Effect of neonatal nociceptin or nocistatin imprinting on the brain concentration of biogenic amines and their metabolites

Tekes, Kornélia; Gyenge, Melinda; Sótonyi, Péter; Csaba, G.

doi:10.1016/j.braindev.2008.05.007

Cited by 10 publications

(8 citation statements)

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“…Considering that during parturition, the intensity of pain and duration of delivery is individual, the variable endorphin production could influence the aggressivity of adults. Imprinting with the pain-stimulating nociceptin or pain killer nocistatin influences the brain biogenic amine levels in adults, region specifically (Tekes et al 2009c). In addition, the effects at weaning also could be settled on the perinatal imprinting.…”

Section: Hormonal Imprinting Of the Central Nervous Systemmentioning

confidence: 99%

“…As a consequence of the mother's alcohol consumption, the nocistatin level of CSF and blood increases (Tekes et al 2007a). Other molecules (benzpyrene, vitamins A and D) also can imprint the brain, is manifested in the change of biogenic amine levels of the brain and CSF (Tekes et al 2007a, b, 2009a, b, c). Perinatal stress —which disturbs the whole endocrine system—also life-long influences the brain biogenic amine and CSF nociceptin level (Tekes et al 2010).…”

Section: Hormonal Imprinting Of the Central Nervous Systemmentioning

confidence: 99%

“…In the F1 generation of DES-imprinted mothers, the frequency of tumors increased (Newbold et al 2000). Imprinting with receptor level acting vitamins A and D influenced the brain biogenic amine levels of F1 progenies (Tekes et al 2009a, b, c) as well as the hormone production of immune cells (Csaba et al 2007). Morphine exposure at puberty caused the increase of anxiety and sensitivity to morphine (Byrnes 2005) in the offspring.…”

Section: The Transgenerational Imprintingmentioning

confidence: 99%

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The biological basis and clinical significance of hormonal imprinting, an epigenetic process

Csaba

2011

Clin Epigenet

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The biological phenomenon, hormonal imprinting, was named and defined by us (Biol Rev, 1980, 55, 47-63) 30 years ago, after many experimental works and observations. Later, similar phenomena were also named to epigenetic imprinting or metabolic imprinting. In the case of hormonal imprinting, the first encounter between a hormone and its developing target cell receptor—usually at the perinatal period—determines the normal receptor-hormone connection for life. However, in this period, molecules similar to the target hormone (members of the same hormone family, synthetic drugs, environmental pollutants, etc), which are also able to bind to the receptor, provoke faulty imprinting also with lifelong—receptorial, behavioral, etc.,—consequences. Faulty hormonal imprinting could also be provoked later in life in continuously dividing cells and in the brain. Faulty hormonal imprinting is a disturbance of gene methylation pattern, which is epigenenetically inherited to the further generations (transgenerational imprinting). The absence of the normal or the presence of false hormonal imprinting predispose to or manifested in different diseases (e.g., malignant tumors, metabolic syndrome) long after the time of imprinting or in the progenies.

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Section: Hormonal Imprinting Of the Central Nervous Systemmentioning

confidence: 99%

Section: Hormonal Imprinting Of the Central Nervous Systemmentioning

confidence: 99%

Section: The Transgenerational Imprintingmentioning

confidence: 99%

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The biological basis and clinical significance of hormonal imprinting, an epigenetic process

Csaba

2011

Clin Epigenet

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“…Nocistatinimprinting hatá-sára éppen ellenkezőleg, a biogén aminszintek csökke-nése domináns [44]. Más anyagokkal történő perinatalis imprinting ugyancsak befolyásolja a késői agyi nocistatinszintet, amely benzpirénimprinting hatására szignifikánsan csökken a liquorban mérve [45], és béta-endorfi n-imprinting hatására nő a vérplazmában [36].…”

