Increased Fos Expression in Preoptic Calcitonin Gene-Related Peptide (CGRP) Neurones following Mating but not the Luteinizing Hormone Surge in Female Rats

1995 ◽  
Vol 7 (5) ◽  
pp. 377-385 ◽  
Author(s):  
Allan E. Herbison ◽  
Ian S. King ◽  
Keith K. C. Tan ◽  
Sandra Dye
Keyword(s):  
Luteinizing Hormone ◽  
Calcitonin Gene Related Peptide ◽  
Female Rats ◽  
Related Peptide ◽  
Calcitonin Gene ◽  
Fos Expression ◽  
Luteinizing Hormone Surge

scholarly journals Enhanced post-traumatic headache-like behaviors and diminished contribution of peripheral CGRP in female rats following a mild closed head injury

Cephalalgia ◽  
2020 ◽  
Vol 40 (7) ◽  
pp. 748-760 ◽  
Author(s):  
Dara Bree ◽  
Kimberly Mackenzie ◽  
Jennifer Stratton ◽  
Dan Levy
Keyword(s):  
Monoclonal Antibody ◽  
Head Injury ◽  
Closed Head Injury ◽  
Calcitonin Gene Related Peptide ◽  
Female Rats ◽  
Related Peptide ◽  
Increased Risk ◽  
Calcitonin Gene ◽  
Closed Head ◽  
Post Traumatic

Introduction Females are thought to have increased risk of developing post-traumatic headache following a traumatic head injury or concussion. However, the processes underlying this susceptibility remain unclear. We previously demonstrated the development of post-traumatic headache-like pain behaviors in a male rat model of mild closed head injury, along with the ability of sumatriptan and an anti-calcitonin-gene-related peptide monoclonal antibody to ameliorate these behaviors. Here, we conducted a follow-up study to explore the development of post-traumatic headache-like behaviors and the effectiveness of these headache therapies in females subjected to the same head trauma protocol. Methods Adult female Sprague Dawley rats were subjected to a mild closed head injury using a weight-drop device (n = 126), or to a sham procedure (n = 28). Characterization of headache and pain related behaviors included assessment of changes in cutaneous cephalic and extracephalic tactile pain sensitivity, using von Frey monofilaments. Sensitivity to headache/migraine triggers was tested by examining the effect of intraperitoneal administration of a low dose of glyceryl trinitrate (100 µg/kg). Treatments included acute systemic administration of sumatriptan (1 mg/kg) and repeated systemic administration of a mouse anti-calcitonin gene-related peptide monoclonal antibody (30 mg/kg). Serum levels of calcitonin gene-related peptide were measured at baseline and at various time points post head injury in new cohorts of females (n = 38) and males (n = 36). Results Female rats subjected to a mild closed head injury developed cutaneous mechanical hyperalgesia, which was limited to the cephalic region and was resolved 4 weeks later. Cephalic pain hypersensitivity was ameliorated by treatment with sumatriptan but was resistant to an early and prolonged treatment with the anti-calcitonin gene-related peptide monoclonal antibody. Following the resolution of the head injury-evoked cephalic hypersensitivity, administration of glyceryl trinitrate produced a renewed and pronounced cephalic and extracephalic pain hypersensitivity that was inhibited by sumatriptan, but only partially by the anti-calcitonin gene-related peptide treatment. Calcitonin gene-related peptide serum levels were elevated in females but not in males at 7 days post head injury. Conclusions Development of post-traumatic headache-like pain behaviors following a mild closed head injury, and responsiveness to treatment in rats is sexually dimorphic. When compared to the data obtained from male rats in the previous study, female rats display a prolonged state of cephalic hyperalgesia, increased responsiveness to a headache trigger, and a poorer effectiveness of an early and prolonged anti-calcitonin gene-related peptide treatment. The increased risk of females to develop post-traumatic headache may be linked to enhanced responsiveness of peripheral and/or central pain pathways and a mechanism independent of peripheral calcitonin gene-related peptide signaling.

