Tonic inhibition originates from synapses close to the soma.
Central neurons are subject to a tonic barrage of randomly occurring spontaneous inhibitory events (mIP-SCs) resulting from the action potential-independent release of gamma-aminobutyric acid (GABA). Do the terminals making synapses onto somatic versus dendritic sites, which arise from specific populations of interneurons, differ in their ability to generate mIPSCs? We have combined the techniques of whole-cell patch-clamp recording and computational simulation to demonstrate that in granule cells of the dentate gyrus, most of the action potential-independent inhibition taking place as mIPSCs originates from proximal sites. Indeed, removal of the bulk (> 50%) of the dendritic tree did not change the characteristics of mIPSCs. These results are consistent with a functional segregation of GABAergic terminals synapsing at proximal versus distal portions of central neurons. Thus, proximal GABAergic terminals are responsible for tonic inhibition targeted at the soma.
Soltesz
I
I
Department of Anesthesiology and Pain Management, University of Texas Southwestern Medical Center, Dallas 75235, USA.
Smetters
D K
DK
Mody
I
I
D000200:Action Potentials; D000818:Animals; D003198:Computer Simulation; D003712:Dendrites / Q000502:physiology; D004594:Electrophysiology; D007700:Kinetics; D008297:Male; D008954:Models, Biological; D009411:Nerve Endings / Q000502:physiology; D009474:Neurons / Q000502:physiology* / Q000648:ultrastructure; D018408:Patch-Clamp Techniques; D051381:Rats; D017208:Rats, Wistar; D013569:Synapses / Q000502:physiology*; D005680:gamma-Aminobutyric Acid / Q000378:metabolism*
D005680:gamma-Aminobutyric Acid