Effect of brain monoamines on the secretion of adrenocorticotrophic hormone

1982 ◽  
Vol 101 (2) ◽  
pp. 180-186 ◽  
Author(s):  
Alka Amar ◽  
S. Mandal ◽  
A. K. Sanyal
Keyword(s):  
Dopaminergic Neurons ◽  
Adrenal Glands ◽  
Plasma Corticosterone ◽  
Albino Rats ◽  
Adrenocorticotrophic Hormone ◽  
Brain Monoamines ◽  
Acth Secretion ◽  
Acute Increase

Abstract. The role of brain monoamines (5-HT, NA and DA) in the secretion of adrenocorticotrophic hormone (ACTH) was studied in view of contradictory reports. Plasma corticosterone levels and the rate of synthesis of corticosterone in vitro by the adrenal gland were estimated in albino rats and have been taken as the index of ACTH activity. These estimations were done in unstressed and stressed, and in untreated and treated rats. Drugs were administered intracerebroventricularly to the rats to cause selective degeneration of tryptaminergic, noradrenergic or dopaminergic neurons. The results show that plasma corticosterone levels and the rate of synthesis of corticosterone were significantly decreased after selective degeneration of tryptaminergic neurons in unstressed rats. After selective degeneration of either tryptaminergic or noradrenergic neurons, the acute increase in the plasma corticosterone levels and rate of synthesis of corticosterone in vitro by adrenal glands in stressed rats were significantly inhibited. These results have been interpreted to suggest that the central tonic control on adrenal glands may be 5-HT mediated and that during stress ACTH secretion may be both 5-HT and NA mediated. DA does not seem to have significant role in the regulation of ACTH secretion.

Ghrelin Stimulates Adrenocorticotrophic Hormone (ACTH) Secretion by Human ACTH-Secreting Pituitary Adenomas In Vitro

2007 ◽  
Vol 19 (3) ◽  
pp. 208-212 ◽  
Author(s):  
F. Pecori Giraldi ◽  
L. G. Bucciarelli ◽  
A. Saccani ◽  
M. Scacchi ◽  
S. Pesce ◽  
...  
Keyword(s):  
Pituitary Adenomas ◽  
Adrenocorticotrophic Hormone ◽  
Acth Secretion ◽  
Acth Secreting

Differential activation of the pituitary-adrenocortical axis after stress in the rat: use of two genetically selected lines (Roman low- and high-avoidance rats) as a model

1989 ◽  
Vol 123 (3) ◽  
pp. 477-485 ◽  
Author(s):  
C.-D. Walker ◽  
R. W. Rivest ◽  
M. J. Meaney ◽  
M. L. Aubert
Keyword(s):  
Glucocorticoid Receptor ◽  
Conditioned Avoidance ◽  
Plasma Corticosterone ◽  
Type I ◽  
Pituitary Cells ◽  
Acth Secretion ◽  
Rapid Acquisition ◽  
Basal Plasma

ABSTRACT We have examined the activation of the pituitary-adrenal axis in two lines of rats, the Roman high (RHA)- and low (RLA)-avoidance rats known to be emotionally different. These rats are selected for rapid acquisition of a conditioned avoidance response (RHA) compared with failure to acquire this response (RLA). In this study the endocrine response (ACTH, corticosterone, aldosterone) of RLA and RHA rats to two types of stress was examined: exposure to openfield stress for 10 min (Op) or exposure to ether vapours for 3 min (E). Basal plasma ACTH concentrations were lower in RLA than in RHA rats (RLA: 110·8 ± 24·5 ng/l; RHA: 252·7 ± 60·8 ng/l, P<0·05) but the absolute values of ACTH reached after both types of stress were comparable between RLA and RHA rats. Plasma corticosterone and aldosterone under resting conditions were not different between RLA and RHA rats. Plasma corticosterone was higher in RLA following openfield stress (P<0·05) while no differences between RLA and RHA were observed after ether stress (RHA: basal = 66±14·nmol/l, Op =384± 55, E= 606± 75; RLA: basal=121±52, Op = 612 ±92, E= 698 ± 89). Stressinduced increases in plasma aldosterone were higher in the RLA line after both types of stress (RHA: basal = 175±36 pmol/l, Op = 546±53, E= 563± 47; RLA: basal = 272 ± 64, Op =1246 ± 91, E= 863 ± 72). Pituitary responsiveness to exogenous corticotrophinreleasing factor (CRF) in vivo and in vitro differed in the two lines: administration of ovine CRF (10 μg/kg body weight, i.p.) resulted in significant increases in ACTH secretion but the response was significantly lower in RHA rats (RHA: 511·1 ±41·5 ng/l; RLA: 831·4 ± 70·3 ng/l, P<0·01). Dispersed pituitary cells from the RHA line exhibited a smaller response to CRF (10 nmol/l) treatment in vitro compared with cells derived from the RLA rats (RHA: 750 ± 83% of control; RLA: 1374 ±79, P<0·01) suggesting differences in pituitary sensitivity to CRF between the two lines. Additional differences at the pituitary level were observed since the type II glucocorticoid receptor population in RHA rats was higher than in RLA rats (RHA: 246±13 fmol [3H]RU28362 bound/mg protein; RLA: 173±18, P<0·01). Similarly, hippocampal type I glucocorticoid receptor population was increased in RHA rats (RHA: 172·2 ± 8·3 fmol [3H]aldosterone bound/mg protein; RLA: 116·7±7·3, P< 0·01). It is concluded that first, differences in pituitary activity between RLA and RHA rats are distinct from changes observed at the adrenal level, secondly, increased stress-induced ACTH output in the RLA line is associated with enhanced pituitary sensitivity to CRF and possibly with diminished corticosterone inhibitory feedback action on CRF and ACTH secretion, and thirdly, the possible involvement of differences in the pattern of CRF secretion between RLA and RHA rats on resting pituitary ACTH secretion cannot be excluded. Journal of Endocrinology (1989) 123, 477–485