Calcitonin inhibition of prolactin secretion in isolated rat pituitary cells

1988 ◽  
Vol 116 (2) ◽  
pp. 279-286 ◽  
Author(s):  
G. V. Shah ◽  
R. M. Epand ◽  
R. C. Orlowski
Keyword(s):  
Salmon Calcitonin ◽  
Calcitonin Gene Related Peptide ◽  
Prolactin Secretion ◽  
Female Rats ◽  
Pituitary Cells ◽  
Prolactin Release ◽  
Related Peptide ◽  
Calcitonin Gene ◽  
Untreated Female ◽  
Rat Pituitary Cells

ABSTRACT Salmon calcitonin inhibited TRH-stimulated release of prolactin in isolated pituitary cells from untreated female rats. These cells were still capable of responding to the fresh addition of TRH after the removal of calcitonin. Calcitonin gene-related peptide had only a weak effect in inhibiting prolactin release in these cells. Pituitary cells isolated from female rats which had been treated with weekly s.c. injections of 1 mg oestradiol dipropionate for 4 weeks, exhibited a marked increase in the magnitude of the inhibition of prolactin release by salmon calcitonin. Both basal and TRH-stimulated release of prolactin were inhibited by concentrations of 0·1 nmol salmon calcitonin/l or higher. Prolactin release from these cells was also inhibited at somewhat higher concentrations by calcitonin gene-related peptide. Our results demonstrate that calcitonin can directly inhibit basal as well as TRH-stimulated prolactin release by acting directly at the pituitary. The results strongly suggest that the peptide may be involved in the regulation of prolactin release in certain physiological conditions. J. Endocr. (1988) 116, 279–286

Basal tail skin temperature elevation and augmented response to calcitonin gene-related peptide in ovariectomized rats

1995 ◽  
Vol 146 (3) ◽  
pp. 431-437 ◽  
Author(s):  
T Kobayashi ◽  
O Ushijima ◽  
J-T Chen ◽  
M Shiraki ◽  
T Ohta ◽  
...  
Keyword(s):  
Skin Temperature ◽  
Temperature Response ◽  
Calcitonin Gene Related Peptide ◽  
Female Rats ◽  
Ovariectomized Rats ◽  
Dependent Manner ◽  
Related Peptide ◽  
Ovx Rats ◽  
Calcitonin Gene ◽  
Drastic Increase

Abstract Hyper-release of calcitonin gene-related peptide (CGRP) plays a direct and pivotal role in the induction of menopausal hot flushes (HFs), in which a drastic increase in skin temperature occurs. However, it is not possible to investigate whether CGRP induces skin temperature increase and whether skin temperature response to CGRP changes and contributes to the occurrence of HFs in postmenopausal women who are in oestrogen deficiency. By using rats' tail skin temperature (TST), a good marker to evaluate skin temperature regulation, we examined the effects of CGRP and calcitonin (3, 10 and 30 μg/kg, i.v.) on TST in female rats and further investigated the TST change induced by CGRP (10 μg/kg, i.v.) in ovariectomized (OVX) rats compared with that in sham-operated (Sham) rats. We found that CGRP, but not calcitonin, induced a TST increase in a dose-dependent manner and that the TST change induced by CGRP (0·6 ±0·2 °C for OVX rats vs 0·3 ±0·1 °C for Sham rats, P<0·05) and also the basal TST (26·0 ± 0·2 °C for OVX rats vs 25·5 ±0·1 °C for Sham rats) were significantly greater in OVX rats (P<0·05). Furthermore, treatment with oestradiol (30 μg/kg, s.c.) for 8 days partially inhibited the augmented TST response to CGRP in OVX rats and almost completely inhibited (P<0·05) the basal TST elevation, with the concomitant recovery of the serum oestradiol level to that in Sham rats. These results suggest that the augmented skin temperature response to CGRP and the elevation of basal skin temperature that are found in OVX rats, animals which are oestradiol deficient, may also occur in menopausal women and contribute to their HFs. Journal of Endocrinology (1995) 146, 431–437

scholarly journals Enhanced post-traumatic headache-like behaviors and diminished contribution of peripheral CGRP in female rats following a mild closed head injury

