Open AccessBotulinum neurotoxin type A modulates vesicular release of glutamate from satellite glial cells
Author(s) -
Silva Larissa Bittencourt da,
Poulsen Jeppe Nørgaard,
ArendtNielsen Lars,
Gazerani Parisa
Publication year - 2015
Publication title -
journal of cellular and molecular medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.44
H-Index - 130
eISSN - 1582-4934
pISSN - 1582-1838
DOI - 10.1111/jcmm.12562
Subject(s) - ionomycin , glutamate receptor , neurotoxin , chemistry , calcium , stimulation , pharmacology , microbiology and biotechnology , biochemistry , biology , endocrinology , receptor , organic chemistry
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 ( SGC s) of rat trigeminal ganglion; whether cultured SGC s would release glutamate in a time‐ and calcium‐dependent manner following calcium‐ionophore ionomycin stimulation; and if botulinum neurotoxin type A (Bo NTA ), in a dose‐dependent manner, could block or decrease vesicular release of glutamate. SGC s were isolated from the trigeminal ganglia ( TG ) of adult Wistar rats and cultured for 7 days. The presence of SNAP s in TG sections and isolated SGC s were investigated using immunohistochemistry and immunocytochemistry, respectively. SGC s were stimulated with ionomycin (5 μM for 4, 8, 12 and 30 min.) to release glutamate. SGC s were then pre‐incubated with Bo NTA (24 hrs with 0.1, 1, 10 and 100 pM) to investigate if Bo NTA could potentially block ionomycin‐stimulated glutamate release. Glutamate concentrations were measured by ELISA . SNAP ‐25 and SNAP ‐23 were present in SGC s in TG sections and in cultured SGC s. Ionomycin significantly increased glutamate release from cultured SGC s 30 min. following the treatment ( P < 0.001). Bo NTA (100 pM) significantly decreased glutamate release ( P < 0.01). Results from this study demonstrated that SGC s, when stimulated with ionomycin, released glutamate that was inhibited by Bo NTA , possibly through cleavage of SNAP ‐25 and/or SNAP ‐23. These novel findings demonstrate the existence of vesicular glutamate release from SGC s, which could potentially play a role in the trigeminal sensory transmission. In addition, interaction of Bo NTA with non‐neuronal cells at the level of TG suggests a potential analgesic mechanism of action of Bo NTA .