Selective serotonin reuptake inhibitors and neuroendocrine function

Raap, D. K.; Kar, Louis D. Van de

doi:10.1016/s0024-3205(99)00169-1

Cited by 119 publications

(77 citation statements)

References 196 publications

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“…The present data confirm that acute oral administration of citalopram increases HPA axis activity (Raap and Van de Kar, 1999;Hennig and Netter, 2002). The acute facilitatory effect of SSRIs on the HPA axis is thought to be mediated by increased release of corticotrophin-releasing hormone (CRH) in the paraventricular nucleus of the hypothalamus, which leads to increased corticotropin (ACTH) release at pituitary level (Raap and Van de Kar, 1999).…”

Section: Discussionsupporting

confidence: 80%

“…The acute facilitatory effect of SSRIs on the HPA axis is thought to be mediated by increased release of corticotrophin-releasing hormone (CRH) in the paraventricular nucleus of the hypothalamus, which leads to increased corticotropin (ACTH) release at pituitary level (Raap and Van de Kar, 1999). This, in turn, results in greater secretion of cortisol from the adrenal gland into the plasma, which can be detected by salivary monitoring.…”

Section: Discussionmentioning

confidence: 99%

“…A possible explanation of this difference is that prolactin release may be more buffered by inhibitory serotonin autoreceptor activity (Raap and Van de Kar, 1999). For example, increases in plasma prolactin levels are seen after 3 weeks of oral paroxetine administration but not after 1 week, despite the presence of similar plasma levels of paroxetine on both occasions (Cowen and Sargent, 1997).…”

Section: Discussionmentioning

confidence: 99%

“…Drugs that potentiate serotonin (5-HT) function can produce increases in the secretion of cortisol and prolactin (Raap and Van de Kar, 1999). For example, intravenous administration of selective serotonin re-uptake inhibitors (SSRIs) produces a reliable increase in plasma prolactin as well as in plasma and salivary cortisol (Laakmann et al, 1990;Seifritz et al, 1996).…”

Section: Introductionmentioning

confidence: 99%

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Comparison of the Effects of Citalopram and Escitalopram on 5-Ht-Mediated Neuroendocrine Responses

Nadeem

Attenburrow

Cowen

2004

Neuropsychopharmacol

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Acute oral administration of selective serotonin re-uptake inhibitors (SSRIs) increases plasma cortisol by facilitating brain serotonin activity. Recently, salivary cortisol sampling has grown in popularity as a noninvasive means of assessing HPA axis activity. The aim of the present study was to find out whether acute oral administration of the SSRI, citalopram, increases salivary cortisol in healthy volunteers and whether the increase produced by an equivalent dose of its active isomer, escitalopram, is greater. A total of 15 healthy subjects were tested on three occasions receiving either oral citalopram (20 mg), escitalopram (10 mg), or placebo in a double-blind, randomized, crossover design. Salivary cortisol and plasma cortisol and prolactin were measured for 240 min after each treatment. Relative to placebo, both citalopram and escitalopram increased salivary and plasma cortisol levels with no evidence of consistent differences between them. Plasma prolactin concentration was not altered by either active treatment. Plasma and salivary cortisol responses after citalopram but not escitalopram correlated significantly. The present study does not support an enhanced effect of escitalopram on 5-HT-mediated neuroendocrine responses.

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Section: Discussionsupporting

confidence: 80%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Comparison of the Effects of Citalopram and Escitalopram on 5-Ht-Mediated Neuroendocrine Responses

Nadeem

Attenburrow

Cowen

2004

Neuropsychopharmacol

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“…The administration of oxytocin has been shown to decrease the fear-induced activity of the amygdala (Kirsch et al, 2005). There are suggestions that some of the therapeutic effects of antidepressants in social anxiety disorders are through oxytocin release in the PVN (Raap and Van de Kar, 1999). Many oxytocin-containing cells of the PVN have estradiol receptors in the adult, such that these may be a site of gender based activating (as opposed to organizing) effects of hormones (Bodo and Rissman, 2006) and blood levels of oxytocin are higher in women than men (Ozsoy et al, 2009).…”

Section: Neuroendocrine Hypothesismentioning

confidence: 99%

Sexual Differentiation and the Neuroendocrine Hypothesis of Autism

Aiello

Whitaker‐Azmitia

2011

The Anatomical Record

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The phenotypic expression of autism spectrum disorders varies widely in severity and characteristics and it is, therefore, likely that a number of etiological factors are involved. However, one finding which has been found consistently is that there is a greater incidence of autism in boys than girls. Recently, attention has been given to the extreme male hypothesis-that is that autism behaviors are an extreme form of typical male behaviors, including lack of empathy and language deficits but an increase in so-called systemizing behaviors, such as attention to detail and collecting. This points to the possibility that an alteration during sexual differentiation of the brain may occur in autism. During sexual differentiation of the brain, two brain regions are highly sexually dimorphicthe amygdala and the hypothalamus. Both of these regions are also implicated in the neuroendocrine hypothesis of autism, wherein a balance between oxytocin and cortisol may contribute to the disorder. We are thus proposing that the extreme male hypothesis and the neuroendocrine hypothesis are in fact compatible in that sexual differentiation of the brain towards an extreme male phenotype would result in the neuroendocrine changes proposed in autism. We have preliminary data, treating developing rat pups with the differentiating hormone 17-b estradiol during a critical time and showing changes in social behaviors and oxytocin, to support this hypothesis. Further studies should be undertaken to confirm the role of extremes of normal sexual differentiation in producing the neuroendocrine changes associated with autism. Anat Rec, 294:1663-1670, 2011. V V C 2011 Wiley-Liss, Inc.Key words: autism; oxytocin; cortisol; sexual differentiation; extreme male TWO HYPOTHESESSimply stated, the hypothesis which we are proposing in this article, and the work currently ongoing in our lab, is that enhanced sexual differentiation of the brain, towards the male phenotype, leads to changes in the neuroendocrine factors, oxytocin and cortisol. These factors are involved in the processing and evaluation of social bonding experiences and any disruption in their typical function can lead to the primary defining characteristic of the autism phenotype-inadequate social bonding. The Extreme Male Hypothesis of AutismAutism is a disorder of brain development and thus any factors which regulate brain development and are known to be altered in autism should be considered as possibly contributing to the phenotype. For example, much of our previous work and work of others, has focused on the known role of serotonin in brain development as well as the well known hyperserotonemia which occurs in autism (Whitaker-Azmitia, 2005). More recently, researchers have proposed a role for sexual differentiation of the brain in the phenotypic behaviors of

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