2019 ◽  
Author(s):  
Dara Bree ◽  
Kimberly Mackenzie ◽  
Jennifer Stratton ◽  
Dan Levy
Keyword(s):  
Monoclonal Antibody ◽  
Head Injury ◽  
Closed Head Injury ◽  
Calcitonin Gene Related Peptide ◽  
Systemic Administration ◽  
Female Rats ◽  
Related Peptide ◽  
Increased Risk ◽  
Calcitonin Gene ◽  
Closed Head

AbstractIntroductionFemales are thought to have increased risk of developing posttraumatic headache (PTH) following a traumatic head injury, or concussion. However, the processes underlying this susceptibility remain unclear. We previously explored the development of PTH-like pain behaviors in a novel rat model of mild closed head injury, along with the ability of sumatriptan and an anti-calcitonin-gene-related peptide monoclonal antibody to ameliorate these behaviors. Here, we explored the development of PTH-like behaviors and the effectiveness of these headache therapies in females subjected to the same head trauma protocol.MethodsAdult female Sprague Dawley rats were subjected to a mild closed head injury using a weight-drop device. Characterization of headache and pain related behaviors included assessment of changes in cutaneous cephalic and extracephalic tactile pain sensitivity, using von Frey monofilaments. Sensitivity to headache/migraine triggers was tested by examining the effect of systemic administration of a low-dose of glyceryl trinitrate (GTN). Treatments included acute systemic administration of sumatriptan and repeated systemic administration of a mouse anti-calcitonin-gene-related peptide monoclonal antibody. Serum levels of calcitonin-gene-related peptide were measured at various time points in females and males after the head injury.ResultsFemale rats subjected to a mild closed head injury developed cutaneous mechanical hyperalgesia, that was limited to the cephalic region, and was resolved 4 weeks later. Cephalic pain hypersensitivity was ameliorated by treatment with sumatriptan, but was resistant to an early and prolonged treatment with the anti-CGRP monoclonal antibody. Following the resolution of the head injury-evoked cephalic hypersensitivity, administration of GTN produced a renewed and pronounced cephalic and extracephalic pain hypersensitivity that was inhibited by sumatriptan, but only partially by the anti-CGRP treatment. CGRP serum levels were elevated in females but not in males at 7 days post head injury.ConclusionsDevelopment of PTH-like pain behaviors following a mild closed head injury, and responsiveness to treatment in rats is sexually dimorphic. When compared to males, female rats display a prolonged state of cephalic hyperalgesia, increased responsiveness to a headache trigger, and a poorer effectiveness of an early and prolonged anti-CGRP treatment. The increased risk of females to develop PTH may be linked to enhanced responsiveness of peripheral and/or central pain pathways and a mechanism independent of peripheral CGRP signaling.

scholarly journals Calcitonin Gene–related Peptide Is Involved in Inflammatory Pain but Not in Postoperative Pain

2014 ◽  
Vol 121 (5) ◽  
pp. 1068-1079 ◽  
Author(s):  
Kumiko Ishida ◽  
Tomoyuki Kawamata ◽  
Satoshi Tanaka ◽  
Takayuki Shindo ◽  
Mikito Kawamata
Keyword(s):  
Postoperative Pain ◽  
Knockout Mice ◽  
Inflammatory Pain ◽  
Calcitonin Gene Related Peptide ◽  
Wild Type ◽  
Heat Stimulation ◽  
Related Peptide ◽  
Pain Scores ◽  
Calcitonin Gene ◽  
Fos Expression

