Effects of eledoisin on thyrotrophin secretion in rats

1985 ◽  
Vol 110 (1) ◽  
pp. 90-94
Author(s):  
Terunori Mitsuma ◽  
Tsuyoshi Nogimori ◽  
De Heng Sun ◽  
Masahiro Chaya
Keyword(s):  
Central Nervous System ◽  
Thyroid Hormone ◽  
Inhibitory Effect ◽  
Thyrotrophin Releasing Hormone ◽  
Tsh Secretion ◽  
Pretreated Group ◽  
The Central Nervous System ◽  
Thyroid Hormone Levels ◽  
Tsh Levels

Abstract. The effect of peripheral administration of eledoisin on thyrotrophin-releasing hormone (TRH) and thyrotrophin (TSH) secretion in rats were studied. Eledoisin (500 μg/kg) was injected iv, and the rats were serially decapitated. TRH, TSH and thyroid hormone were measured by radioimmunoassay. The hypothalamic immunoreactive TRH (ir-TRH) content increased significantly after eledoisin injection, whereas its plasma concentration tended to decrease, but not significantly. Plasma TSH levels decreased significantly in a dose-related manner with a nadir at 40 min after the injection. Plasma thyroid hormone levels did not change significantly. Plasma ir-TRH and TSH responses to cold were inhibited by eledoisin, but the plasma TSH response to TRH was not affected. In the pimozide- or para-chlorophenylalanine-pretreated group, the inhibitory effect of eledoisin on TSH levels was prevented, but not in the l-dopa- or 5-hydroxytryptophan-pretreated group. These drugs alone did not affect plasma TSH levels at the dose used. The inactivation of TRH immunoreactivity by plasma or hypothalamus in vitro after eledoisin injection did not differ from that of controls. These findings suggest that eledoisin acts on the hypothalamus to inhibit TRH release, and its effects are modified by amines of the central nervous system.

Bombesin inhibits thyrotrophin secretion in rats

1985 ◽  
Vol 108 (1) ◽  
pp. 79-84 ◽  
Author(s):  
Terunori Mitsuma ◽  
Tsuyoshi Nogimori ◽  
Masahiro Chaya
Keyword(s):  
Thyroid Hormone ◽  
Plasma Concentrations ◽  
Treated Group ◽  
Inhibitory Effect ◽  
Thyrotrophin Releasing Hormone ◽  
Tsh Secretion ◽  
The Central Nervous System ◽  
Thyroid Hormone Levels ◽  
Tsh Levels

Abstract. The effects of peripheral administration of bombesin on thyrotrophin-releasing hormone (TRH) and thvrotrophin (TSH) secretion in rats were studied. Bombesin (200 μg/kg) was injected iv, and the rats were serially decapitated. TRH, TSH and thyroid hormone were measured by radioimmunoassay. The hypothalamic immunoreactive TRH (ir-TRH) content increased significantly after bombesin injection, whereas plasma concentrations tended to decrease, but not significantly. Plasma TSH levels decreased significantly in a dose-related manner with a nadir at 40 min after the injection. Plasma thyroid hormone levels did not change significantly. Plasma ir-TRH and TSH responses to cold were inhibited by bombesin, but the plasma TSH response to TRH was not affected. In the pimozide- or para-chlorophenylalanine pre-treated group, the inhibitory effect of bombesin on TSH levels was prevented, but not in the l-Dopa- or 5-hydroxytryptophan pre-treated group. These drugs alone had no effect on plasma TSH levels in terms of the dose used. The inactivation of TRH immunoreactivity in plasma or hypothalamus in vitro after bombesin injection did not differ from that of the controls. These findings suggest that bombesin acts on the hypothalamus to inhibit TRH release, and that its effects are at least partially modified by amines of the central nervous system.

