China
Africa
Explore chapters and articles related to this topic
Treatment of Chronic Fatigue Syndrome
Published in Jay A. Goldstein, Chronic Fatigue Syndromes, 2020
Negative allosteric modulators of GABA-gated chloride ion conductance include pregnenolone and DHEA. The brain has higher levels of these compounds than any other organ, and brain concentrations are independent of production peripherally.36 Some neurosteroids appear to have anxiolytic properties in animals.37 Neurosteroids have considerable potential in treating CFS and related disorders such as premenstrual syndrome, anxiety disorders, fibromyalgia, and sleep disorders.
Synthesis, Enzyme Localization, and Regulation of Neurosteroids
Published in Sheryl S. Smith, Neurosteroid Effects in the Central Nervous System, 2003
Neurosteroids, by definition, are those steroids that are synthesized in the central (CNS) and peripheral (PNS) nervous systems, independently of the steroidogenic activity of endocrine glands (gonads and adrenals). They pertain to the same chemical group as classical steroid hormones, their precursors and metabolites, and they derive from cholesterol.
Stress-Responsive Neurohormones in Depression and Anxiety
Published in Siegfried Kasper, Johan A. den Boer, J. M. Ad Sitsen, Handbook of Depression and Anxiety, 2003
Ströhle Andreas, Holsboer Florian
In the last decade, considerable evidence has emerged indicating that certain steroids may alter neuronal excitability via their action at the cell surface via interaction with certain neurotransmitter receptors. For steroids with these particular properites, the term “neuroactive steroids” has been used (31-33). Other authors use the term neurosteroids, which can be misconstrued, because these steroids are not specifically synthesized in neurons. Whereas it seems attractive to differentiate genomic from nongenomic actions upon neurons, it could be demonstrated that transitions may also exist between these two modes of action [34]. Steroids that are believed to have limited effects at membrane sites, such as allopregnanolone (3α,5α-THP) and allotetrahydrodeoxycorticosterone (3α,5α-THDOC), can be oxidized intracellularly and then exert genomic actions through progesterone receptors. Thus, the steroid molecule provides a rather flexible structure that can be modified, depending on the tissue, to satisfy specific demands.
Therapeutic potential of GABAA receptor subunit expression abnormalities in fragile X syndrome
Published in Expert Review of Precision Medicine and Drug Development, 2022
Mathijs B. van der Lei, R. Frank Kooy
In addition to the benzodiazepine binding site, synaptic and extrasynaptic GABAA receptors contain binding sites for neurosteroids. Neurosteroids are synthesized within the central nervous system and interact with GABAA receptors to enhance inhibition and alter neuronal excitability [79,80]. Interestingly, at low nanomolar concentrations neurosteroids work as positive allosteric modulators to enhance the activity of GABAA receptors, but at relatively high concentrations neurosteroids have to unique feature to directly activate GABAA receptors even in the absence of GABA [81–83]. Neurosteroids are especially sensitive for the extrasynaptic binding site at the δ subunit of the GABAA receptor, as shown by a reduced response to neurosteroids in δ subunit knockout mice [84]. The following section discusses two current synthetic available neurosteroids, even as their potential for fragile X syndrome (Table 4).
24 hour patterning in gene expression of pineal neurosteroid biosynthesis in young chickens (Gallus gallus domesticus L.)
Published in Chronobiology International, 2021
Magdalena Chustecka, Natalia Blügental, Pawel Marek Majewski, Iwona Adamska
Neurosteroids have a wide range of functions, from genomic action to regulation of neurophysiological processes; however, not all processes involving neurosteroids are fully understood and explained. Neurosteroids can act as allosteric modulators of GABA (Covey et al. 2001; Herbison 2001; Lambert et al. 2003), AMPA (Rupprecht et al. 2001), NMDA (Mameli et al. 2005; Mathis et al. 1994, 1996) and many other receptors (Dubrovsky 2005; Klangkalya and Chan 1988; Maurice 2004; Pereira et al. 2002). Processes affected by neurosteroids include: neuroprotection (Charalampopoulos et al. 2004), i.e., regulation of myelination of fibers (Hussain et al. 2011), and regulation of organogenesis and neurogenesis (Charalampopoulos et al. 2008). Neurosteroids also appear to regulate behavioral and neurophysiological processes, influencing depression, stress, cognition, and sleep. Involvement in behavior covers mostly reproductive, feeding, and locomotion activity (Do Rego et al. 2009).
Change in gene expression levels of GABA, glutamate and neurosteroid pathways due to acoustic trauma in the cochlea
Published in Journal of Neurogenetics, 2021
Meltem Cerrah Gunes, Murat Salih Gunes, Alperen Vural, Fatma Aybuga, Arslan Bayram, Keziban Korkmaz Bayram, Mehmet Ilhan Sahin, Muhammet Ensar Dogan, Sevda Yesim Ozdemir, Yusuf Ozkul
Acoustic trauma causes damage to the peripheral and central auditory system. Glutamate excitotoxicity damages the auditory SGNs causing loss of postsynaptic terminals and cell dysfunction (Kujawa & Liberman, 2015). Excitation generated by glutamatergic neurons is compensated by cortical inhibition (Froemke, 2015). One week after the noise exposure, especially ipsilateral elevation of the number of GABAergic interneurons containing the calcium-binding protein Parvalbumin(PV) was observed and this was thought to be a compensatory mechanism (C. Liu et al., 2018). Neurosteroids take part in the regulation of neuronal function by modulating the expression of GABAA and NMDA receptor subgroups (Compagnone & Mellon, 2000). To elucidate this relationship in glutamate, GABA and neurosteroid pathways in acoustic trauma, we investigated mice exposed to intense noise and examined expressions of related genes in the cochlea.