Related Experiment Video
Updated: Sep 27, 2026

Measuring Spinal Presynaptic Inhibition in Mice By Dorsal Root Potential Recording In Vivo
Published on: March 29, 2014
Pre- and postsynaptic inhibition mediated by GABA(B) receptors in rat ventrolateral periaqueductal gray neurons
Kun Yang1, Hidemasa Furue, Eiichi Kumamoto
1Department of Integrative Physiology, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan. yankun@post.saga-med.ac.jp
Abstract:
The present study examined the actions of a GABA(B)-receptor agonist, baclofen, on synaptic transmission in rat ventrolateral periaqueductal gray (PAG) neurons of brainstem slices by using whole-cell voltage-clamp recordings. Baclofen (10 microM) induced a slow outward current (peak amplitude: 30.1+/-3.1pA, n=13) at -70mV, which persisted in the presence of tetrodotoxin (0.5 microM) and was diminished in the presence of postsynaptic intracellular K(+)-channel blockers (Cs(+) and TEA) and GDP-beta-S, indicating a direct postsynaptic depression mediated by K(+) channels and G proteins. Baclofen (10 microM) also decreased the frequency of both glutamatergic spontaneous EPSC (by 36+/-7%, n=11) and GABAergic spontaneous IPSC (by 37+/-12%, n=6) without changes in their amplitudes, indicating its presynaptic inhibitions. Taken together, the activation of postsynaptic GABA(B) receptors inhibits ventrolateral PAG neurons directly. At the same time, activating presynaptic GABA(B) receptors on glutamatergic and GABAergic nerve terminals inhibits glutamate and GABA release, respectively. The overall effects might influence an output of ventrolateral PAG neurons that build up the descending pain control system to the spinal dorsal horn.
More Related Videos
Related Concept Videos
Excitatory and Inhibitory Effects of Neurotransmitters
Ligand-Gated Ion Channel Receptor: Gating Mechanism
G-Protein Gated Ion Channels
Sensory organs,...

