Central Serous Chorioretinopathy and Blood Serotonin Concentrations

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Abstract

Background: To investigate blood serotonin (5-hydroxytryptamine (5-HT)) concentrations and their relationships with selected characteristics in patients with central serous chorioretinopathy (CSC). Methods: This was a prospective study including 93 patients with active CSC. Blood concentrations of 5-HT, adrenocorticotropic hormone, and cortisol were measured in patients with CSC. Selected patient characteristics, including disease history (acute or chronic), medication use, smoking history, mood status, best-corrected visual acuity (BCVA), subfoveal choroidal thickness (SCT), findings on fluorescein and indocyanine green angiography, and anatomical changes were evaluated during follow-up. Results: Eleven of the 93 patients had low 5-HT concentrations (<57 ng/mL) (12%, eight men and three women; mean age 55 years); we identified no significant relationship with acute/chronic disease status. The patients with low 5-HT were significantly more likely to have five or more fluorescein leakage sites ( p = 0.0275), recurrence of subretinal fluids ( p < 0.0001), and failure to achieve significant improvement in BCVA during follow-up ( p = 0.862) than patients with 5-HT within the normal range. Conclusions: Blood serotonin concentrations may influence the pathophysiology and prognosis of CSC.

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Orexin activation counteracts decreases in nonexercise activity thermogenesis (NEAT) caused by high-fat diet.

P.E. Bunney, A.N. Zink, A.A. Holm … (2017)

Overweight and obesity result from an imbalance between caloric intake and energy expenditure, including expenditure from spontaneous physical activity (SPA). Changes in SPA and resulting changes in non-exercise activity thermogenesis (NEAT) likely interact with diet to influence risk for obesity. However, previous research on the relationship between diet, physical activity, and energy expenditure has been mixed. The neuropeptide orexin is a driver of SPA, and orexin neuron activity can be manipulated using DREADDs (Designer Receptors Exclusively Activated by Designer Drugs). We hypothesized that HFD decreases SPA and NEAT, and that DREADD-mediated activation of orexin neuron signaling would abolish this decrease and produce an increase in NEAT instead. To test these ideas, we characterized behaviors to determine the extent to which access to a high-fat diet (HFD) influences the proportion and probability of engaging in food intake and activity. We then measured NEAT following access to HFD and following a DREADD intervention targeting orexin neurons. Two cohorts of orexin-cre male mice were injected with an excitatory DREADD virus into the caudal hypothalamus, where orexin neurons are concentrated. Mice were then housed in continuous metabolic phenotyping cages (Sable Promethion). Food intake, indirect calorimetry, and SPA were automatically measured every second. For cohort 1 (n=8), animals were given access to chow, then switched to HFD. For cohort 2 (n=4/group), half of the animals were given access to HFD, the other access to chow. Then, among animals on HFD, orexin neurons were activated following injections of clozapine n-oxide (CNO). Mice on HFD spent significantly less time eating (p<0.01) and more time inactive compared to mice on chow (p<0.01). Following a meal, mice on HFD were significantly more likely to engage in periods of inactivity compared to those on chow (p<0.05). NEAT was decreased in animals on HFD, and was increased to the NEAT level of control animals following activation of orexin neurons with DREADDs. Food intake (kilocalories) was not significantly different between mice on chow and HFD, yet mice on chow expended more energy per unit of SPA, relative to that in mice consuming HFD. These results suggest that HFD consumption reduces SPA and NEAT, and increases inactivity following a meal. Together, the data suggest a change in the efficiency of energy expenditure based upon diet, such that SPA during HFD burns fewer calories compared to SPA on a standard chow diet.

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Central serous chorioretinopathy: Recent findings and new physiopathology hypothesis.

