Skip to main content
. Author manuscript; available in PMC: 2007 Oct 30.
Published in final edited form as: Pain. 2007 Apr 24;130(1-2):166–176. doi: 10.1016/j.pain.2007.03.012

Figure 2.

Figure 2

Mast cell degranulation triggers prolonged excitation of meningeal nociceptors. (A) Schematic localization of the recording site for meningeal nociceptors in the trigeminal ganglion (TG). The figure also illustrates the trigeminovascular pathway from the meninges to the central trigeminal nucleus caudalis (TNC). (B) Selected 30 minutes recording periods demonstrating the neuronal activity (bin size 1 sec) of an affected C-unit meningeal nociceptor at baseline (top) and then at various time points following MC degranulation with 48/80 (bottom traces). Average discharge rates are given in parentheses. (C) Peri-stimulus time histogram showing the response of the same meningeal nociceptor (top trace, bin size 0.5 sec) to a suprathreshold 38kPa mechanical stimulus (bottom trace) applied to the neuron’s dural receptive field following bone removal at the end of the experiment. (D) Time course changes (mean ± SE) in neuronal discharge rate of the affected A-δ and C-units following MC degranulation. (E) The effect of local craniotomy and mast cell depletion on baseline neuronal ongoing discharge level. Note the high level of neuronal activity in neurons in which their receptive field was interrupted by a craniotomy. (F) Time course effect of MC degranulation on meningeal nociceptors showing the increase in ongoing discharge rate (mean ± SEM) and its blockade by prior administration of the MC stabilizer SCG. * p<0.01, Fisher PLSD test.