothalamus facilitates sexual receptivity through the deactivation of medial preoptic nucleus mu-opioid receptors

Sanathara

Moraes

Kanjiya

et al. 2011

Hormones and Behavior

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Sexual receptivity, lordosis, can be induced by sequential estradiol and progesterone or extended exposure to high levels of estradiol in the female rat. In both cases estradiol initially inhibits lordosis through activation of β-endorphin (β-END) neurons of the arcuate nucleus of the hypothalamus (ARH) that activate μ-opioid receptors (MOP) in the medial preoptic nucleus (MPN). Subsequent progesterone or extended estradiol exposure deactivate MPN MOP to facilitate lordosis. Opioid receptor-like receptor-1 (ORL-1) is expressed in ARH and ventromedial hypothalamus (VMH). Infusions of its endogenous ligand, orphanin FQ (OFQ/N, aka nociceptin), into VMH-ARH region facilitates lordosis. Whether OFQ/N acts in ARH and/or VMH and whether OFQ/N is necessary for steroid facilitation of lordosis is unclear. In Exp I, OFQ/N infusions in VMH and ARH that facilitated lordosis also deactivated MPN MOP indicating that OFQ/N facilitation of lordosis requires deactivation of ascending ARH-MPN projections by directly inhibiting ARH β-END neurons and/or through inhibition of excitatory VMH-ARH pathways to proopiomelanocortin neurons. It is unclear whether OFQ/N activates the VMH output motor pathways directly or via the deactivation of MPN MOP. In Exp II we tested whether ORL-1 activation is necessary for estradiol-only or estradiol + progesterone lordosis facilitation. Blocking ORL-1 with UFP-101 inhibited estradiol-only lordosis and MPN MOP deactivation but had no effect on estradiol + progesterone facilitation of lordosis and MOP deactivation. In conclusion, steroid facilitation of lordosis inhibits ARH β-END neurons to deactivate MPN MOP, but estradiol-only and estradiol + progesterone treatment appear to use different neurotransmitter systems to inhibit ARH-MPN signaling.

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Hormonal-Neural Integration in the Female Rat Ventromedial Hypothalamus: Triple Labeling for Estrogen Receptor-α, Retrograde Tract Tracing from the Periaqueductal Gray, and Mating-Induced Fos Expression

Cited by 43 publications

References 54 publications

Membrane-Initiated Estradiol Signaling Regulating Sexual Receptivity

Membrane-Initiated Estradiol Signaling Regulating Sexual Receptivity

Oestrogen receptors in the central nervous system and evidence for their role in the control of cardiovascular function

Orphanin FQ in the mediobasal hypothalamus facilitates sexual receptivity through the deactivation of medial preoptic nucleus mu-opioid receptors

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