Alejandra Daruich, Alexandre Matet, Ali Dirani … (2015)

Central serous chorioretinopathy (CSCR) is a major cause of vision threat among middle-aged male individuals. Multimodal imaging led to the description of a wide range of CSCR manifestations, and highlighted the contribution of the choroid and pigment epithelium in CSCR pathogenesis. However, the exact molecular mechanisms of CSCR have remained uncertain. The aim of this review is to recapitulate the clinical understanding of CSCR, with an emphasis on the most recent findings on epidemiology, risk factors, clinical and imaging diagnosis, and treatments options. It also gives an overview of the novel mineralocorticoid pathway hypothesis, from animal data to clinical evidences of the biological efficacy of oral mineralocorticoid antagonists in acute and chronic CSCR patients. In rodents, activation of the mineralocorticoid pathway in ocular cells either by intravitreous injection of its specific ligand, aldosterone, or by over-expression of the receptor specifically in the vascular endothelium, induced ocular phenotypes carrying many features of acute CSCR. Molecular mechanisms include expression of the calcium-dependent potassium channel (KCa2.3) in the endothelium of choroidal vessels, inducing subsequent vasodilation. Inappropriate or over-activation of the mineralocorticoid receptor in ocular cells and other tissues (such as brain, vessels) could link CSCR with the known co-morbidities observed in CSCR patients, including hypertension, coronary disease and psychological stress.

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Digital indocyanine green videoangiography of central serous chorioretinopathy.

L Yannuzzi, D Guyer, M Slakter … (1994)

The pathogenesis of central serous chorioretinopathy (CSC) is poorly understood. Abnormalities in the choroidal circulation have been hypothesized to be causative factors. Fluorescein angiography has not been particularly useful in identifying specific choroidal defects in CSC, largely because of inherent limitations in imaging with this technique. Recent technologic advances in digital indocyanine green videoangiography allow enhanced imaging of the choroid and other subretinal structures in comparison with fluorescein angiography. We performed digital indocyanine green videoangiography in 29 consecutive eyes with CSC and compared our results with clinical and fluorescein angiographic findings. Several newly recognized subretinal abnormalities in CSC were noted with digital indocyanine green videoangiography, including (1) presumed hyperpermeability of the choroidal circulation surrounding active retinal pigment epithelial leaks, (2) additional focal and multifocal areas of presumed choroidal hyperpermeability not associated with abnormalities detectable by fluorescein angiography or clinical examination, and (3) multiple presumed "occult" serous retinal pigment epithelial detachments with a characteristic indocyanine green videoangiographic pattern. We suggest that the pathogenesis of CSC may be due to a choroidal vascular hyperpermeability with and without associated active pigment epithelial leaks and multiple presumed "occult" serous retinal pigment epithelial detachments. Based on these findings, a hypothetical model can be constructed related to the pathogenesis of CSC, beginning with choroidal abnormalities that secondarily affect the retinal pigment epithelium and neurosensory retina.

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Contributors

Kenji Yamashiro: Role: Academic Editor

Journal

Journal ID (nlm-ta): J Clin Med

Journal ID (iso-abbrev): J Clin Med

Journal ID (publisher-id): jcm

Title: Journal of Clinical Medicine

Publisher: MDPI

ISSN (Electronic): 2077-0383

Publication date (Electronic): 03 February 2021

Publication date Collection: February 2021

Volume: 10

Issue: 4

Electronic Location Identifier: 558

Affiliations

Department of Ophthalmology, Hyogo College of Medicine, Nishinomiya 6638501, Japan; kimutake@ 123456hyo-med.ac.jp (T.K.); takas4i_cartar@ 123456hotmail.com (T.A.); yuki.kom0923@ 123456gmail.com (Y.K.); piwhiss@ 123456gmail.com (H.I.)

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[* ]Correspondence: fgomi@ 123456hyo-med.ac.jp ; Tel.: +81-798-45-6111

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Fumi Gomi https://orcid.org/0000-0003-0807-8817

Article

Publisher ID: jcm-10-00558

DOI: 10.3390/jcm10040558

PMC ID: 7913142

PubMed ID: 33546112

SO-VID: 7790f078-c13e-47af-96f6-8212564aa01b

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Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ( http://creativecommons.org/licenses/by/4.0/).

Central Serous Chorioretinopathy and Blood Serotonin Concentrations

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Serotonin and BEYOND

Most cited references 39

Orexin activation counteracts decreases in nonexercise activity thermogenesis (NEAT) caused by high-fat diet.

Central serous chorioretinopathy: Recent findings and new physiopathology hypothesis.

Digital indocyanine green videoangiography of central serous chorioretinopathy.

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