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A local GABAergic system within rat trigeminal ganglion cells
Author(s) -
Hayasaki H.,
Sohma Y.,
Kanbara K.,
Maemura K.,
Kubota T.,
Watanabe M.
Publication year - 2006
Publication title -
european journal of neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.346
H-Index - 206
eISSN - 1460-9568
pISSN - 0953-816X
DOI - 10.1111/j.1460-9568.2006.04602.x
Subject(s) - glutamate decarboxylase , gabaergic , glutamate receptor , trigeminal ganglion , immunocytochemistry , in situ hybridization , microbiology and biotechnology , biology , extracellular , gamma aminobutyric acid , inhibitory postsynaptic potential , ganglion , gabaa receptor , medicine , protein subunit , chemistry , receptor , endocrinology , messenger rna , neuroscience , biochemistry , enzyme , sensory system , gene
We investigated the GABAergic system within the Sprague–Dawley rat (2–3‐weeks old) trigeminal ganglion (TG). Reverse transcription‐polymerase chain reaction (RT‐PCR) analysis revealed expression of glutamate decarboxylase (GAD) 65 and GAD67 mRNAs and mRNAs encoding GABA A receptor subunits α1–6, β1–3, γ1–3, and δ. In situ hybridization revealed that GAD65 and GAD67 mRNAs were expressed in neuronal cell bodies but not satellite cells. Immunohistochemical analysis showed that only GAD65 was expressed in all neuronal cell bodies, and approximately 70% of all neurons exhibited GABA immunoreactivity. Satellite cells were strongly immunopositive for GABA. GABA A receptor α1, α5, β2/3 and γ1/2/3 subunit immunoreactivities were observed in the majority of neurons, but no immunoreactivity for α2 was observed. Two types of cells were identified in TG based on cell size and morphology, type A and B. The percentage of cells expressing α3, α4, α6, and δ subunits appeared to be dependent on cell size, as δ and α6 expression were only observed in small (B‐type) neurons. In whole‐cell patch clamp experiments, GABA application induced inward Cl – currents in all neurons examined. The EC 50 for GABA varied from 5.3 to 240 µ m , and the Hill Coefficient ( nH ) varied between 0.98 and 2.6 at −60 mV. We found that GABA was released from TG cells by increasing extracellular K + concentration to 100 m m . We speculate that GABA acts as a nonsynaptically released diffusible neurotransmitter, which may modulate somatic inhibition of neurons within the TG.