Rapid modulation of TRH and TRH-like peptide release in rat brain and peripheral tissues by prazosin

Sattin, Albert; Pekary, A. Eugene; Blood, James

doi:10.1016/j.peptides.2011.06.012

Cited by 6 publications

(2 citation statements)

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“…Contraction of the epididymis, prostate and vas deferens during ejaculation is mediated by peptidergic and noradrenergic neurons [46]. Blockade of the α 1 -adrenoreceptors with prazosin, a therapeutic for hypertension which has more recently been shown to be effective in the treatment of PTSD, stim- ulates release of TRH and TRH-like peptides in epididymis and prostate, 2 tissues with the highest concentrations of α 1 -adrenoreceptors in rats, suggesting a role for these peptides in the ejaculatory process [47]. Serum testosterone and glucose levels undergo significant variation during the 24-h photoperiod as previously reported [48,49] and seen in ▶ table 1.…”

Section: Discussionmentioning

confidence: 99%

TRH and TRH-Like Peptide Levels Co-Vary with Reproductive and Metabolic Rhythms

Pekary

Sattin

2016

Horm Metab Res

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Photoperiod-synchronized rhythms in non-CSN tissues persist in total darkness. Clock genes involved in maintaining regular biorhythms within the suprachiasmatic nucleus (SCN) of the hypothalamus are expressed in extra-CNS tissues and continue periodic expression in vitro. Understanding the details of how the SCN clock is coupled with peripheral clocks is only incompletely understood and may involve a multiplicity of feedback systems. The present study is an extension of our previous work showing that brain levels of TRH (pGlu-His-Pro-NH) and TRH-like peptides (X-TRH: pGlu-X-Pro-NH, where "X" can be any amino acid residue) fluctuate throughout the day-night cycle. Male rats were maintained in a stable environment, lights on 6-18 h. TRH and TRH-like peptides in liver, pancreas, testis, prostate, epididymis, and heart were measured at 3, 10, 16, and 22 h. The greatest change in peptide level was a 12-fold increase for TRH in prostate at 16 h relative to the corresponding value at 3 h. The TRH, Tyr-TRH and Phe-TRH levels in liver declined steadily to about 40% of the 3-h values by 22 h. Changes, in the order of decreasing number of significant increases (↑) and/or decreases (↓), were: testis (5↑, 1↓), liver (3↓), epididymis (2↑), prostate (1↑, 1↓) and heart (1↑). Peptide levels in liver and testis correlated with serum leptin and serum corticosterone, respectively, which are potent releasers of these peptides. Testosterone and glucose were also highly correlated. These tripeptides may participate in the regulation of metabolic and reproductive functions, which change during the day-night cycle.

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Section: Discussionmentioning

confidence: 99%

TRH and TRH-Like Peptide Levels Co-Vary with Reproductive and Metabolic Rhythms

Pekary

Sattin

2016

Horm Metab Res

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“…Prohormone convertases are also capable of influencing TRH expression, as drug-induced hypothyroidism can result in increased levels of PC1/3 and PC2 expression and thus increased pro-TRH levels within the ventromedial nucleus and lateral hypothalamus (Espinosa et al, 2007). Pekary and colleagues have identified other modulators of TRH and TRH-like peptide release including: ghrelin (Pekary et al, 2012), prazosin (Sattin et al 2011), corticosterone (Pekary et al, 2008), lipopolysaccharides (LPS) (Pekary et al, 2007), and leptin (Pekary et al, 2010). Additionally, corticotrophin releasing hormone (CRH) has demonstrated a capacity to decrease TRH levels in multiple regions of the brain (Tsigos and Chrousos, 2002).…”

Section: Trh Synthesis Processing and Clearancementioning

confidence: 99%

The role of Thyrotropin Releasing Hormone in aging and neurodegenerative diseases

Daimon¹,

Chirdon²,

Maudsley³

et al. 2013

AJAD

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Thyrotropin releasing hormone (TRH) is primarily known as the central regulator of the hypothalamic-pituitary-thyroid (HPT) axis. However, TRH also exerts a variety of central nervous system effects independent from its activity in the HPT axis. With advancing age, decreases in TRH synthesis, expression, and activity have been demonstrated. Associated with this emerging evidence suggests that TRH is implicated in neurodegenerative diseases of aging, including Alzheimer’s disease and Parkinson’s disease. TRH and its synthetic analogs have been recognized as trophic factors in neurons of the diencephalon and spinal cord, and as neuroprotectants against oxidative stress, glutamate toxicity, caspase-induced cell death, DNA fragmentation, and inflammation. In this review, we will provide an overview of some of the roles of TRH, outside of the HPT axis, associated with pathological aging and neurodegeneration and we shall discuss the potential of TRH and TRH analogs for the treatment of neurodegenerative diseases.

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