CORTICOTROPHIN RELEASE INDUCED BY SURGICAL TRAUMA AFTER TRANSECTION OF VARIOUS AFFERENT NERVOUS PATHWAYS TO THE HYPOTHALAMUS

1972 ◽  
Vol 53 (3) ◽  
pp. 389-395 ◽  
Author(s):  
G. B. MAKARA ◽  
E. STARK ◽  
J. MARTON ◽  
T. MÉSZÁROS
Keyword(s):  
Corticosterone Level ◽  
Plasma Corticosterone ◽  
Surgical Trauma ◽  
Plasma Corticosterone Level ◽  
Nerve Fibres ◽  
Hypothalamic Area ◽  
Medial Basal Hypothalamus ◽  
Median Forebrain Bundle ◽  
Significant Difference ◽  
Acth Release

SUMMARY Corticotrophin (ACTH) release induced by surgical trauma under pentobarbitone anaesthesia was studied in rats. The plasma corticosterone level was used as an index of 'rapid' ACTH release. One hour after surgical trauma the plasma corticosterone level had risen in rats with various cuts around the medial basal hypothalamus except in the group with lateral cuts. After stress no significant difference was found between the plasma levels of the controls and those of the rats with anterior, 'low' superior, 'low' anterosuperior, and 'short' posterior cuts. In contrast, in rats with 'high' superior, 'high' anterosuperior, 'long' posterior and lateral cuts the plasma corticosterone level was lower than in the appropriate sham-operated controls. It is suggested that the nerve fibres initiating ACTH release after surgical trauma ascend the spinal cord to the medulla and mid-brain whence the pathways pass forward in the region of the dorsal longitudinal fasciculus and/or the median forebrain bundle to the lateral hypothalamic area, and from there to the medial basal hypothalamus.

AFFERENT PATHWAYS OF STRESSFUL STIMULI: CORTICOTROPHIN RELEASE AFTER PARTIAL DEAFFERENTATION OF THE MEDIAL BASAL HYPOTHALAMUS

1969 ◽  
Vol 44 (2) ◽  
pp. 187-193 ◽  
Author(s):  
G. B. MAKARA ◽  
E. STARK ◽  
M. PALKOVITS ◽  
T. RÉVÉSZ ◽  
K. MIHÁLY
Keyword(s):  
Escherichia Coli ◽  
Corticosterone Level ◽  
Plasma Corticosterone ◽  
Neural Pathways ◽  
Plasma Corticosterone Level ◽  
Nerve Fibres ◽  
Afferent Pathways ◽  
Medial Basal Hypothalamus ◽  
Noise And Vibration ◽  
Acth Release

SUMMARY Corticotrophin (ACTH) release induced by various stressful stimuli has been studied in rats with antero-lateral deafferentation of the medial basal hypothalamus (MBH). The plasma corticosterone level was determined as an index of ACTH release. In rats with antero-lateral deafferentation of the MBH, ACTH release was prevented after exposure to noise and vibration, sham adrenalectomy and s.c. injection of 1% formalin. ACTH release induced by the injection of histamine (1 mg./100 g., i.p.) and capsaicin (0·25 mg./100 g., s.c.) was significantly less than in the controls. Escherichia coli lipopolysaccharide (25 μg./100 g., i.p.) induced an ACTH release that could not be distinguished from that in the controls. We suggest that (a) noise and vibration, sham adrenalectomy and injection of 1% formalin trigger ACTH release through neural pathways arriving at the MBH from anterior, lateral and dorsal directions, (b) histamine or capsaicin releases ACTH partly through antero-lateral neural afferents to the MBH. In contrast, the ACTH-releasing stimulus of bacterial endotoxin injection reaches the hypothalamo—hypophysial unit by humoral pathways and/or posterior nerve fibres.

