Selective persistent reduction in choline acetyltransferase activity in basal forebrain of the rat after thyroid deficiency during early life

Patel, Ambrish J.; Hayashi, Masao; Hunt, Anthony

doi:10.1016/0006-8993(87)90556-7

Cited by 78 publications

(51 citation statements)

References 17 publications

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“…Accordingly, it has been shown that early maternal hypothyroxinemia alters fetal brain histogenesis and cytoarchitecture in rats (Lavado-Autric et al 2003), and unrecognized hypothyroidism in women in the first trimester of pregnancy may adversely affect the neuropsychological development of the progeny (Haddow et al 1999, Pop et al 2003, Morreale de Escobar et al 2004. There is also evidence both in embryonic and adult mammals supporting a key role of TH in the development and maintenance of basal forebrain cholinergic neurons typically involved in AD (Patel et al 1987, Calzà et al 1997. Therefore, we hypothesized that seladin-1 might be a mediator of the effects of TH in the brain.…”

Section: Seladin-1 As a Mediator Of The Effects Of Thyroid Hormones (mentioning

confidence: 99%

Neuroprotective effects of the Alzheimer's disease-related gene seladin-1

Peri

Serio

2008

Journal of Molecular Endocrinology

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The endocrine and the nervous system are closely correlated throughout life, starting from the embryo and until the late stages of life. Alzheimer's disease (AD) is the most common neurodegenerative disease associated with ageing. Unfortunately, an effective way to prevent or to cure this disease does not exist, so far. There is evidence that estrogens exert neuroprotective properties, although their efficacy against AD is still a matter of debate. In 2000 a new neuroprotective gene, i.e. seladin-1 (for SELective AD INdicator-1) was identified and found to be down regulated in AD vulnerable brain regions. Seladin-1 inhibits the activation of caspase-3, a key modulator of apoptosis. This protein has also enzymatic activity. In fact, it has been demonstrated that the seladin-1 gene encodes 3-b-hydroxysterol D-24-reductase, which catalyzes the synthesis of cholesterol from desmosterol. In recent years, it has been demonstrated that an appropriate amount of membrane cholesterol determines the generation of a barrier against toxic insults and prevents the production of b-amyloid, the histopathological hallmark of AD. This review will summarize the studies that have been focused on the characterization of the biological properties of seladin-1 since its first identification. In particular, the relationship between seladin-1-mediated neuroprotection and estrogens, IGF1 and thyroid hormones, will be described and discussed.

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Section: Seladin-1 As a Mediator Of The Effects Of Thyroid Hormones (mentioning

confidence: 99%

Neuroprotective effects of the Alzheimer's disease-related gene seladin-1

Peri

Serio

2008

Journal of Molecular Endocrinology

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“…These findings suggest that seladin-1 is a predominant product of multipotent cells and that the defective seladin-1 expression detected in AD-vulnerable brain regions may be linked to an impaired neuronal stem cell compartment, which could be a potential risk factor for the development of this disease. Interestingly, there is evidence both in embryonic and in adult mammals that TH plays a key role in the development and maintenance of basal forebrain cholinergic neurons typically involved in AD (Patel et al 1987, Calzàet al 1997.…”

Section: Introductionmentioning

confidence: 99%

Thyroid hormones promote cell differentiation and up-regulate the expression of the seladin-1 gene in in vitro models of human neuronal precursors

Benvenuti¹,

Luciani²,

Cellai³

et al. 2008

Journal of Endocrinology

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Thyroid hormones (TH) play an important role in the development of human brain, by regulating the expression of specific genes. Selective Alzheimer's disease indicator-1 (seladin-1) is a recently discovered gene with neuroprotective properties, which has been found to be down-regulated in brain regions affected by Alzheimer's disease. Seladin-1 has anti-apoptotic properties mainly due to the inhibition of the activation of caspase 3. The aim of this study was to determine whether seladin-1 may be regarded as a new mediator of the effects of TH in the developing brain. In order to demonstrate this hypothesis, the effects of TH both on cell differentiation and on the expression of seladin-1 were assessed in two different cell models, i.e. fetal human neuroepithelial cells (FNC) and human mesenchymal stem cells (hMSC), which can be differentiated into neurons. 3,3 0 ,5-Triiodothyronine (T 3 ) determined different biological responses (inhibition of cell adhesion, induction of migration, and increase in the expression of the neuronal marker neurofilament-M and Na C and Ca 2C channel functionality) in both FNC and hMSC, which express TH receptors. Then, we showed that TH significantly increase the expression levels of seladin-1, and that T 3 effectively prevents camptothecin-induced apoptosis. However, in hMSC-derived neurons the expression of seladin-1 was not affected by TH. Our results demonstrated for the first time that seladin-1 is a novel TH-regulated gene in neuronal precursors. In view of its anti-apoptotic activity, it might be hypothesized that one of the functions of the increased seladin-1 levels in the developing brain may be to protect neuronal precursor cells from death.

