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Special Issue "Steroids, Central Neurotransmission, Mood, Memory and Mental State"

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Endocrinology and Metabolism".

Deadline for manuscript submissions: closed (31 May 2021).

Special Issue Editor

Prof. Dr. George Fink
E-Mail Website
Guest Editor
Florey Institute of Neuroscience and Mental Health, The University of Melbourne, Melbourne, Victoria, Australia
Interests: neuroendocrinology; neurohormones and neuropeptides; central neural transmission; feedback systems; gonadotropin releasing hormone (GnRH); GnRH self priming effect; pituitary responsiveness to neurohormones; stress and stress effects; corticotropin releasing factor (CRF): PTSD: allostasis; stress as a cause of peptic ulceration; neuropharmacology; psychopharmacology
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Special Issue Information

Dear colleagues,

Steroid hormones secreted by the gonads and adrenal glands affect mood, memory, and mental state in humans. Thus, for example, the increased incidence of mood disorder around the time of menstruation, puerperium, and the menopause has been associated with the coincident fall of plasma estradiol concentrations. Estradiol has also been implicated in and used as adjunct treatment for schizophrenia.

Studies in rodents and humans have shown that estrogen affects central neurotransmission, such as the central serotonin system. In turn, manipulation of central serotonin neurons affects the intracellular mineralocorticoid and glucocorticoid receptors in the hippocampus. These receptors bind cortisol (human) or corticosterone (rodents) secreted by the adrenal cortex at rest in a circadian mode and in larger spurts in response to stress. In addition, steroid hormones also affect synaptogenesis, dendritic branching, myelination and other mechanisms involved in neuroplasticity. Finally, neurosteroids, synthesized within the central nervous system, have proved to be potent allosteric agonists as well as direct activators of GABA-A receptors, thereby providing innovative therapies for epilepsy, brain injury, Fragile X syndrome, and chemical neurotoxicity.

This Special Issue will review the themes outlined above with a focus on novel fundamental and clinical advances.

Prof. Dr. George Fink
Guest Editor

Illustrative references:

Fink G, Sumner BE, Rosie R, Grace O, Quinn JP. Estrogen control of central neurotransmission: effect on mood, mental state, and memory. Cell Mol Neurobiol. 1996 Jun;16(3):325-44. Review

Fink G, Sumner BE, McQueen JK, Wilson H, Rosie R. Sex steroid control of mood, mental state and memory. Clin Exp Pharmacol Physiol. 1998 Oct;25(10):764-75. Review.

Fink G, Sumner B, Rosie R, Wilson H, McQueen J. Androgen actions on central serotonin neurotransmission: relevance for mood, mental state and memory. Behav Brain Res. 1999 Nov 1;105(1):53-68. Review.

Sumner BE, Grant KE, Rosie R, Hegele-Hartung Ch, Fritzemeier KH, Fink G. Raloxifene blocks estradiol induction of the serotonin transporter and 5-hydroxytryptamine2A receptor in female rat brain. Neurosci Lett. 2007 Apr 24;417(1):95-9. Epub 2007 Feb 15.

Moses-Kolko EL1, Berga SL, Greer PJ, Smith G, Cidis Meltzer C, Drevets WC. Widespread increases of cortical serotonin type 2A receptor availability after hormone therapy in euthymic postmenopausal women. Fertil Steril. 2003 Sep;80(3):554-9.

Kulkarni J, Butler S, Riecher-Rössler A. Estrogens and SERMS as adjunctive treatments for schizophrenia. Front Neuroendocrinol. 2019 Apr;53:100743. doi:10.1016/j.yfrne.2019.03.002. Epub 2019 Mar 25.

Seckl JR, Dickson KL, Fink G. Central 5,7-dihydroxytryptamine lesions decrease hippocampal glucocorticoid and mineralocorticoid receptor messenger ribonucleic Acid expression. J Neuroendocrinol. 1990 Dec 1;2(6):911-6. doi: 10.1111/j.1365-2826.1990.tb00659.x.

Reddy DS, Estes WA. Clinical Potential of Neurosteroids for CNS Disorders. Trends Pharmacol Sci. 2016 Jul;37(7):543-561. doi: 10.1016/j.tips.2016.04.003. Epub 2016 May 5.

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Research

Article
PPAR-α Hypermethylation in the Hippocampus of Mice Exposed to Social Isolation Stress Is Associated with Enhanced Neuroinflammation and Aggressive Behavior
Int. J. Mol. Sci. 2021, 22(19), 10678; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms221910678 - 01 Oct 2021
Viewed by 389
Abstract
Social behavioral changes, including social isolation or loneliness, increase the risk for stress-related disorders, such as major depressive disorder, posttraumatic stress disorder (PTSD), and suicide, which share a strong neuroinflammatory etiopathogenetic component. The peroxisome-proliferator activated receptor (PPAR)-α, a newly discovered target involved in [...] Read more.
Social behavioral changes, including social isolation or loneliness, increase the risk for stress-related disorders, such as major depressive disorder, posttraumatic stress disorder (PTSD), and suicide, which share a strong neuroinflammatory etiopathogenetic component. The peroxisome-proliferator activated receptor (PPAR)-α, a newly discovered target involved in emotional behavior regulation, is a ligand-activated nuclear receptor and a transcription factor that, following stimulation by endogenous or synthetic ligands, may induce neuroprotective effects by modulating neuroinflammation, and improve anxiety and depression-like behaviors by enhancing neurosteroid biosynthesis. How stress affects epigenetic mechanisms with downstream effects on inflammation and emotional behavior remains poorly understood. We studied the effects of 4-week social isolation, using a mouse model of PTSD/suicide-like behavior, on hippocampal PPAR-α epigenetic modification. Decreased PPAR-α expression in the hippocampus of socially isolated mice was associated with increased levels of methylated cytosines of PPAR-α gene CpG-rich fragments and deficient neurosteroid biosynthesis. This effect was associated with increased histone deacetylases (HDAC)1, methyl-cytosine binding protein (MeCP)2 and decreased ten-eleven translocator (TET)2 expression, which favor hypermethylation. These alterations were associated with increased TLR-4 and pro-inflammatory markers (e.g., TNF-α,), mediated by NF-κB signaling in the hippocampus of aggressive mice. This study contributes the first evidence of stress-induced brain PPAR-α epigenetic regulation. Social isolation stress may constitute a risk factor for inflammatory-based psychiatric disorders associated with neurosteroid deficits, and targeting epigenetic marks linked to PPAR-α downregulation may offer a valid therapeutic approach. Full article
(This article belongs to the Special Issue Steroids, Central Neurotransmission, Mood, Memory and Mental State)
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