β-Neoendorphin inhibits thyrotrophin secretion in rats

1983 ◽  
Vol 104 (4) ◽  
pp. 437-442 ◽  
Author(s):  
Terunori Mitsuma ◽  
Tsuyoshi Nogimori
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Plasma Concentrations ◽  
Inhibitory Effect ◽  
Thyrotrophin Releasing Hormone ◽  
Specific Radioimmunoassay ◽  
Tsh Secretion ◽  
Pretreated Group ◽  
The Central Nervous System ◽  
Tsh Levels

Abstract. The effects of β-neoendorphin on thyrotrophin-releasing hormone (TRH) and thyrotrophin (TSH) secretion in rats were studied. β-neoendorphin (500 μg/kg) was injected iv, and the rats were decapitated serially. TRH, TSH, thyroxine (T4) and 3,3',5-triiodothyronine (T3) were measured by means of a specific radioimmunoassay for each. Hypothalamic immunoreactive TRH (ir-TRH) content increased significantly after β-neoendorphin injection, and plasma concentrations tended to decrease, but not significantly so. Plasma TSH levels decreased significantly in a dose-related manner with a nadir at 40 min. Plasma T4 and T3 levels did not change after the injection. Plasma ir-TRH and TSH responses to cold were significantly inhibited by β-neoendorphin, but the plasma TSH response to TRH was not. Naloxone partially prevented the inhibitory effect of β-neoendorphin on TSH release. In the haloperidol- or 5-hydroxytryptophan-pretreated group, the inhibitory effect of β-neoendorphin on TSH release was prevented, but not in the l-dopa- or para-chlorophenylalanine-pretreated group. These drugs alone did not affect plasma TSH levels at the dose used. These findings suggest that β-neoendorphin acts on the hypothalamus by inhibiting TRH release, which may be modified by amines of the central nervous system.

Dynorphin (1–13) effects on thyrotrophin-releasing hormone and thyrotrophin secretion in rats

1983 ◽  
Vol 103 (3) ◽  
pp. 359-364 ◽  
Author(s):  
Terunori Mitsuma ◽  
Tsuyoshi Nogimori
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Inhibitory Effect ◽  
Thyrotrophin Releasing Hormone ◽  
Releasing Hormone ◽  
Tsh Secretion ◽  
Pretreated Group ◽  
Basal Plasma ◽  
The Central Nervous System ◽  
Tsh Levels

Abstract. The effects of dynorphin (1-13) on thyrotrophin-releasing hormone (TRH) and thyrotrophin (TSH) secretion in rats were studied. Dynorphin (500 μg/kg) was injected iv, and the rats were serially decapitated. TRH and TSH, thyroxine (T4) and 3,3',5-triiodothyronine (T3) were measured by radioimmunoassay. The hypothalamic immunoreactive TRH did not change significantly after dynorphin injection. Basal plasma TSH levels significantly decreased in a dose-related manner with a nadir at 40 min after dynorphin injection. The effect of dynorphin on TSH release was partially prevented by naloxone. The plasma TSH response to cold was significantly inhibited by dynorphin. The plasma TSH response to TRH did not differ from that of the control. In the l-DOPA or 5-hydrotryptophan-pretreated group, the inhibitory effect of dynorphin on TSH release was prevented, but not in the haloperidolor para-chlorophenylalanine-pretreated group. These drugs alone did not affect plasma TSH levels. The plasma T4 and T3 levels did not change significantly after dynorphin injection. The findings suggest that dynorphin acts on the hypothalamus by inhibiting TRH release, which may be modified by amines of the central nervous system.