Abstract Background: The aim of this study was to clarify the roles of calcitonin gene–related peptide (CGRP) in postoperative pain and inflammatory pain. Methods: αCGRP knockout mice that the authors have developed and wild-type mice were used. Pain behaviors were assessed after incision and complete Freund’s adjuvant (CFA) injection. Changes in CGRP and c-Fos expression in the dorsal horn were also examined. Results: Guarding pain scores in αCGRP knockout mice were lower than those in wild-type mice at 24 h (3.8 ± 1.6 vs. 6.8 ± 1.5, P = 0.044) and 48 h (1.8 ± 1.7 vs. 6.0 ± 1.5, P = 0.001) after CFA injection (n = 8 to 9). Withdrawal latencies to heat stimulation in αCGRP knockout mice were higher than those in wild-type mice at 24 to 72 h after CFA injection (4.9 ± 1.0 vs. 3.4 ± 0.8 at 24 h, P = 0.04; 5.1 ± 0.3 vs. 3.2 ± 0.9 at 48 h, P = 0.047; and 5.4 ± 1.6 vs. 3.5 ± 0.5 s at 72 h, P = 0.045) (n = 11 to 13), but withdrawal thresholds to mechanical stimulation were comparable. CGRP expression was increased at 24 h after CFA injection in wild-type mice, and the c-Fos–positive profile was increased at 4 h after CFA injection (ipsilateral vs. contralateral: 12.3 ± 4.6 vs. 1.3 ± 1.9, P &lt; 0.0001) and maintained at 24 h (10.0 ± 4.1 vs. 0.8 ± 1.3, P &lt; 0.0001) (n = 4 to 6). Conclusion: These results suggest that contribution of the αCGRP system depends on the modality of pain and the stage of inflammation.

Contribution of intraganglionic CGRP to migraine-like responses in male and female rats

Cephalalgia ◽  
2019 ◽  
Vol 40 (7) ◽  
pp. 689-700
Author(s):  
Erika Ivanna Araya ◽  
Joelle de Melo Turnes ◽  
Amanda Ribeiro Barroso ◽  
Juliana Geremias Chichorro
Keyword(s):  
Mechanical Allodynia ◽  
Light Sensitivity ◽  
Calcitonin Gene Related Peptide ◽  
Female Rats ◽  
Male Rats ◽  
Male And Female ◽  
Related Peptide ◽  
Male And Female Rats ◽  
Mechanical Threshold ◽  
Calcitonin Gene

Objective To evaluate whether intraganglionic calcitonin gene-related peptide induced differential migraine-like responses in male and female rats. Methods Calcitonin gene-related peptide was injected in the trigeminal ganglion of male and female rats followed by assessment of periorbital mechanical allodynia with von Frey hairs. The influence of systemic treatment with sumatriptan or intraganglionic treatment with minocycline and propentofylline was determined on the calcitonin gene-related peptide-induced mechanical allodynia in male and female rats. One additional group was exposed to an aversive light 24 h after calcitonin gene-related peptide priming, followed by evaluation of periorbital mechanical threshold, and another group was tested in the elevated-plus maze. Results Intraganglionar calcitonin gene-related peptide-induced periorbital mechanical allodynia in female (0.5 to 6 h) and male rats (0.5 to 4 h). Systemic sumatriptan briefly attenuated the mechanical allodynia, but intraganglionar minocycline or propentofylline injection was effective only in male rats. Calcitonin gene-related peptide induced photic sensitivity in female and male rats (lasting 4 h and 1 h, respectively), as well as anxiety-like behavior. Conclusions Intraganglionar calcitonin gene-related peptide may play a major role in migraine-like responses, including periorbital mechanical allodynia, light sensitivity and anxiety like-behavior. Female rats are likely to be more susceptible to calcitonin gene-related peptide effects and a better understanding of the sexual dimorphism in calcitonin gene-related peptide signaling may help to improve migraine therapy.

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