A postsynaptic G-protein in hippocampal long-term potentiation.
The effects of guanosine triphosphate (GTP)-binding protein (G-protein) blockade on hippocampal LTP at stratum radiatum-CA1 synapses was studied. Bath application of 20 mM lithium chloride (LiCl) inhibited long-term potentiation (LTP) of extracellularly-recorded excitatory postsynaptic potentials (EPSPs). Inclusion of 100 mM LiCl in intracellular recording electrodes was shown to block postsynaptic G-proteins by bath-application of baclofen, an agonist at the G-protein linked gamma-aminobutyric acid (GABAB) receptor. Under normal conditions, GABAB receptor activation causes a hyperpolarization postsynaptically, and a decrease in neurotransmitter release presynaptically. With LiCl in the recording electrodes, the postsynaptically-mediated hyperpolarization was blocked, while the presynaptically-mediated depression of EPSPs was unaffected. With postsynaptic G-proteins blocked in this manner, LTP at these synapses was inhibited. These studies provide evidence for the involvement of a postsynaptic G-protein in LTP of stratum radiatum-CA1 synapses.
Department of Pharmacology and Toxicology, Queen's University, Kingston, ON, Canada.
B A
BA
Ballyk
J W
JW
Goh
D000818:Animals; D002712:Chlorides / Q000494:pharmacology; D019204:GTP-Binding Proteins / Q000037:antagonists & inhibitors / Q000502:physiology*; D006624:Hippocampus / Q000187:drug effects / Q000502:physiology*; D066298:In Vitro Techniques; D008094:Lithium / Q000494:pharmacology; D018021:Lithium Chloride; D008297:Male; D009419:Nerve Tissue Proteins / Q000037:antagonists & inhibitors / Q000502:physiology*; D009473:Neuronal Plasticity / Q000187:drug effects / Q000502:physiology*; D051381:Rats; D017208:Rats, Wistar; D013347:Subcellular Fractions / Q000737:chemistry; D013569:Synapses
D002712:Chlorides; D009419:Nerve Tissue Proteins; D008094:Lithium; D019204:GTP-Binding Proteins; D018021:Lithium Chloride