AFFERENT PATHWAYS OF STRESSFUL STIMULI: CORTICOTROPHIN RELEASE AFTER HYPOTHALAMIC DEAFFERENTATION

1970 ◽  
Vol 47 (4) ◽  
pp. 411-NP ◽  
Author(s):  
G. B. MAKARA ◽  
E. STARK ◽  
M. PALKOVITS
Keyword(s):  
Intraperitoneal Administration ◽  
Corticosterone Level ◽  
Plasma Corticosterone ◽  
Afferent Input ◽  
Neural Pathways ◽  
Plasma Corticosterone Level ◽  
Afferent Pathways ◽  
Medial Basal Hypothalamus ◽  
E Coli ◽  
Acth Release

SUMMARY Corticotrophin (ACTH) release induced by stressful stimuli has been studied in rats with completely deafferentated medial basal hypothalamus (MBH) pituitary islands or median eminence (ME)-stalk pituitary islands. The plasma corticosterone level was used as index of ACTH release. In rats with MBH pituitary islands, capsaicin failed to raise the plasma corticosterone level, but the intraperitoneal administration of E. coli endotoxin, histamine, insulin or a large subcutaneous dose of formaldehyde caused ACTH release which could not be distinguished from that in the controls. Histamine and insulin induced ACTH release even in rats with a ME-stalk pituitary island. It is suggested that E. coli endotoxin, histamine, insulin hypoglycaemia and large doses of formaldehyde may be classified as 'humoral' stimuli of ACTH release, since a neural afferent input to the MBH is not essential for their action. On the other hand, the integrity of some neural pathways to the MBH is essential for the ACTH-releasing effect of capsaicin.

Effects of paraventricular lesions on stimulated ACTH release and CRF in stalk-median eminence of the rat

1981 ◽  
Vol 240 (4) ◽  
pp. E441-E446 ◽  
Author(s):  
G. B. Makara ◽  
E. Stark ◽  
M. Karteszi ◽  
M. Palkovits ◽  
G. Rappay
Keyword(s):  
Median Eminence ◽  
Corticosterone Level ◽  
Plasma Corticosterone ◽  
Surgical Trauma ◽  
Acth Level ◽  
Plasma Acth ◽  
Medial Basal Hypothalamus ◽  
Plasma Acth Level ◽  
Basal Plasma ◽  
Corticosterone Response

The effects of destroying the paraventricular nucleus (PVN) of the rat hypothalamus on pituitary-adrenal function were studied. Four days after PVN lesions were placed with a rotating knife, the basal plasma corticosterone level was normal, but the corticosterone response to electrical stimulation of the medial basal hypothalamus, surgical trauma, and ether-venesection stress was significantly inhibited. Four and 8 days after PVN lesioning and adrenalectomy, the basal plasma ACTH level was lower, and the rise of plasma ACTH level elicited by a 3-min ether inhalation was significantly smaller than in the adrenalectomized controls. Corticotropin-releasing factor (CRF) activity in the stalk-median eminence extracts from PVN-lesioned rats was significantly less than in the control extracts. The weight of the adrenals was decreased by both 2 and 4 wk after PVN destruction, and 2 wk after hemiadrenalectomy, the compensatory adrenal hypertrophy was inhibited. The plasma corticosterone response to ether-venesection stress was inhibited only temporarily because it returned to normal by the end of the 4th postoperative week. The results are consistent with the hypothesis that a substantial portion of CRF-containing fibers in the stalk-median eminence region either originate from or run though the PVN or its immediate vicinity.

The hypophyseal–adrenocortical response to various different stressing procedures in ACTH-treated rats

1968 ◽  
Vol 46 (4) ◽  
pp. 567-571 ◽  
Author(s):  
E. Stark ◽  
Zs. Ács ◽  
G. B. Makara ◽  
K. Mihály
Keyword(s):  
Corticosterone Level ◽  
Plasma Corticosterone ◽  
Release Mechanism ◽  
Significant Elevation ◽  
Plasma Corticosterone Level ◽  
Corticosterone Concentration ◽  
Corticotrophin Releasing Factor ◽  
Adrenocortical Response ◽  
The Difference ◽  
Acth Release

Twenty-four hours after the last of 14 daily injections of ACTH, the administration of ether, histamine, 1% formalin, or lysine-8-vasopressin produced no rise in the plasma corticosterone level in rats but raised it significantly in saline-treated control animals. As assayed by the plasma corticosterone concentration, ACTH release was found to be inhibited when hypophyseal–adrenocortical responsiveness was not impaired and the peripheral corticosterone level was normal or less than normal. Endotoxin induced nearly the same statistically significant elevation in the ACTH-treated and saline-treated animals. It would appear that it is the high corticosterone level produced by the last ACTH injection that suppresses the corticotrophin-releasing factor (CRF) 24 h later (feedback action) when this level returns to normal or less than normal; and that certain stressors liberate CRF whereas others do not. An explanation for the latter assumption may be found either in the difference in intensity between the stimuli or, more probably, in that the high corticosterone level inhibits the ACTH release mechanism for certain individual stressors, but not for others.