scholarly journals Striatal Syntaixin 1A Plays a Protective Role Against Iminodipropionitrile Induced Tic Disorder Through Interaction with Dopamine Transporter

2022 ◽  
Author(s):  
Xiumei Liu ◽  
Xueming Wang ◽  
Xiaoling Zhang ◽  
Aihua Cao
Keyword(s):  
Dopamine Transporter ◽  
Dopaminergic Neurons ◽  
Stereotyped Behavior ◽  
Protective Role ◽  
Snare Complex ◽  
Pathological State ◽  
Tic Disorder

Abstract An important mechanism of Tic disorder (TD) is dysfunction in the dopamine (DA) system. Our pilot observation found the expression of Syntaxin 1A (STX1A), a presynaptic SNARE complex, changed in the striatum of TD animals. The present study aimed to clarify the biological role of striatal STX1A in the pathological state of TD and the specific mechanism of its regulation of the dopaminergic system. The TD rat model was established using iminodipropionitrile (IDPN). Adenovirus was used to modulate the expression of STX1A and dopamine transporter (DAT) in vivo and vitro. Primary culture of striatal dopaminergic neurons was performed for in-vitro observation of the DA reuptake, CO-IP analysis of the interaction between STX1A and DAT. First, using immunofluorescence staining, Western blotting, and qPCR, we found that the IDPN induced TD model had reduced striatal STX1A expression. In vitro, the DA content in the supernatant was significantly lower in the STX1A overexpressed group, and the intracellular DA content was significantly higher. Overexpression of STX1A in vivo partially counteracts the IDPN-induced TD-like behaviors, including bite time and head shaking time. Meanwhile, in-vivo knockdown of STX1A can aggravates TD-like behaviors. Further, DAT was overexpressed in vivo, and the TD-like behavior was alleviated. Interestingly, overexpression of DAT in the striatum resulted in increased levels of STX1A. In order to clarify the interaction between DAT and STX1A, the CO-IP analysis was conducted based on the protein of purified striatal dopaminergic neurons. Compared to the IgG control, the blots of DAT and STX1A showed significant binding of each other. Striatal STX1A expression is decreased in TD development, and STX1A plays an anti-TD role possibly through interaction with DAT, which maintains the DA reuptake. The exorbitant DA signal caused by STX1A inhibition drives the pathological stereotyped behavior.

Release of galanin from isolated perfused porcine adrenal glands: role of splanchnic nerves

1991 ◽  
Vol 261 (1) ◽  
pp. E31-E40 ◽  
Author(s):  
J. J. Holst ◽  
M. Ehrhart-Bornstein ◽  
T. Messell ◽  
S. S. Poulsen ◽  
H. Harling
Keyword(s):  
Nerve Stimulation ◽  
Adrenal Glands ◽  
Splanchnic Nerve ◽  
High Concentration ◽  
Vitro Model ◽  
Arterial Plasma ◽  
Regulatory Functions ◽  
Splanchnic Nerve Stimulation