EFFECT OF THYROID STATUS ON THE THYROTROPHIN-RELEASING HORMONE-DEGRADING ACTIVITY OF RAT SERUM

1976 ◽  
Vol 71 (1) ◽  
pp. 13-19 ◽  
Author(s):  
N. WHITE ◽  
S. L. JEFFCOATE ◽  
E. C. GRIFFITHS ◽  
K. C. HOOPER
Keyword(s):  
Thyroid Hormone ◽  
Human Serum ◽  
Thyroid Function ◽  
Thyroid Status ◽  
Rat Serum ◽  
Thyrotrophin Releasing Hormone ◽  
Releasing Hormone ◽  
Tsh Levels

SUMMARY The TRH-degrading activity of rat serum in vitro is five times more potent than that of human serum. In rats, it is significantly reduced in hypothyroidism (thiouracil-induced) and significantly increased in hyperthyroidism (T3 or T4-induced). This suggests a possible role in the regulation of adenohypophysial-thyroid function which is probably, in turn, dependent on thyroid hormone, rather than TSH, levels.

Deficient pulsatile thyrotropin secretion in the low-thyroid-hormone state of severe non-thyroidal illness

1994 ◽  
Vol 130 (2) ◽  
pp. 132-136 ◽  
Author(s):  
Nicola Custro ◽  
Vincenza Scafidi ◽  
Salvatore Gallo ◽  
Alberto Notarbartolo
Keyword(s):  
Thyroid Hormone ◽  
Healthy Subjects ◽  
Normal Subjects ◽  
Healthy Individuals ◽  
Circadian Variations ◽  
Tsh Secretion ◽  
Thyroid Hormone Levels ◽  
Rhythmic Change ◽  
Serum Tsh ◽  
Tsh Levels

Custro N, Scafidi V, Gallo S, Notarbartolo A. Deficient pulsatile thyrotropin secretion in the low-thyroid-hormone state of severe non-thyroidal illness. Eur J Endocrinol 1994;130:132–6. ISSN 0804–4643. Twenty-four-hour thyrotropin (TSH) profiles in eight severely ill patients were compared with those of six healthy subjects. The profiles were assessed using the cosinor method to evaluate circadian variations and using the Pulsar algorithm to analyze episodic secretion. In the normal subjects, the typical periodicity of TSH secretion showed a mean level in the rhythm (mesor) of 2.03 mU/l, The amplitude (half the extent of rhythmic change in the cycle) was 0.58 mU/l; the acrophase (the delay from midnight (0 degrees) of the highest level in the rhythm) was −9.9 degrees. In contrast, severely ill patients showed only slight and anticipated elevations of serum TSH levels (mesor 0.93 mU/l, amplitude 0.22 mU/l, acrophase +82.4 degrees). Moreover, whereas the episodic TSH secretion in healthy individuals consisted of 5–8 pulses/24 h, mainly clustered around midnight, only one pulse of reduced amplitude was detected in two of the eight severely ill patients and no pulses in the other six. Since earlier studies have indicated that the loss of TSH pulsatility is associated with the relative insensitivity of the thyrotrophs to low thyroid hormone levels and our analytical procedures have demonstrated that 24 h pulsatile pattern of TSH closely overlapped with baseline TSH secretion, it seems reasonable to assume that low-thyroid-hormone state, deficient pulsatile TSH secretion and altered nyctohemeral TSH periodicity do not coincide by chance, but that there is a causal relationship between such abnormalities in severely ill patients. Nicola Custro, Cattedra di Patologia Medica, Via del Vespro, n.141, 90127 Palermo, Italy

Thyroidal inhibition of chicken pituitary growth hormone: alterations in secretion and accumulation of newly synthesized hormone

1991 ◽  
Vol 131 (1) ◽  
pp. 39-48 ◽  
Author(s):  
R. J. Denver ◽  
S. Harvey
Keyword(s):  
Thyroid Hormone ◽  
Mammalian Species ◽  
Inhibitory Effect ◽  
Stimulatory Action ◽  
Thyrotrophin Releasing Hormone ◽  
Gh Secretion ◽  
Direct Inhibitory Effect ◽  
Hormone Exposure

