Opiate-Thyroid Hormone Interactions in the Regulation of Thyrotropin Secretion in the Rat

Berglund, Lee Ann; Millard, W.J.; Gabriel, Steven M.; Simpkins, James W.

doi:10.1159/000125602

Cited by 12 publications

(4 citation statements)

References 22 publications

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“…Future studies should measure rT 3 concentrations and deiodinase expression and activity in the brain to more directly address this issue, and those studies are currently underway by our group. Finally, we were unable to control for any additional confounds, such as pharmacological agents, as such opiates, administered close to the time of death that could affect the HPT-axis [35]. These potential confounds should be carefully controlled for in a future, larger study.…”

Section: Discussionmentioning

confidence: 99%

Thyroid Hormone Levels in the Prefrontal Cortex of Post-Mortem Brains of Alzheimers Disease Patients

Davis¹,

Podolanczuk²,

Donahue³

et al. 2008

CAS

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Converging evidence suggests a possible link between thyroid state and Alzheimer’s disease (AD), including a higher probability of dementia in individuals with higher TSH levels and a two-fold risk of AD in patients with hypothyroidism. Thyroid hormones modulate factors associated with AD, including amyloid precursor protein expression in the brain, suggesting a possible role for thyroid hormone in AD pathology. The present study is the first to directly evaluate brain thyroid hormone levels in AD. Triiodothyronine (T3) and thyroxine (T4) levels were measured with radioimmunoassay (RIA) in post-mortem samples of prefrontal cortex of patients with pathologically confirmed AD, including Braak stage I–II (n=8), Braak stage V–VI (n=8), and controls without any primary neurological disease (n=8). T4 levels did not differ between groups. T3 levels were significantly lower in Braak stage V–VI brains relative to controls, but there was no statistically significant difference between T3 levels in Braak stage I–II versus controls. Results suggest that the conversion of T4 to T3 may be affected in advanced AD, perhaps due to alterations in deiodinase activity. Reduced conversion of T4 to T3 in AD may be associated with both AD pathology and the clinical presentation of dementia.

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Section: Discussionmentioning

confidence: 99%

Thyroid Hormone Levels in the Prefrontal Cortex of Post-Mortem Brains of Alzheimers Disease Patients

Davis¹,

Podolanczuk²,

Donahue³

et al. 2008

CAS

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“…These two regions of the hypothalamus are critical for anterior pituitary regulation, as the PVN contains the cell bodies of hypophysiotropic TRH neurons that send axonal projections to the ME and release TRH into the hypophysial portal circulation (Lechan and Toni 1992). While the regulation of the hypothalamic-pituitary-thyroid axis in opiate withdrawal is yet undetermined, chronic morphine treatment itself significantly decreases serum TSH, T3 and T4 levels, suggesting an inhibitory effect on TSH secretion through negative feedback sensitivity to thyroid hormones (Berglund et al 1990). Consequently, during the resolution phase of the opiate withdrawal, 24 h following its precipitation as studied in our work, a compensatory change may also take place in the hypothalamic-pituitary-thyroid axis that allows restoration of thyroid homeostasis.…”

Section: Discussionmentioning

confidence: 99%

Effect of precipitated morphine withdrawal on post‐translational processing of prothyrotropin releasing hormone (proTRH) in the ventrolateral column of the midbrain periaqueductal gray

