CGRP in the trigeminal nucleus, spinal cord and hypothalamus: effect of gonadal steroids

Moussaoui, Saliha; Duval, Pierre; Lenoir, Véronique; Garret, C.; Kerdelhué, B.

doi:10.1016/s0143-4179(96)90037-2

Cited by 23 publications

(21 citation statements)

References 16 publications

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“…However, further work in a larger group of symptomatic women would be required to establish a causative effect. Furthermore, animal 13,14 . Conflicting findings have also been reported in a previous study by Valentini and co-workers, where CGRP levels were shown to be lower in postmenopausal women.…”

Section: Discussionmentioning

confidence: 99%

“…We have recently demonstrated that CGRP is expressed in adipose tissue at mRNA and protein level and that CGRP expression is higher in adipose tissue from postmenopausal women, suggesting a potential mechanism by which adipose tissue may contribute to the increased prevalence and severity of vasomotor symptoms 12 . Previously, animal studies have shown higher tissue levels of CGRP in an estrogen-deficient state 13,14 suggesting that secretion and activity of CGRP may be influenced by the sex hormones. However, to date, there have been no studies investigating the effect of natural menopause on serum CGRP levels and whether this is directly or indirectly associated with vasomotor symptoms and CVD risk.…”

Section: Introductionmentioning

confidence: 99%

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Effects of menopausal status on circulating calcitonin gene-related peptide and adipokines: implications for insulin resistance and cardiovascular risks

Gupta

Harte²,

Sturdee

et al. 2008

Climacteric

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Effects of menopausal status on circulating calcitonin gene-related peptide and adipokines: implications for insulin resistance and cardiovascular risks

Gupta

Harte²,

Sturdee

et al. 2008

Climacteric

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“…In addition, Gollapudi and Oblinger (1999a) have shown that ER-α is present in PC12 cells [neural crest derivatives that are nerve growth factor (NGF)-dependent] and that estrogens have cytoprotective (cell survival) effects that involves NGF and the antiapoptotic molecule Bcl-X L (Gollipudi and Oblinger 1999b). Furthermore, estrogens stimulate neurotransmitter levels (in CNS neurons; Gibbs et al 1994;Okamura et al 1994aOkamura et al , 1994bYuri and Kawata 1994;Dufourny and Warembourg 1999;Miller et al 1999), upregulate neuronal-nitric oxide synthase in autonomic and/or sensory nerves in the vagina (Berman et al 1998), or downregulate CGRP in sensory neurons (Moussaoui et al 1996;Duval et al 1998;Yang et al 1998). These types of regulation could occur in peripheral autonomic and sensory neurons that innervate the uterus.…”

Section: Discussionmentioning

confidence: 99%

“…We have preliminary data that some spinohypothalamic neurons are ER-α immunoreactive. In addition, transmitters in primary afferent nerves, including at least CGRP (Moussaoui et al 1996) and neurokinins (Duval et al 1998), can be influenced by estradiol (i.e., in the spinal cord they are downregulated by estradiol). Consequently, if such neurons receive primary afferent input, they may have their activity modulated by estrogens either directly (if they contain ER) or indirectly (if some of their afferent input neurons contain ER).…”

Section: Discussionmentioning

confidence: 99%

Estrogen receptor-α and -β immunoreactivity and mRNA in neurons of sensory and autonomic ganglia and spinal cord

Papka

Storey-Workley

Shughrue³

et al. 2001

Cell and Tissue Research

162

120

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Estrogen receptor-alpha immunoreactivity and mRNAs are present in neurons in locales that innervate genital organs, e.g., parasympathetic pelvic autonomic ganglia, sensory dorsal root and nodose ganglia, and autonomic areas of the lumbosacral spinal cord. With the availability of probes for the beta-isoform of the estrogen receptor, we studied this receptor in autonomic, sensory, and spinal cord neurons and compared it with the distribution of the alpha-receptor. Estrogen receptor-alpha and -beta immunoreactivity were located in the nuclei of neurons, were in subpopulations of parasympathetic neurons in pelvic ganglia, and sensory neurons of dorsal root and nodose ganglia. Both receptor subtypes were present in the lumbosacral spinal cord: in neurons of the outer laminae of the dorsal horn, lateral collateral and medial collateral pathways, sacral parasympathetic nucleus, dorsal intermediate gray, and lamina X. Similar numbers of spinal cord neurons were immunoreactive for estrogen receptor-beta and estrogen receptor-alpha. However, estrogen receptor-beta-immunoreactive neurons appeared less numerous in the outer dorsal horn, but more numerous in the deeper layers of the spinal cord than estrogen receptor-alpha neurons. Retrograde tracing from the uterus revealed "uterine-related" neurons in dorsal root and pelvic ganglia that contained estrogen receptor-alpha and -beta. In situ hybridization revealed both estrogen receptor-alpha and -beta mRNA transcripts in sensory neurons of the dorsal root and nodose ganglia, parasympathetic neurons of pelvic ganglia, and spinal cord neurons in the dorsal horn, sacral parasympathetic nucleus, and dorsal intermediate gray of L6-S1 segments. These studies show that both estrogen receptor-alpha and -beta are synthesized by autonomic and sensory neurons in parts of the nervous system that have connections with the female reproductive system. Such neurons contain neurotransmitters that have important functions in the female reproductive organs; thus, it is likely that estrogen can influence the activity of such neurons and consequently, through them, the activities of the reproductive organs.

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“…Puri et al [28] found there was no change in the levels of mRNA for CGRP during different stages of the mouse estrous cycle within the trigeminal ganglion. Another study [31] reported that tissue levels of CGRP within the TNC were unchanged during stages of the rat estrous cycle with a high estrogen milieu (eg, diestrus, early proestrus) but were lower during stages of high progesterone milieu (eg, late proestrus, estrus). Nonhormonal factors such as prostaglandins can also enhance CGRP release through their effect on TRPA1 receptors [32].…”

Section: Modulation Of Neuropeptide Synthesismentioning

confidence: 99%

New Theories in the pathogenesis of menstrual migraine

Martin

2008

Current Science Inc

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Hormonal and nonhormonal factors play a role in the pathophysiology of menstrual migraine, but estrogen withdrawal appears to be the most potent of these factors. It is postulated that estrogen withdrawal directly enhances excitability of trigeminal afferents, modulates the synthesis of neuropeptides, activates/deactivates specific neurotransmitter systems, and influences the function of microglia. These changes could activate and/or sensitize the trigeminal system and increase the likelihood of migraine headache during perimenstrual time periods. Three new theories are advanced in this article to explain the pathophysiology of menstrual migraine. Only through an understanding of the mechanisms involved in menstrual migraine can we gain insight into the management of this severe and debilitating form of migraine headache.

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CGRP in the trigeminal nucleus, spinal cord and hypothalamus: effect of gonadal steroids

Cited by 23 publications

References 16 publications

Effects of menopausal status on circulating calcitonin gene-related peptide and adipokines: implications for insulin resistance and cardiovascular risks

Effects of menopausal status on circulating calcitonin gene-related peptide and adipokines: implications for insulin resistance and cardiovascular risks

Estrogen receptor-α and -β immunoreactivity and mRNA in neurons of sensory and autonomic ganglia and spinal cord

New Theories in the pathogenesis of menstrual migraine

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