ACTH (Rat, Mouse) – RIA Kit

Catalog #: RK-001-21

Size: 125 tubes

Price: $924

Sensitivity: 91.6 pg/ml
Linear Range: 10 – 1280 pg/ml
Radioactivity: Each kit contains 1.5 µCi of Iodine 125.
Cross Reactivity:
Peptide %
ACTH (Rat, Mouse) 100
ACTH (Human) 100
ACTH (18-39) (Human) 100
ACTH (1-24) (Human, Rat, Mouse) 0
ACTH (7-38) (Human) 0
a-MSH 0
LH-RH (Human, Porcine, Rat) 0
PACAP-38 (Human, Ovine, Rat) 0
b-Endorphin (Rat) 0
CRI 0

Standard Curve:

Disclaimer: This package conforms to the 49 CFR173.421 for expected radioactive material limited quantity, N.O.S. UN2910.

Adrenocorticotropic Hormone

Abstract

Altered expression of adrenocorticotropic hormone in the epileptic gerbil hippocampus following spontaneous seizure.

We investigated the temporal alterations of adrenocorticotropic hormone (ACTH) immunoreactivity in the hippocampus after seizure onset. Expression of ACTH was observed within interneurons in the pre-seizure group of seizure sensitive gerbils, whereas its immunoreactivities were rarely detected in seizure resistant gerbil. Three hr after the seizure, ACTH immunoreactivity was significantly increased in interneurons within all hippocampal regions. On the basis of their localization and morphology through immunofluorescence staining, these cells were identified as GABAA α1-containing interneurons. At the 12 hr postictal period, ACTH expression in these regions was down-regulated, in a similar manner to the pre-seizure group of gerbils. These findings support the increase in ACTH synthesis that contributes to a reduction of corticotrophin-releasing factor via the negative feedback system which in turn provides an opportunity to enhance the excitability of GABAergic interneurons. Therefore, ACTH may play an important role in the reduction of excitotoxicity in all hippocampal regions.

Technical details influence the diagnostic accuracy of the 1 µg ACTH stimulation test.

Objective: To examine the factors causing inadequate cortisol responses to the 1 µg ACTH stimulation test. Design: Random test assignment (by age and gender) at 0800 or 1600 h.
Methods: We recruited 20 healthy adults to each of the three age groups (<40 years, 40-55 years, and >55 years; half females in each group). ACTH stimulation tests were performed in an outpatient clinic at the NIH Clinical Research Center. Plasma cortisol was measured just before, and 30 and 60 min after the administration of 1 mg ACTH (1-24). The ACTH concentration in diluted and administered solutions was measured.
Results: Twenty-five volunteers (19 at 1600 h) had a subnormal cortisol response (peak cortisol 10.4-17.5 µg/dl), using a criterion <18 mg/dl (497 nmol/l), for a specificity of 58% (confidence interval (CI) 45-71%). Afternoon testing had a significant impact on failure rates (odds ratio 6.98, CI 2.17-22.43), while gender and age did not. The stock solution contained 1 µg ACTH, but after administration through tubing it contained only 0.5-0.8 µg.
Conclusions: The high rate of abnormal results, especially in the afternoon, and loss of ACTH through tubing suggest that morning testing and minimal tubing should be adopted to avoid an inappropriate diagnosis of adrenal insufficiency. Earlier time points and standardized protocols would facilitate comparison of studies.

Wade M, Baid S, Calis K, Raff H, Sinaii N, Nieman L. Technical details influence the diagnostic accuracy of the 1 microg ACTH stimulation test. Eur J Endocrinol. 2010;162(1):109-13.

C-terminal fragments of ACTH stimulate feeding in fasted rats.

We investigated the central effect of ACTH 1-39 (ACTH) and peptides derived from the N-terminus (ACTH 1-10, Acetyl-ACTH 1-13-amide [alpha-MSH]) and C-terminus (ACTH 18-39 and ACTH 22-39) of this peptide on feeding in 16 hour-fasted or rats fed ad libitum. As expected, ACTH reduced feeding in fed and previously fasted rats, although this anorectic effect was more pronounced in fasted rats. The N-terminal-derived peptide alpha-MSH, but not ACTH 1-10, reduced cumulative food intake over 2 h after its injection intracerebroventricularly (icv) in 16 h-fasted, but not in fed rats. In contrast, the C-terminal fragments produced a long-lasting increase in feeding in fasted, but not in fed rats. The anorectic effects of N-terminal fragments of ACTH are recognised to be mediated via melanocortin MC4 receptors. However, the orexigenic effects of the C-terminal fragments do not appear to be conducted via MC4 receptors, since neither ACTH 18-39 nor ACTH 22-39 stimulated cAMP accumulation nor inhibited the ACTH-stimulated cAMP accumulation in HEK-293 cells transfected with the recombinant MC4 receptor.

