Effect of subarachnoid haemorrhage on trigeminovascular calcitonin-gene-related peptide and substance P of the rat dura mater versus cerebral vasculature

1994 ◽  
Vol 127 (1-2) ◽  
pp. 103-111 ◽  
Author(s):  
A. G. Arand ◽  
M. Zuccarello ◽  
B. A. Skidmore ◽  
R. J. Berger ◽  
J. T. Keller
Keyword(s):  
Substance P ◽  
Subarachnoid Haemorrhage ◽  
Dura Mater ◽  
Calcitonin Gene Related Peptide ◽  
Cerebral Vasculature ◽  
Related Peptide ◽  
Calcitonin Gene

Release of Histamine from Dural Mast Cells by Substance P and Calcitonin Gene-Related Peptide

Cephalalgia ◽  
1997 ◽  
Vol 17 (3) ◽  
pp. 166-174 ◽  
Author(s):  
A Ottosson ◽  
L Edvinsson
Keyword(s):  
Mast Cells ◽  
Substance P ◽  
Histamine Release ◽  
Dura Mater ◽  
Neurogenic Inflammation ◽  
Calcitonin Gene Related Peptide ◽  
Sampling Procedure ◽  
Related Peptide ◽  
Calcitonin Gene ◽  
Peritoneal Mast Cells

The aim of the present study was to examine if the neuropeptides substance P (SP), calcitonin gene-related peptide (CGRP), neuropeptide Y (NPY) and vasoactive intestinal peptide (VIP) can stimulate histamine release from mast cells in the dura mater and thereby play a role in cranial vasoregulation and local neurogenic inflammation. Dura mater mast cells were compared with peritoneal mast cells in the rat. Histamine was released from dura mater mast cells by compound 48/80, SP and CGRP but from peritoneal mast cells only by compound 8/80 and SP. NPY and VIP released quite small amounts of histamine from dural mast cells. The release on SP and CGRP from rat dura mater mast cells was blocked by the receptor antagonists FK888 and CGRP8-37 respectively, suggesting receptor mediated release mechanisms. None of the stimuli released histamine from human or porcine dural mast cells, possibly because the sampling procedure injures and incapacitates the cells.

Innervation of the dura mater encephali of cat and rat: ultrastructure and calcitonin gene-related peptide-like and substance P-like immunoreactivity

1993 ◽  
Vol 188 (3) ◽  
Author(s):  
Karl Me�linger ◽  
Ulrike Hanesch ◽  
Matthias Baumg�rtel ◽  
Brigitte Trost ◽  
RobertF. Schmidt
Keyword(s):  
Substance P ◽  
Dura Mater ◽  
Calcitonin Gene Related Peptide ◽  
Dura Mater Encephali ◽  
Related Peptide ◽  
Calcitonin Gene

Cerebrovascular changes following administration of gammaglobulins against substance P or calcitonin gene related peptide in monkey with subarachnoid haemorrhage

1993 ◽  
Vol 7 (5) ◽  
pp. 507-518 ◽  
Author(s):  
Yoshiaki Shiokawa ◽  
Jens Juul Holst ◽  
J. Torben ◽  
N. Rasmussen ◽  
Peter Schmidt ◽  
...  
Keyword(s):  
Substance P ◽  
Subarachnoid Haemorrhage ◽  
Calcitonin Gene Related Peptide ◽  
Related Peptide ◽  
Calcitonin Gene

Twenty six-week repeat dose oral rat toxicity study of cizolirtine, a substance-P and calcitonin gene-related peptide release modulator

2021 ◽  
Vol 122 ◽  
pp. 104916
Author(s):  
Antonio Guzmán ◽  
Gregorio Encina ◽  
Antonio R. Fernández de Henestrosa ◽  
Cristina Vila ◽  
Araceli Tortajada ◽  
...  
Keyword(s):  
Substance P ◽  
Calcitonin Gene Related Peptide ◽  
Toxicity Study ◽  
Repeat Dose ◽  
Related Peptide ◽  
Calcitonin Gene ◽  
Peptide Release ◽  
Dose Oral

Calcitonin gene-related peptide receptors in rat trigeminal ganglion do not control spinal trigeminal activity

2012 ◽  
Vol 108 (2) ◽  
pp. 431-440 ◽  
Author(s):  
Oana Covasala ◽  
Sören L. Stirn ◽  
Stephanie Albrecht ◽  
Roberto De Col ◽  
Karl Messlinger
Keyword(s):  
Trigeminal Ganglion ◽  
Dura Mater ◽  
Calcitonin Gene Related Peptide ◽  
Afferent Input ◽  
Nitric Oxide Donor ◽  
Cgrp Receptor ◽  
Related Peptide ◽  
Trigeminal Neurons ◽  
Calcitonin Gene ◽  
Evoked Activity

Calcitonin gene-related peptide (CGRP) is regarded as a key mediator in the generation of primary headaches. CGRP receptor antagonists reduce migraine pain in clinical trials and spinal trigeminal activity in animal experiments. The site of CGRP receptor inhibition causing these effects is debated. Activation and inhibition of CGRP receptors in the trigeminal ganglion may influence the activity of trigeminal afferents and hence of spinal trigeminal neurons. In anesthetized rats extracellular activity was recorded from neurons with meningeal afferent input in the spinal trigeminal nucleus caudalis. Mechanical stimuli were applied at regular intervals to receptive fields located in the exposed cranial dura mater. α-CGRP (10−5 M), the CGRP receptor antagonist olcegepant (10−3 M), or vehicle was injected through the infraorbital canal into the trigeminal ganglion. The injection of volumes caused transient discharges, but vehicle, CGRP, or olcegepant injection was not followed by significant changes in ongoing or mechanically evoked activity. In animals pretreated intravenously with the nitric oxide donor glyceryl trinitrate (GTN, 250 μg/kg) the mechanically evoked activity decreased after injection of CGRP and increased after injection of olcegepant. In conclusion, the activity of spinal trigeminal neurons with meningeal afferent input is normally not controlled by CGRP receptor activation or inhibition in the trigeminal ganglion. CGRP receptors in the trigeminal ganglion may influence neuronal activity evoked by mechanical stimulation of meningeal afferents only after pretreatment with GTN. Since it has previously been shown that olcegepant applied to the cranial dura mater is ineffective, trigeminal activity driven by meningeal afferent input is more likely to be controlled by CGRP receptors located centrally to the trigeminal ganglion.

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