Abstract
This study investigated the presence of cell membrane docking proteins synaptosomal-associated protein, 25 and 23 kD (SNAP-25 and SNAP-23) in satellite glial cells (SGCs) of rat trigeminal ganglion; whether cultured SGCs would release glutamate in a time- and calcium-dependent manner following calcium-ionophore ionomycin stimulation; and if botulinum neurotoxin type A (BoNTA), in a dose-dependent manner, could block or decrease vesicular release of glutamate. SGCs were isolated from the trigeminal ganglia (TG) of adult Wistar rats and cultured for 7 days. The presence of SNAPs in TG sections and isolated SGCs were investigated using immunohistochemistry and immunocytochemistry, respectively. SGCs were stimulated with ionomycin (5 μM for 4, 8, 12 and 30 min.) to release glutamate. SGCs were then pre-incubated with BoNTA (24 hrs with 0.1, 1, 10 and 100 pM) to investigate if BoNTA could potentially block ionomycin-stimulated glutamate release. Glutamate concentrations were measured by ELISA. SNAP-25 and SNAP-23 were present in SGCs in TG sections and in cultured SGCs. Ionomycin significantly increased glutamate release from cultured SGCs 30 min. following the treatment (P < 0.001). BoNTA (100 pM) significantly decreased glutamate release (P < 0.01). Results from this study demonstrated that SGCs, when stimulated with ionomycin, released glutamate that was inhibited by BoNTA, possibly through cleavage of SNAP-25 and/or SNAP-23. These novel findings demonstrate the existence of vesicular glutamate release from SGCs, which could potentially play a role in the trigeminal sensory transmission. In addition, interaction of BoNTA with non-neuronal cells at the level of TG suggests a potential analgesic mechanism of action of BoNTA.
Highlights
The trigeminovascular system, which consists of neurons, blood vessels and non-neuronal cells, is an important player in craniofacial nociception [1, 2]
We have recently demonstrated that trigeminal satellite glial cells (SGCs) in rats contain glutamate and express excitatory amino acid transporters (EAAT) and that the cultured SGCs can be stimulated with potassium chloride (10 mM) to release glutamate [11]
The present study show that both synaptosomal-associated protein of 25 kD (SNAP-25) and SNAP-23 are present in trigeminal SGCs
Summary
The trigeminovascular system, which consists of neurons, blood vessels and non-neuronal cells (glial cells), is an important player in craniofacial nociception [1, 2]. Dysfunction of this system is considered a potential mechanism underlying the development and/or maintenance of painful conditions such as migraine headaches [3]. One of the substances proposed to contribute to neuron-glia cross talk is excitatory amino acid glutamate, and disruption of glutamate metabolism by SGCs could lead to increased level of glutamate within the TG [9, 10]. We demonstrated that intraganglionic injection of glutamate in vivo evoked afferent discharges, which were increased by the EAAT1 and EAAT2 blocker, (3S)-3-[[3-[[4-(trifluoromethyl)benzoyl]amino]phe-
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