Release of substance P, calcitonin gene-related peptide and prostaglandin E2 from rat dura mater encephali following electrical and chemical stimulation in vitro
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Abstract
Neurogenic inflammation of the dura, expressed in plasma extravasation and vasodilatation,
putatively contributes to different types of headache. A novel in vitro preparation
of the fluid-filled skull cavities was developed to measure mediator release from
dura mater encephali upon antidromic electrical stimulation of the trigeminal ganglion
and after application of a mixture of inflammatory mediators (serotonin, histamine
and bradykinin, 10(-5) M each, pH 6.1) to the arachnoid side of rat dura. The release
of calcitonin gene-related peptide, substance P and prostaglandin E2 from dura mater
was measured in 5-min samples of superfusates using enzyme immunoassays. Orthodromic
chemical and antidromic electrical stimulation of dural afferents caused significant
release of calcitonin gene-related peptide (2.8- and 4.5-fold of baseline). The neuropeptide
was found to be increased during the 5-min stimulation period and returned to baseline
(20.9 +/- 12 pg/ml) in the sampling period after stimulation. In contrast, release
of substance P remained at baseline levels (19.3 +/- 11 pg/ml) throughout the experiment.
Prostaglandin E2 release was elevated during chemical and significantly also after
antidromic electrical stimulation (6- and 4.2-fold of baseline, which was 305 +/-
250 pg/ml). Prostaglandin E2 release outlasted the stimulation period for at least
another 5 min. The data support the hypothesis of neurogenic inflammation being involved
in headaches and provide new evidence for prostaglandin E2 possibly facilitating meningeal
nociceptor excitation and, hence, pain.