We found a high concentration of galanin in extracts of porcine adrenal glands (114 pmol/g). By immunohistochemistry, galanin was localized to groups of medullary cells previously shown to produce norepinephrine. To study mechanisms for the release of galanin, we developed the following in vitro model: isolated perfused porcine adrenals with intact splanchnic nerve supply. When the nerves were electrically stimulated, epinephrine and norepinephrine secretion increased 276- and 291-fold, respectively, and galanin release increased up to 1,300-fold. Acetylcholine at 10(-6) M stimulated galanin release, and hexamethonium almost abolished the response to nerve stimulation. Galanin infusions had no effect on epinephrine and norepinephrine secretion in concentrations of 10(-8) and 10(-7) M, but increased both cortisol and aldosterone secretion (P less than 0.05). Splanchnic nerve stimulation in anesthetized pigs increased the concentration of galanin in the caval vein but not in arterial plasma. It is concluded that galanin, coreleased with catecholamines from the adrenal glands, may have endocrine functions but that galanin may also have local regulatory functions in the adrenals.

scholarly journals Ventral pallidal GABAergic neurons control wakefulness associated with motivation through the ventral tegmental pathway

2020 ◽  
Author(s):  
Ya-Dong Li ◽  
Yan-Jia Luo ◽  
Wei Xu ◽  
Jing Ge ◽  
Yoan Cherasse ◽  
...  
Keyword(s):  
Dopaminergic Neurons ◽  
Gabaergic Neurons ◽  
Population Activity ◽  
Lateral Habenula ◽  
Optogenetic Stimulation ◽  
Ventral Tegmental ◽  
Stimulation Of

Abstract The ventral pallidum (VP) regulates motivation, drug addiction, and several behaviors that rely on heightened arousal. However, the role and underlying neural circuits of the VP in the control of wakefulness remain poorly understood. In the present study, we sought to elucidate the specific role of VP GABAergic neurons in controlling sleep–wake behaviors in mice. Fiber photometry revealed that the population activity of VP GABAergic neurons was increased during physiological transitions from non-rapid eye movement (non-REM, NREM) sleep to either wakefulness or REM sleep. Moreover, chemogenetic and optogenetic manipulations were leveraged to investigate a potential causal role of VP GABAergic neurons in initiating and/or maintaining arousal. In vivo optogenetic stimulation of VP GABAergic neurons innervating the ventral tegmental area (VTA) strongly promoted arousal via disinhibition of VTA dopaminergic neurons. Functional in vitro mapping revealed that VP GABAergic neurons, in principle, inhibited VTA GABAergic neurons but also inhibited VTA dopaminergic neurons. In addition, optogenetic stimulation of terminals of VP GABAergic neurons revealed that they promoted arousal by innervating the lateral hypothalamus, but not the mediodorsal thalamus or lateral habenula. The increased wakefulness chemogenetically evoked by VP GABAergic neuronal activation was completely abolished by pretreatment with dopaminergic D1 and D2/D3 receptor antagonists. Furthermore, activation of VP GABAergic neurons increased exploration time in both the open-field and light–dark box tests but did not modulate depression-like behaviors or food intake. Finally, chemogenetic inhibition of VP GABAergic neurons decreased arousal. Taken together, our findings indicate that VP GABAergic neurons are essential for arousal related to motivation.

ANALYSIS OF THE INHIBITION OF THE ACTH RELEASE BY HYPOTHALAMIC IMPLANTS OF ATROPINE

1973 ◽  
Vol 73 (4) ◽  
pp. 651-659 ◽  
Author(s):  
J. Kaplanski ◽  
P. G. Smelik
Keyword(s):  
Adrenal Glands ◽  
Plasma Corticosterone ◽  
Corticosterone Concentration ◽  
Hypothalamic Region ◽  
Adrenal System ◽  
Cholinergic Synapses ◽  
Adrenocortical Responses ◽  
Acth Release

ABSTRACT The effect of anterior hypothalamic atropine implants on the secretion of corticotrophin in the rat, as indicated by the corticosteroid production by adrenal glands incubated in vitro and/or by the plasma corticosterone concentration, was studied. It was found that atropine implants markedly inhibit the adrenocortical responses evoked by all the stress stimuli tested, except for that to a CRF preparation. The onset of the blockade was very fast; the duration of the inhibition lasted for about 2 h. Smaller amounts of atropine (2×15 μg) were also effective when implanted bilaterally into the anterior hypothalamic region. It is concluded that cholinergic synapses in the hypothalamus may be involved in the activation of the pituitary-adrenal system after stressful stimuli.

