GABA(B) receptors couple to potassium and calcium channels on identified lateral perforant pathway projection neurons

Citation
Xy. Wang et Na. Lambert, GABA(B) receptors couple to potassium and calcium channels on identified lateral perforant pathway projection neurons, J NEUROPHYS, 83(2), 2000, pp. 1073-1078
Citations number
35
Categorie Soggetti
Neurosciences & Behavoir
Journal title
JOURNAL OF NEUROPHYSIOLOGY
ISSN journal
00223077 → ACNP
Volume
83
Issue
2
Year of publication
2000
Pages
1073 - 1078
Database
ISI
SICI code
0022-3077(200002)83:2<1073:GRCTPA>2.0.ZU;2-B
Abstract
GABA(B) receptors couple to potassium and calcium channels on identified la teral perforant pathway projection neurons. J. Neurophysiol. 83: 1073-1078, 2000. Activation of presynaptic GABA(B) receptors inhibits neurotransmitte r release at most cortical synapses, at least in part because of inhibition of voltage-gated calcium channels. One synapse where this is not the case is the lateral perforant pathway synapse onto dentate granule cells in the hippocampus. The current study was conducted to determine whether the neuro ns that make these synapses express GABA(B) receptors that can couple to io n channels. Perforant pathway projection neurons were labeled by injecting retrograde tracer into the dorsal hippocampus. The GABA(B) receptor agonist baclofen (10 mu M) activated inwardly rectifying potassium channels and in hibited currents mediated by voltage-gated calcium channels in retrogradely labeled neurons in layer II of the lateral entorhinal cortex. These effect s were reversed by coapplication of the selective GABA(B) receptor antagoni st CGP 55845A (1 mu M). Equivalent effects were produced by 100 mu M adenos ine, which inhibits neurotransmitter release at lateral perforant pathway s ynapses. The effects of baclofen and adenosine on inward currents were larg ely occlusive. These results suggest that the absence of GABA(B) receptor-m ediated presynaptic inhibition at lateral perforant pathway synapses is not simply due to a failure to express these receptors and imply that GABA(B) receptors can either be selectively localized or regulated at terminal vers us somatodendritic domains.