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Brain Res. 1993 May 14;611(1):81-6.

A postsynaptic G-protein in hippocampal long-term potentiation.

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Department of Pharmacology and Toxicology, Queen's University, Kingston, ON, Canada.


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.

[Indexed for MEDLINE]

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