Schematics

More Information

Adrenocorticotropic hormone (ACTH), also known as corticotropin, is a polypeptide tropic hormone produced and secreted by the anterior pituitary gland. It is an important component of the hypothalamic-pituitary-adrenal axis and is often produced in response to biological stress (along with corticotropin-releasing hormone from the hypothalamus). Its principal effects are increased production and release of corticosteroids and, as its name suggests, cortisol from the adrenal cortex.
ACTH is synthesized from pre-pro-opiomelanocortin (pre-POMC). The removal of the signal peptide during translation produces the 241-amino acid polypeptide POMC, which undergoes a series of post-translational modifications such as phosphorylation and glycosylation before it is proteolytically cleaved by endopeptidases to yield various polypeptide fragments with varying physiological activity. These fragments include NPP, Melanotropin Gamma (γ-MSH), Potential Peptide, Corticotropin (Adrenocorticotropic Hormone, or ACTH), Melanotropin Alpha (Melanocyte-Stimulating Hormone, or α-MSH), Corticotropin-like Intermediate Peptide (CLIP), Lipotropin Beta (β-LPH), Lipotropin Gamma (γ-LPH), Melanotropin Beta (β-MSH), Beta-Endorphin, and Met-Enkephalin. POMC, ACTH and β-lipotropin are secreted from corticotropes in the anterior lobe (or adenohypophysis) of the pituitary gland in response to the hormone corticotropin-releasing hormone (CRH) released by the hypothalamus.
In order to regulate the secretion of ACTH, many substances secreted within this axis exhibit slow/intermediate and fast feedback-loop activity. Glucocorticoids secreted from the adrenal cortex work to inhibit CRH secretion by the hypothalamus, which in turn decreases anterior pituitary secretion of ACTH. Glucocorticoids may also inhibit the rates of POMC gene transcription and peptide synthesis. The latter is an example of a slow feedback loop, which works on the order of hours to days, whereas the former works on the order of minutes.
ACTH is also related to the circadian rhythm in many organisms. The half-life of ACTH in human blood is about ten minutes.

Neuronostatin encoded by the somatostatin gene regulates neuronal, cardiovascular, and metabolic functions.
Samson et al. J Biol Chem. 2008 Nov 14;283(46):31949-59.

Hypothalamic-pituitary-adrenal axis hyporesponsiveness to restraint stress in mice deficient for large-conductance calcium- and voltage-activated potassium (BK) channels
Brunton et al. Endocrinology. 2007 Nov;148(11):5496-506.

Neonatal REM sleep is regulated by corticotropin releasing factor
Feng et al. Behav Brain Res. 2007 Aug 22;182(1):95-102.

The effect of long-term exposure to combinations of growth promoters in Long Evans rats Part 1: Endocrine adrenal function
Silvan et al. Anal Chim Acta. 2007 Mar 14;586(1-2):246-51.

Central Neuropeptide B Administration Activates Stress Hormone Secretion and Stimulates Feeding in Male Rats
Samson et al. J Neuroendocrinol. 2004 Oct;16(10):842-9.

Effect of bupropion on hippocampal neurotransmitters and on peripheral hormonal concentrations in the rat.
Piacentini et al. J Appl Physiol. 2003 Aug;95(2):652-6.

Neuropeptide W Acts in Brain to Control Prolactin, Corticosterone, and Growth Hormone Release
Baker et al. Endocrinology. 2003 Jul;144(7):2816-21.

Prolactin-releasing peptide and its homolog RFRP-1 act in hypothalamus but not in anterior pituitary gland to stimulate stress hormone secretion.
Samson et al. Endocrine. 2003 Feb-Mar;20(1-2):59-66.

Hypocretin/orexin suppresses corticotroph responsiveness in vitro.
Samson et al. Am J Physiol Regul Integr Comp Physiol. 2001 Oct;281(4):R1140-5.


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