Nillni

Lee

Légràdi

et al. 2002

Journal of Neurochemistry

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We have demonstrated that during opiate withdrawal, preprothyrotropin releasing hormone (preproTRH) mRNA is increased in neurons of the midbrain periaqueductal gray matter (PAG) while the concentration of TRH remained unaltered, suggesting that the processing of proTRH may be different in this region of the brain. The aim of the present study was to determine which of the proTRH-derived peptides are affected by opiate withdrawal in the PAG. These changes were compared to other TRH-containing areas such as the hypothalamic paraventricular nucleus (PVN), median eminence (ME) and the lateral hypothalamus (LH). Control and morphine-treated rats 24 h following naltrexone-precipitated withdrawal were decapitated and the brain microdissected. Pooled samples from each animal group were acid extracted, and peptides were electrophoretically separated then analyzed by specific radioimmunoassay. Opiate withdrawal caused a significant change in the level of some post-translational processing products derived from the TRH precursor. In the PAG, opiate withdrawal resulted in an accumulation of the intervening preproTRH 83)106 peptide from the N-terminal side of the prohormone, while the levels of the C-terminal preproTRH 208-285 peptide were reduced, with no change in preproTRH 25)50 or TRH, itself, as compared to control animals. Immunohistochemical analysis also showed significant increases in cellular preproTRH 83)106 peptide immunolabeling in the PAG. Opiate withdrawal in the lateral hypothalamus, unlike from the PAG, was accompanied by an increase in the concentration of TRH. In addition, western blot analysis showed that during opiate withdrawal, the mature form of the prohormone convertase 2 (PC2) increased only in PAG as compared with their respective controls. Thus, these results demonstrate a region-specific regulation of TRH prohormone processing in the brain, which may engage PC2, further suggesting a role for specific proTRH-derived peptides in the manifestations of opiate withdrawal.

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“…In long-term periods depending on the dose and duration of use and other factors, different mechanisms are gradually involved. 1 Molina et al ( 1994 ), 2 Berglund et al ( 1990 ), 3 Al Sagair ( 2005 ), 4 Bryant et al ( 1987 ), 5 Payabvash et al ( 2006 ), 6 Zhang et al ( 2004 ), 7 Divsalar et al ( 2010 ), 8 Rahimi et al ( 2014 ), 9 Bryant et al ( 1988 ), 10 Radosevich et al ( 1984 ), 11 May et al ( 1988 ), 12 Ipp et al ( 1980 ), 13 Molina et al ( 1994 ), 14 Zandomeneghi et al ( 1988 ), 15 Liu and Cheng ( 2011 ), 16 Sheldon and Quin ( 2005 ), 17 Headrick et al ( 2012 ), 18 Mansour et al ( 1970 ), 19 Asgary et al ( 2008 ), 20 de Luis et al ( 2005 ), 21 Jimenez and Fuentes ( 1993 ), 22 Bolte et al ( 2009 ).…”

Section: The Mechanisms Of Actionmentioning

confidence: 99%

The Impact of Opium Consumption on Blood Glucose, Serum Lipids and Blood Pressure, and Related Mechanisms

Najafipour

Beik

2016

Front. Physiol.

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Aim: Substance abuse has become a universal crisis in our modern age. Among illegal substances, opium and its derivatives have been ranked second in terms of usage after cannabis in the world. In many Asian regions, the use of opium enjoys a high social acceptance; hence, some common people and even medical practitioners believe that opium lowers blood glucose and pressure and treat dyslipidemia. How much this belief is scientifically justified?Method: The results of available studies on both humans and animals searched in different search engines up to mid-2016 were integrated (78 articles). Upon the findings we try to offer a more transparent picture of the effects of opium on the mentioned factors along with the probable underlying mechanisms of its action.Results: Taken together, a variety of evidences suggest that the consumption of opium has no scientific justification for amendment of these biochemical variables. The mechanisms proposed so far for the action of opium in the three above disorders are summarized at the end of the article. Short term effects seems to be mostly mediated through central nervous system (neural and hormonal mechanisms), but long term effects are often due to the structural and functional alterations in some body organs.Conclusion: Although opium may temporarily reduce blood pressure, but it increases blood glucose and most of blood lipids. Moreover its long term use has negative impacts and thus it aggravates diabetes, dyslipidemia and hypertension. Accordingly, it is necessary to inform societies about the potential disadvantages of unauthorized opium consumption.

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Opiate-Thyroid Hormone Interactions in the Regulation of Thyrotropin Secretion in the Rat

Cited by 12 publications

References 22 publications

Thyroid Hormone Levels in the Prefrontal Cortex of Post-Mortem Brains of Alzheimers Disease Patients

Thyroid Hormone Levels in the Prefrontal Cortex of Post-Mortem Brains of Alzheimers Disease Patients

Effect of precipitated morphine withdrawal on post‐translational processing of prothyrotropin releasing hormone (proTRH) in the ventrolateral column of the midbrain periaqueductal gray

The Impact of Opium Consumption on Blood Glucose, Serum Lipids and Blood Pressure, and Related Mechanisms

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