ABSTRACT Hypothyroidism reduces GH synthesis and release in several mammalian species, in which thyroid hormone directly stimulates GH gene transcription. In contrast, hypothyroidism stimulates GH secretion in birds, in which thyroid hormone directly inhibits pituitary GH release. We have, therefore, investigated the effects of thyroid status on the accumulation of newly synthesized GH in the pituitaries of 8- to 10-week-old Leghorn cockerels in vitro and in vivo. The incorporation of [35S]methionine into immunoprecipitable GH ([35S] GH) was increased, over a 4-h incubation period, in glands from birds made hypothyroid by injections of methimazole (50 mg/kg day for 10 days) in comparison with glands from vehicle-injected controls. Treatment with tri-iodothyronine (T3, 100 μg/kg per day for 10 days) in vivo did not significantly alter the accumulation of [35S]GH in vitro but did block the release of [35S]GH in response to a GH secretagogue (thyrotrophin-releasing hormone; exposure to 280 nmol/l for 30 min) and reduced immunoassayable pituitary GH content. Pretreatment of glands from euthyroid birds with T3 (100 nmol/l) in vitro (for 20 h) reduced the basal accumulation of [35S]GH as well as that induced by another GH secretagogue (GH-releasing factor; 100 nmol/l) during a 6-h labelling period. These results show that, unlike the generally stimulatory action of thyroid hormone in mammals, in birds, T3 exerts a direct inhibitory effect on the accumulation of newly synthesized pituitary GH. Journal of Endocrinology (1991) 131, 39–48

Neural Stem Cells to Glial Cells an Important Factor for Brain Injury

2020 ◽  
Author(s):  
Prithiv K R Kumar
Keyword(s):  
Stem Cells ◽  
Central Nervous System ◽  
Nervous System ◽  
Neural Stem Cells ◽  
Glial Cells ◽  
Brain Injuries ◽  
The Body ◽  
The Central Nervous System ◽  
Near Future

Stem cells have the capacity to differentiate into any type of cell or organ. Stems cell originate from any part of the body, including the brain. Brain cells or rather neural stem cells have the capacitive advantage of differentiating into the central nervous system leading to the formation of neurons and glial cells. Neural stem cells should have a source by editing DNA, or by mixings chemical enzymes of iPSCs. By this method, a limitless number of neuron stem cells can be obtained. Increase in supply of NSCs help in repairing glial cells which in-turn heal the central nervous system. Generally, brain injuries cause motor and sensory deficits leading to stroke. With all trials from novel therapeutic methods to enhanced rehabilitation time, the economy and quality of life is suppressed. Only PSCs have proven effective for grafting cells into NSCs. Neurons derived from stem cells is the only challenge that limits in-vitro usage in the near future.

scholarly journals Beyond Oncological Hyperthermia: Physically Drivable Magnetic Nanobubbles as Novel Multipurpose Theranostic Carriers in the Central Nervous System

Molecules ◽  
2020 ◽  
Vol 25 (9) ◽  
pp. 2104 ◽  
Author(s):  
Eleonora Ficiarà ◽  
Shoeb Anwar Ansari ◽  
Monica Argenziano ◽  
Luigi Cangemi ◽  
Chiara Monge ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Brain Tumors ◽  
Ad Hoc ◽  
Superparamagnetic Iron Oxide ◽  
Conventional Radiotherapy ◽  
The Central Nervous System ◽  
Magnetic Resonance Imaging Mri ◽  
The Brain

Magnetic Oxygen-Loaded Nanobubbles (MOLNBs), manufactured by adding Superparamagnetic Iron Oxide Nanoparticles (SPIONs) on the surface of polymeric nanobubbles, are investigated as theranostic carriers for delivering oxygen and chemotherapy to brain tumors. Physicochemical and cyto-toxicological properties and in vitro internalization by human brain microvascular endothelial cells as well as the motion of MOLNBs in a static magnetic field were investigated. MOLNBs are safe oxygen-loaded vectors able to overcome the brain membranes and drivable through the Central Nervous System (CNS) to deliver their cargoes to specific sites of interest. In addition, MOLNBs are monitorable either via Magnetic Resonance Imaging (MRI) or Ultrasound (US) sonography. MOLNBs can find application in targeting brain tumors since they can enhance conventional radiotherapy and deliver chemotherapy being driven by ad hoc tailored magnetic fields under MRI and/or US monitoring.