CHOLINERGIC INFLUENCES ON HYPOTHALAMIC-PITUITARY-ADRENOCORTICAL ACTIVITY OF STRESSED RATS: AN APPROACH UTILIZING CHOLINE DEFICIENT DIETS

1978 ◽  
Vol 89 (4) ◽  
pp. 737-743 ◽  
Author(s):  
N. Sithichoke ◽  
L. J. Malasanos ◽  
S. F. Marotta
Keyword(s):  
Drinking Water ◽  
Cholinergic System ◽  
Adrenal Glands ◽  
Plasma Corticosterone ◽  
Male Rats ◽  
Cholinergic Activity ◽  
Deficient Diet ◽  
Adrenocortical Activity ◽  
Hpa Response

ABSTRACT Male rats were placed on choline (Ch) deficient diets for 3 to 14 days, without and with Ch (normal and large doses) supplemented in the drinking water, to determine whether altering the availability of Ch would affect the cholinergic system in relation to the latter's role in modulating the hypothalamic-pituitary-adrenocortical (HPA) system of non-stressed and stressed animals. The results indicate that the basal nonstressed activity of the HPA system, as assessed by adrenal and plasma corticosterone concentrations, was not affected by placing the animals on these diets for as long as 14 days. Furthermore, the in vitro production of corticosterone by these adrenal glands, in the presence or absence of adrenocorticotrophin, was similar to those observed in animals on a regular rat diet; however, the HPA responses to auditory (100 db) stress, and to a lesser extent hypercapnic (9 % CO2) stress, were impaired on the Ch deficient diet (14 days), and these responses were partially corrected by supplementing the diet with Ch in the drinking water. Thus, the data suggest that altering the dietary intake of Ch may affect cholinergic activity, which in turn affects the HPA response to stressors.

scholarly journals Role of PGF2alpha and oxytocin in parturition in the brushtail possum (Trichosurus vulpecula)

Reproduction ◽  
2002 ◽  
pp. 429-434 ◽  
Author(s):  
C Veitch ◽  
L Brown ◽  
C Sernia ◽  
RT Gemmell
Keyword(s):  
Corpus Luteum ◽  
Uterine Contraction ◽  
Adrenal Glands ◽  
Tammar Wallaby ◽  
Brushtail Possum ◽  
Uterine Contractions ◽  
Prostaglandin F ◽  
Birth Position

Maturation of the fetal pituitary and adrenal glands allows the secretion of cortisol, which in turn leads to an increase in prostaglandin and mesotocin production. The production of prostaglandin and mesotocin results in an increase in uterine contractions and initiates birth in marsupials. The major metabolite of PGF(2alpha), 13,14-dihydro-15-keto-prostaglandin F(2alpha) (PGFM), has been found in the plasma of the possum at the time of birth and administration of PGF(2alpha) to female possums induced the adoption of the birth position. Evidence that mesotocin is an integral hormone of birth in the tammar wallaby indicates that both PGF(2alpha) and mesotocin or oxytocin are required for marsupial birth. The presence of PGF(2alpha) receptors in the uterus and corpus luteum of the possum, and the in vitro uterine responsiveness to PGF(2alpha) or oxytocin, were examined. PGF(2alpha) receptors were not observed in possum uteri and the inability of PGF(2alpha) to cause contractions indicates that PGF(2alpha) is not involved directly in contraction of the uterus at parturition. The presence of oxytocin and mesotocin receptors in the uterus of possoms and the ability of oxytocin to induce uterine contraction in vitro supports the view that mesotocin is required for expulsion of the young from the uterus. Low numbers of PGF(2alpha) receptors were found in the possum corpus luteum at birth, indicating an involvement of PGF(2alpha) in regression of the corpus luteum.

scholarly journals Triggering Receptor Expressed on Myeloid Cells 2 Protects Dopaminergic Neurons by Promoting Autophagy in the Inflammatory Pathogenesis of Parkinson’s Disease

2021 ◽  
Vol 15 ◽  
Author(s):  
Wei Huang ◽  
Qiankun Lv ◽  
Yunfei Xiao ◽  
Zhen Zhong ◽  
Binbin Hu ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Dopaminergic Neurons ◽  
Human Genetics ◽  
Neurodegenerative Disorder ◽  
Inflammatory Factors ◽  
Inflammatory Mechanism

Parkinson’s disease is a neurodegenerative disorder with an inflammatory response as the core pathogenic mechanism. Previous human genetics findings support the view that the loss of TREM2 function will aggravate neurodegeneration, and TREM2 is one of the most highly expressed receptors in microglia. However, the role of TREM2 in the inflammatory mechanism of PD is not clear. In our study, it was found both in vivo and in vitro that the activation of microglia not only promoted the secretion of inflammatory factors but also decreased the level of TREM2 and inhibited the occurrence of autophagy. In contrast, an increase in the level of TREM2 decreased the expression of inflammatory factors and enhanced the level of autophagy through the p38 MAPK/mTOR pathway. Moreover, increased TREM2 expression significantly decreased the apoptosis of dopaminergic (DA) neurons and improved the motor ability of PD mice. In summary, TREM2 is an important link between the pathogenesis of PD and inflammation. Our study provides a new view for the mechanism of TREM2 in PD and reveals TREM2 as a potential therapeutic target for PD.

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