Acute inositol does not attenuate m-CPP-induced anxiety, mydriasis and endocrine effects in panic disorder

Benjamin, Jonathan; Nemetz, Hannah; Fux, Mendel; Bleichman, Igor; Agam, Galila

doi:10.1016/s0022-3956(97)00021-6

Cited by 15 publications

(5 citation statements)

References 25 publications

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“…DAG activates protein kinase C (PKC) and IP3 activates intracellular calcium (Ca2+) release, an essential step in oocyte maturation and so of fertilization process. There are nine inositol stereoisomers, and myoinositol is the most represented in cellular content [6]. All stereoisomers act as mediator of insulin action inside the cell [7]: myoinositol (MYO) and D-chiro-inositol (DCI) are inositol-containing phosphoglycan (IPG) mediators, generated by hydrolysis of glycosylphosphatidylinositol that inhibits cyclic AMP-dependent protein kinase (the first) and activates pyruvate dehydrogenase (the second one) [8].…”

Section: Inositolmentioning

confidence: 99%

Inositol and In Vitro Fertilization with Embryo Transfer

Simi

Genazzani

Obino

et al. 2017

International Journal of Endocrinology

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Recently, studies on inositol supplementation during in vitro fertilization program (IVF) have gained particular importance due to the effect of this molecule on reducing insulin resistance improving ovarian function, oocyte quality, and embryo and pregnancy rates and reducing gonadotropin amount during stimulation. Inositol and its isoforms, especially myoinositol (MYO), are often used as prestimulation therapy in infertile patients undergoing IVF cycle. Inositol supplementation started three months before ovarian stimulation, resulting in significant improvements in hormonal responses, reducing the amount of FSH necessary for optimal follicle development and serum levels of 17beta-estradiol measured the day of hCG injection. As shown by growing number of trials, MYO supplementation improves oocyte quality by reducing the number of degenerated and immature oocytes, in this way increasing the quality of embryos produced. Inositol can also improve the quality of sperm parameters in those patients affected by oligoasthenoteratozoospermia.

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Section: Inositolmentioning

confidence: 99%

Inositol and In Vitro Fertilization with Embryo Transfer

Simi

Genazzani

Obino

et al. 2017

International Journal of Endocrinology

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“…In addition to psychometric measures, plasma cortisol and, in five cases, plasma prolactin as well have been measured. In spite of these differences, the results have concurred in showing an increase of stress hormones after mCPP (Charney et al 1987b, Kahn et al 1988, Klein et al 1991, Germine et al 1994, Wetzler et al 1996, Benjamin et al 1997). In the remaining two studies the oral route was used.…”

Section: Serotoninergic Agentsmentioning

confidence: 83%

Does the panic attack activate the hypothalamic-pituitary-adrenal axis?

Graeff

Garcia-Leal

Del-Ben

et al. 2005

An. Acad. Bras. Ciênc.

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A bibliographic search has been performed in MEDLINE using cortisol and panic as key-words, occurring in the title and/or in the abstract. Human studies were selected, with no time limit. The following publications were excluded: review articles, case reports, panic attacks in disorders other than panic disorder, and studies on changes that occurred in-between panic attacks. The results showed that real-life panic attacks as well as those induced by selective panicogenic agents such as lactate and carbon dioxide do not activate the hypothalamicpituitary-adrenal (HPA) axis. Agonists of the colecystokinin receptor B, such as the colecystokinin-4 peptide and pentagastrin, increase stress hormones regardless of the occurrence of a panic attack and thus, seem to activate the HPA axis directly. The benzodiazepine antagonist flumazenil does not increase stress hormones, but this agent does not reliably induce panic attacks. Pharmacological agents that increased anxiety in both normal subjects and panic patients raised stress hormone levels; among them are the α 2 -adrenergic antagonist yohimbine, the serotonergic agents 1-(m-chlorophenyl) piperazine (mCPP) and fenfluramine, as well as the psychostimulant agent caffeine. Therefore, the panic attack does not seem to activate the HPA axis, in contrast to anticipatory anxiety.

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“…It has been reported that 5HT 2 receptor antagonists (Millson et al 1991(Millson et al , 1992 and 5HT 3 receptor antagonists (Rizzi et al 1993) cause miosis. In contrast, fenfluramine, m-chlorophenylpiperazine and 5-HT 1A receptor agonists were shown to increase pupil size (Benjamin et al 1997;Broocks et al 1998;Prow et al 1996). The mydriatic response is probably mediated by central 5HT 1A receptors evoking the release of noradrenaline on alpha2-adrenoreceptors (Prow et al 1996).…”

Section: Discussionmentioning

confidence: 99%