Bacopa monnieri alleviates aluminium chloride-induced anxiety by regulating plasma corticosterone level in Wistar rats

2020 ◽  
Vol 0 (0) ◽  
Author(s):  
Senthil Murugan Murugaiyan ◽  
Rajesh Bhargavan
Keyword(s):  
Oral Administration ◽  
Corticosterone Level ◽  
Tween 80 ◽  
Treated Group ◽  
Plasma Corticosterone ◽  
Bacopa Monnieri ◽  
Aluminium Chloride ◽  
Control Group ◽  
Plasma Corticosterone Level ◽  
Protective Groups

AbstractObjectivesAluminium is present in food preparations, antacids and many medications. It causes neurodegeneration thereby resulting in a spectrum of neurological disorders such as dementia, Alzheimer’s disease and anxiety. Bacopa monnieri (BM) is widely used in ayurvedic medicine to improve memory functions. Its anxiolytic property was investigated in this study by using elevated plus maze (EPM) and plasma corticosterone level.MethodsThirty rats were assigned into five groups. Control group received distilled water, and 0.5% tween 80, AlCl3 group received Aluminium Chloride (AlCl3), Protective groups (BM100 + AlCl3 group and BM200 + AlCl3 group) received AlCl3 and BM at two different doses, and the BM200 group received BM. The EPM experiment was performed at the end of the 4th week of oral administration of BM and AlCl3 followed by the measurement of plasma corticosterone.ResultsOral administration of AlCl3 to rats increases the levels of anxiety as seen in a decrease in the percentage of entries into the open arms of EPM, an increase in grooming frequency and defecation index. However, the rats in the protective groups shown an increase in the percentage of open arm entries and rearing frequency, and decreased grooming frequency and defecation index. AlCl3 alone treated group showed a significant increase in the plasma corticosterone levels compared to the control group. Whereas the protective groups have shown a significant decrease in the plasma corticosterone levels than the AlCl3 alone treated group.ConclusionsHence the BM has potential role in reverting the anxiogenic effect of AlCl3 in the amygdala as it is evident from the plasma corticosterone levels and the EPM parameters of different groups under study.

scholarly journals Inflammatory Pain and Corticosterone Response in Infant Rats: Effect of 5-HT1A Agonist Buspirone Prior to Gestational Stress

2013 ◽  
Vol 2013 ◽  
pp. 1-7 ◽  
Author(s):  
Irina P. Butkevich ◽  
Viktor A. Mikhailenko ◽  
Tat'yana R. Bagaeva ◽  
Elena A. Vershinina ◽  
Anna Maria Aloisi ◽  
...  
Keyword(s):  
Hpa Axis ◽  
Inflammatory Pain ◽  
Formalin Test ◽  
Corticosterone Level ◽  
Plasma Corticosterone ◽  
Male Rats ◽  
Plasma Corticosterone Level ◽  
Infant Rats ◽  
Corticosterone Response ◽  
Gestational Stress

Our researches have shown that gestational stress causes exacerbation of inflammatory pain in the offspring; the maternal 5-HT1A agonist buspirone before the stress prevents the adverse effect. The serotonergic system and hypothalamo-pituitary-adrenal (HPA) axis are closely interrelated. However, interrelations between inflammatory pain and the HPA axis during the hyporeactive period of the latter have not been studied. The present research demonstrates that formalin-induced pain causes a gradual and prolonged increase in plasma corticosterone level in 7-day-old male rats; twenty-four hours after injection of formalin, the basal corticosterone level still exceeds the initial basal corticosterone value. Chronic treatments of rat dams with buspirone before restraint stress during gestation normalize in the offspring pain-like behavior and induce during the acute phase in the formalin test the stronger corticosterone increase as compared to the stress hormonal elevation in animals with other prenatal treatments. Negative correlation between plasma corticosterone level and the number of flexes+shakes is revealed in buspirone+stress rats. The new data enhance the idea about relativity of the HPA axis hyporeactive period and suggest that maternal buspirone prior to stress during gestation may enhance an adaptive mechanism of the inflammatory nociceptive system in the infant male offspring through activation of the HPA axis peripheral link.

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