Section: A Fájdalomérzés Imprintingjeunclassified

Hormonal imprinting in the central nervous system: causes and consequences

Csaba

2013

Orvosi Hetilap

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A perinatalis hormonális imprinting fogalma először 1980-ban jelent meg és azóta széleskörűen elterjedt. Az imprinting a fejlődő receptor és a megfelelő hormon első találkozásakor megy végbe -valószínűleg a DNS metilációs mintázatának megváltozása által -, és hatása a sejtek utódgenerációiban élethossziglan tart. Szükséges a receptor kötési képességének teljes kialakulásához. A fejlődő receptorhoz azonban egyéb -a célhormonhoz hasonló -molekulák (receptorszinten ható hormonanalógok, gyógyszerek, vegyszerek, környezetszennyező anyagok) is kötődni képesek, ugyancsak életre szóló hibás imprintinget hozva létre. Ez kóros állapotokat okozhat. Később kiderült, hogy egyéb kritikus periódusokban, mint a pubertás, szintén imprinting jöhet létre, sőt differenciálódó sejtekben az élet bármely szakaszában. Az imprinting a szülőről az utódra is átadódik, azaz epigenetikusan öröklődik, valószínűleg emberben is. A központi idegrendszer is (hibásan) imprintálódhat, ami a dopaminerg, szerotonerg és noradrenerg rendszert tartósan befolyásolja, így a szexuális és szociális magatartás zavaraiban is megmutatkozik állatkísérletek-ben. Korunkban a hibás imprinting létrejötte elkerülhetetlen a gyógyszerek, vegyszerek tömege, az ételekben levő hormonszerű anyagok (például szójafi toszteroidok) és a környezetszennyezés miatt. A szerző különösen kiemeli az oxitocinnak, mint imprinternek veszélyességét, mivel igen széles körben alkalmazzák, miközben imprintingje döntő-en érintheti az érzelmi és szociális szférát és egyes betegségek -mint az autizmus, szkizofrénia és Parkinson-kór -fellépését. A perinatalis imprinterek veszélyessége azért is nő, mert az imprinting átöröklődve befolyásolhatja az emberi evolúciót. Orv. Hetil., 2013, 154, 128-135. Kulcsszavak: hormonális imprinting, hibás imprinting, agy, autizmus, szkizofrénia Hormonal imprinting in the central nervous system: causes and consequencesThe notion of the perinatal "hormonal imprinting" has been published at fi rst in 1980 and since that time it spred expansively. The imprintig develops at the fi rst encounter between the developing receptor and the target hormone -possibly by the alteration of the methylation pattern of DNA -and it is transmitted to the progeny generations of the cell. This is needed for the complete development of the receptor's binding capacity. However, molecules similar to the target hormone (hormone-analogues, drugs, chemicals, environmental pollutants) can also bind to the developing receptor, causing faulty imprinting with life-long consequences. This can promote pathological conditions. Later it was cleared that in other critical periods such as puberty, imprinting also can be provoked, even in any age in differentiating cells. The central nervous system (brain) also can be mistakenly imprinted, which durably infl uences the dopaminergic, serotonergic and noradrenergic system and this can be manifested -in animal experiments -in alterations of the sexual and social behavior. In our modern age the faulty hormonal imprintig is inavoidable because of the ...

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“…The highest concentrations of N/OFQ were noticed in the dorsal central gray matter (periaqueductal gray), the locus coeruleus, the ventromedial nucleus of hypothalamus, the septum and the dorsal horn of the spinal cord. Evidence indicates that N/ OFQ has a signifi cant role in regulating the neurotransmission of the central nervous system (24). There is also evidence that N/OFQ has direct effects on different cardiovascular regulatory areas on rodents both in vitro and in vivo (6).…”

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confidence: 99%

Decreased plasma nociceptin/orphanin FQ levels after acute coronary syndromes

Csobay-Novák

Sótonyi

Krepuska

et al. 2012

Acta Physiologica Hungarica

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Foregoing researches made on the N/OFQ system brought up a possible role for this system in cardiovascular regulation. In this study we examined how N/OFQ levels of the blood plasma changed in acute cardiovascular diseases. Three cardiac patient groups were created: enzyme positive acute coronary syndrome (EPACS, n = 10), enzyme negative ACS (ENACS, n = 7) and ischemic heart disease (IHD, n = 11). We compared the patients to healthy control subjects (n = 31). We found signifi cantly lower N/OFQ levels in the EPACS [6.86 (6.21-7.38) pg/ ml], ENACS [6.97 (6.87-7.01) pg/ml and IHD groups [7.58 (7.23-8.20) pg/ml] compared to the control group [8.86 (7.27-9.83) pg/ml]. A signifi cant correlation was detected between N/OFQ and white blood cell count (WBC), platelet count (PLT), creatine kinase (CK), glutamate oxaloacetate transaminase (GOT) and cholesterol levels in the EPACS group.Decreased plasma N/OFQ is closely associated with the presence of acute cardiovascular disease, and the severity of symptoms has a signifi cant negative correlation with the N/OFQ levels. We believe that the rate of N/OFQ depression is in association with the level of ischemic stress and the following infl ammatory response. Further investigations are needed to clarify the relevance and elucidate the exact effects of the ischemic stress on the N/OFQ system. Keywords: acute coronary syndrome, angina pectoris, nociceptin/orphanin FQ, ischemic stressMore than a decade now that a new chapter has been opened in the research of the opioid system with Mollereau cloning a new member of the opioid receptor family, which was named opioid receptor like orphan receptor (ORL-1) because it was reminiscent of the opioid receptors on both structural and functional ground (21). A year later the endogenous ligand of the ORL-1 was identifi ed and named nociceptin (for its hyperalgesic effect on mice when administered intracerebroventricularly) and orphanin-FQ, because of the Phe and Gln amino acids on the ends of the peptide chain (21, 22). The ORL-1 receptor was renamed NOP receptor and the nociceptin/orphanin FQ peptide as N/OFQ in the current nomenclature by NC-IUPHAR.

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Effect of neonatal nociceptin or nocistatin imprinting on the brain concentration of biogenic amines and their metabolites

Cited by 10 publications

References 27 publications

The biological basis and clinical significance of hormonal imprinting, an epigenetic process

The biological basis and clinical significance of hormonal imprinting, an epigenetic process

Hormonal imprinting in the central nervous system: causes and consequences

Decreased plasma nociceptin/orphanin FQ levels after acute coronary syndromes

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