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“…33) Although the brain region responsible for head weaving response has not been conclusively demonstrated, the transgenic mouse model indicate the relevance between head weaving response and these brain region. PM feeding has been reported to result in structural and neurochemical degeneration in hippocampus, 34,35) prefrontal, 36) parietal 37,38) and visual 39) cortices. However, there are few report similar nutritional deficiency protocol as ours.…”

Section: Discussionmentioning

confidence: 99%

Enhanced Behavioral Response to Serotonin-Related Agonists in Postweaning Protein Malnourished Mice

Sato

Nakagawasai

Hayashi

et al. 2012

Biological & Pharmaceutical Bulletin

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We investigated whether postweaning protein malnutrition (PM) affects serotonergic systems. Mice were fed a PM diet or normal protein (control) diet from weaning (21 d of age). Twenty days later, we tested for behavioral effects of the selective serotonin (5-HT) 1A Key words protein malnutrition; serotonin 1A ; serotonin syndrome; head weaving; post-weaning period; mouse Serotonin (5-HT) is involved in the control of numerous physiological functions (e.g. food intake, thermoregulation, sleep patterns and nociception) 1) as well as in some psychiatric disorders such as anxiety and depression.2) These multiple actions are mediated through activation of at least 15 different families of serotonergic receptors.3) The 5-HT 1A receptor is one of the best described receptor subtypes and may be present on presynaptic as well as postsynaptic neurons.4) 5-HT 1A agonists have been successfully used in the treatment of anxiety disorders in human.5) However, excessive stimulation of postsynaptic 5-HT 1A receptor can lead to the 5-HT syndrome, a toxic condition displaying multiple clinical features. 6) In rodents, the administration of high doses of 5-HT 1A agonist, e.g. 8-hydroxy-N,N-dipropyl-2-aminotetralin (8-OH-DPAT), also elicits a 5-HT syndrome with typical major behavioral components such as flat body posture, hind limb abduction, forepaw treading, and head weaving. 7)5-HT concentrations are strongly influenced by undernourishment.8) 5-HT is synthesized from the amino acid precursor tryptophan and therefore is dependent on the latter's bioavailability. Brain levels of both are believed to increase as a result of metabolic adaptation to protein deficiency, which induces a decrease in the molar ratio of bound tryptophan to albumin. 9)However, some studies have reported either a decrease or no changes in brain serotonin levels following protein malnutrition (PM).10-12) Several experimental studies have focused on the consequences of prenatal (i.e., gestation period) and early postnatal (i.e., lactation period) malnutrition. PM during these developmental stages causes various atypical behaviors in rats, such as reduced anxiety, 13) decreased social interaction, 14) increased depressive behavior, 15) prepulse inhibition deficit 16) and impairment of memory-related behavior. 17) Moreover, a reduction in 5-HT 1A receptor levels and 5-HT uptake sites was reported in the hippocampus of prenatal PM rats.12) Since the 5-HT 1A receptor is considered to be a key receptor via which 5-HT participates in hippocampal dependent learning and memory functions, 18) PM may impact on cognitive performances as well. Thus, it is considered that the developmental period extending from gestation to weaning is critical with regards to PM. However, it has become apparent that brain development continues through adolescence.19) The age range for which the brain is vulnerable to the effects of malnutrition is potentially much greater than previously suspected but the threshold for malnutrition necessary to produce the behavioral alterations is unk...

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Selective persistent reduction in choline acetyltransferase activity in basal forebrain of the rat after thyroid deficiency during early life

Cited by 78 publications

References 17 publications

Neuroprotective effects of the Alzheimer's disease-related gene seladin-1

Neuroprotective effects of the Alzheimer's disease-related gene seladin-1

Thyroid hormones promote cell differentiation and up-regulate the expression of the seladin-1 gene in in vitro models of human neuronal precursors

Enhanced Behavioral Response to Serotonin-Related Agonists in Postweaning Protein Malnourished Mice

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