scholarly journals Effects of Platelet-Rich Plasma on Cellular Populations of the Central Nervous System: The Influence of Donor Age

2021 ◽  
Vol 22 (4) ◽  
pp. 1725
Author(s):  
Diego Delgado ◽  
Ane Miren Bilbao ◽  
Maider Beitia ◽  
Ane Garate ◽  
Pello Sánchez ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Cellular Response ◽  
Platelet Rich Plasma ◽  
Biological Response ◽  
In Vitro Models ◽  
Molecular Composition ◽  
Cellular Models ◽  
The Central Nervous System

Platelet-rich plasma (PRP) is a biologic therapy that promotes healing responses across multiple medical fields, including the central nervous system (CNS). The efficacy of this therapy depends on several factors such as the donor’s health status and age. This work aims to prove the effect of PRP on cellular models of the CNS, considering the differences between PRP from young and elderly donors. Two different PRP pools were prepared from donors 65–85 and 20–25 years old. The cellular and molecular composition of both PRPs were analyzed. Subsequently, the cellular response was evaluated in CNS in vitro models, studying proliferation, neurogenesis, synaptogenesis, and inflammation. While no differences in the cellular composition of PRPs were found, the molecular composition of the Young PRP showed lower levels of inflammatory molecules such as CCL-11, as well as the presence of other factors not found in Aged PRP (GDF-11). Although both PRPs had effects in terms of reducing neural progenitor cell apoptosis, stabilizing neuronal synapses, and decreasing inflammation in the microglia, the effect of the Young PRP was more pronounced. In conclusion, the molecular composition of the PRP, conditioned by the age of the donors, affects the magnitude of the biological response.

scholarly journals Design and In Vitro Study of a Dual Drug-Loaded Delivery System Produced by Electrospinning for the Treatment of Acute Injuries of the Central Nervous System

Pharmaceutics ◽  
2021 ◽  
Vol 13 (6) ◽  
pp. 848
Author(s):  
Luisa Stella Dolci ◽  
Rosaria Carmela Perone ◽  
Roberto Di Gesù ◽  
Mallesh Kurakula ◽  
Chiara Gualandi ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Delivery System ◽  
Synergistic Effects ◽  
In Vitro Release ◽  
Health Priorities ◽  
The Central Nervous System ◽  
Vitro Release ◽  
Dual Drug

Vascular and traumatic injuries of the central nervous system are recognized as global health priorities. A polypharmacology approach that is able to simultaneously target several injury factors by the combination of agents having synergistic effects appears to be promising. Herein, we designed a polymeric delivery system loaded with two drugs, ibuprofen (Ibu) and thyroid hormone triiodothyronine (T3) to in vitro release the suitable amount of the anti-inflammation and the remyelination drug. As a production method, electrospinning technology was used. First, Ibu-loaded micro (diameter circa 0.95–1.20 µm) and nano (diameter circa 0.70 µm) fibers were produced using poly(l-lactide) PLLA and PLGA with different lactide/glycolide ratios (50:50, 75:25, and 85:15) to select the most suitable polymer and fiber diameter. Based on the in vitro release results and in-house knowledge, PLLA nanofibers (mean diameter = 580 ± 120 nm) loaded with both Ibu and T3 were then successfully produced by a co-axial electrospinning technique. The in vitro release studies demonstrated that the final Ibu/T3 PLLA system extended the release of both drugs for 14 days, providing the target sustained release. Finally, studies in cell cultures (RAW macrophages and neural stem cell-derived oligodendrocyte precursor cells—OPCs) demonstrated the anti-inflammatory and promyelinating efficacy of the dual drug-loaded delivery platform.

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