Testicular descent. III. The neonatal mouse gubernaculum shows rhythmic contraction in organ culture in response to calcitonin gene-related peptide.

Endocrinology ◽  
1992 ◽  
Vol 131 (6) ◽  
pp. 2881-2884 ◽  
Author(s):  
Y Momose ◽  
A L Griffiths ◽  
J M Hutson
Keyword(s):  
Organ Culture ◽  
Calcitonin Gene Related Peptide ◽  
Neonatal Mouse ◽  
Testicular Descent ◽  
Rhythmic Contraction ◽  
Related Peptide ◽  
Calcitonin Gene

scholarly journals Effect of an anti-androgen on testicular descent and inguinal closure in a marsupial, the tammar wallaby (Macropus eugenii)

Reproduction ◽  
2002 ◽  
pp. 865-874 ◽  
Author(s):  
D Coveney ◽  
G Shaw ◽  
JM Hutson ◽  
MB Renfree
Keyword(s):  
Dorsal Root ◽  
Inguinal Canal ◽  
Prostate Gland ◽  
Tammar Wallaby ◽  
Calcitonin Gene Related Peptide ◽  
Hormonal Control ◽  
Testicular Descent ◽  
Genitofemoral Nerve ◽  
Related Peptide ◽  
Calcitonin Gene

Androgens are essential for testicular descent in eutherian mammals, but little is known about its hormonal control in marsupials. This study reports the effects of daily treatment with the anti-androgen flutamide (10 mg kg(-1)) from day 9 to day 75 after birth on the descent of the testis and inguinal closure in tammar wallabies. By day 75 after birth, the testes of control males had descended and the prostate gland was well developed. The testes of all flutamide-treated males had passed through the inguinal canal and were situated in the base of the scrotum. Three of the nine flutamide-treated males had unilateral inguinal hernias. The size of the inguinal canal, regardless of whether a hernia was present, was significantly wider than that of control males. Development of the prostate gland was significantly inhibited. By day 75 after birth, the phallus was significantly longer in control males than in females, whereas the phallus of flutamide-treated males was similar to that of control females. In flutamide-treated males, the lumbar 1 dorsal root ganglia was feminized and significantly fewer cell bodies expressed calcitonin gene- related peptide. As the anti-androgen treatment resulted in a reduction in the number of calcitonin gene-related peptide-positive cell bodies in the dorsal root ganglion supplying the genitofemoral nerve, the process of inguinal closure in tammar wallabies may be mediated by calcitonin gene-related peptide via the genitofemoral nerve, as indicated in humans. Flutamide treatment inhibited development of the prostate gland and phallus, which are both androgen-dependent structures, but it did not affect the normal descent of the testis, indicating that testicular descent can proceed when the action of androgens is blocked.

Organ culture of the trigeminal ganglion induces enhanced expression of calcitonin gene-related peptide via activation of extracellular signal-regulated protein kinase 1/2

Cephalalgia ◽  
2010 ◽  
Vol 31 (1) ◽  
pp. 95-105 ◽  
Author(s):  
János Tajti ◽  
Anikó Kuris ◽  
László Vécsei ◽  
Cang-Bao Xu ◽  
Lars Edvinsson
Keyword(s):  
Protein Kinase ◽  
Organ Culture ◽  
Glial Cells ◽  
Calcitonin Gene Related Peptide ◽  
Trigeminal Ganglia ◽  
Primary Headaches ◽  
Related Peptide ◽  
Extracellular Signal ◽  
Calcitonin Gene

Background and objective: Clinical and experimental studies have revealed a central role of calcitonin gene-related peptide (CGRP) in primary headaches. The role of extracellular signal-regulated kinase 1 and 2 (ERK1/2) in neuronal and glial cell expression of CGRP- immunoreactivity (-ir) in rat trigeminal ganglia was studied with an organ culture method. Experimental procedures: Sections of adult rat trigeminal ganglia were cultured for up to 48 hours, examined with immunohistochemistry and quantitative real-time polymerase chain reaction (PCR) assay. Specific antibodies against CGRP, phosphorylated ERK1/2 (pERK1/2), total ERK1/2 (tERK1/2), phosphorylated p38 (pp38), phosphorylated C-Jun-N-terminal protein kinase (pJNK), pro-calcitonin (pro-CT), CGRP receptor activity modifying protein 1 (RAMP1), glutamine synthetase (GS) and pro-CT were used. To explore molecular mechanisms involved in the organ culture–induced CGRP-ir in neurons and glial cells, the effects of the MEK/ERK1/2 inhibitor U0126, its inactive analogue U0124, the p38 inhibitor SB203580 and the JNK inhibitor SP600125 were studied. Results: In fresh ganglia, small- and medium-sized neurons were CGRP-ir while some larger neurons displayed RAMP1-ir. Glial cells were negative to both. After organ culture, neurons showed enhanced CGRP- and RAMP1-ir. In addition, some glial cells were RAMP1- and CGRP-ir. Isolated glial cells and neurons were found to contain CGRP mRNA, and showed pro-CT-ir, suggestive of local formation of CGRP. Neurons and glial cells showed enhanced pERK1/2-ir already after two hours of organ culture and this remained elevated for 48 hours. There was transient pJNK-ir in neurons at two hours, while pp38-ir was not altered. U0126 reduced the enhanced pERK1/2-ir, while U0124 had no such effect; the CGRP-ir in neurons and glial cells was reduced at 48 hours and in parallel the CGRP mRNA expression was lower at 24 hours. Conclusion: We suggest that in conditions of elevated CGRP expression, inhibition of ERK1/2 might be an option for novel treatment.

Rat heart organ culture for the study of trophic substances involved in the maintenance of normal sensitivity to norepinephrine: possible involvement of cAMP and search for other factors

1990 ◽  
Vol 68 (7) ◽  
pp. 898-902 ◽  
Author(s):  
Hikaru Tanaka ◽  
Koki Shigenobu
Keyword(s):  
Organ Culture ◽  
Sympathetic Innervation ◽  
High Sensitivity ◽  
Calcitonin Gene Related Peptide ◽  
Right Atrial ◽  
Intracellular Camp ◽  
Rat Serum ◽  
Related Peptide ◽  
Calcitonin Gene

In organ culture conditions, in the absence of in vivo factors, the newborn rat right atria acquire a high sensitivity to agonists similar to that seen before sympathetic innervation and after denervation. In the present study, we examined the effects of various extracts and substances on the development of supersensitivity to norepinephrine (NE) to obtain information on the in vivo factors that regulate myocardial sensitivity. Addition of rat serum, right atrial extract, superior cervical ganglionic extract, vas deferens extract, carbachol, insulin, cortisone, thyroxin, and neuropeptide Y in the culture medium did not prevent the development of supersensitivity. Addition of NE completely inhibited the development of supersensitivity. This effect of NE was blocked by sotalol but not by phentolamine. Addition of calcitonin gene related peptide, forskolin, and 8-bromo-cAMP partially inhibited the development of supersensitivity. These results are consistent with the view that NE released from sympathetic nerve terminals in the newborn atria maintains myocardial sensitivity at normal level by acting on β-adrenergic receptors, and that the effect may be partially mediated by a rise in intracellular cAMP concentration.Key words: rat neonate cardiac muscle, organ culture, sympathetic innervation, norepinephrine, calcitonin gene related peptide, sensitivity, trophic control.

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