Low concentrations of GABA reduce accommodation in primary afferent neurons by an action at GABAB receptors.
The pattern of accommodation of spike activity during sustained membrane depolarization was investigated in primary afferent neurons recorded intracellularly in vitro in the rat. We show that gamma-aminobutyric acid (GABA) and baclofen reduce accommodation in some fast conducting dorsal root ganglion neurons. This effect was restricted to those A delta cells with axons displaying a rather fast conduction velocity (15-25 m/s). GABA-induced blockade of accommodation was not observed in large A beta neurons. Pharmacological studies with baclofen, as opposed to isoguvacine, indicate that this effect is due to GABAB receptors activation. The effect is also shown to be resistant to bicuculline antagonism. In slow conducting afferents, GABAB receptor activation is known to shorten the CA2+ component of action potentials. By contrast, no such component was observed in the A delta cells studied. Furthermore, Ca2+-activated K+ conductances are not implicated in the reduction of accommodation caused by GABAB receptor activation. In conjunction with the actual knowledge about the distribution of GABA receptors on primary afferents, our result indicates that GABAA and GABAB receptors coexist on all categories of A delta and C primary afferents in the rat.
D000818:Animals; D001418:Baclofen / Q000494:pharmacology; D002118:Calcium / Q000378:metabolism; D005260:Female; D005727:Ganglia, Spinal / Q000032:analysis / Q000187:drug effects*; D007473:Ion Channels / Q000187:drug effects; D008297:Male; D009431:Neural Conduction / Q000187:drug effects; D009475:Neurons, Afferent / Q000187:drug effects; D051381:Rats; D011963:Receptors, GABA-A / Q000032:analysis / Q000187:drug effects*; D005680:gamma-Aminobutyric Acid / Q000494:pharmacology*
D007473:Ion Channels; D011963:Receptors, GABA-A; D005680:gamma-Aminobutyric Acid; D001418:Baclofen; D002118:Calcium