Prior Activation of Inositol 1,4,5-Trisphosphate Receptors Suppresses the Subsequent Induction of Long-Term Potentiation in Hippocampal CA1 Neurons

• Published in: Learning & memory (Cold Spring Harbor, N.Y.) Vol. 23; no. 5; pp. 208 - 220
• Main Authors: Fujii, Satoshi, Yamazaki, Yoshihiko, Goto, Jun-Ichi, Fujiwara, Hiroki, Mikoshiba, Katsuhiko
• Format: Journal Article
• Language: English
• Published: United States Cold Spring Harbor Laboratory Press 01.05.2016
• Subjects: Animals; Benzoates - pharmacology; Benzophenanthridines - pharmacology; Biophysics; Boron Compounds - pharmacology; Brain Hemisphere Functions; CA1 Region, Hippocampal - cytology; Conditioning; Dose-Response Relationship, Drug; Electric Stimulation; Enzyme Inhibitors - pharmacology; Excitatory Amino Acid Antagonists - pharmacology; Excitatory Postsynaptic Potentials - drug effects; Excitatory Postsynaptic Potentials - physiology; Glycine - analogs & derivatives; Glycine - pharmacology; Guinea Pigs; Immunosuppressive Agents - pharmacology; In Vitro Techniques; Inositol 1,4,5-Trisphosphate Receptors - metabolism; Long-Term Potentiation - drug effects; Long-Term Potentiation - physiology; Male; Methoxyhydroxyphenylglycol - analogs & derivatives; Methoxyhydroxyphenylglycol - pharmacology; Neurological Organization; Neurology; Neurons - drug effects; Neurons - physiology; Stimulation; Tacrolimus - pharmacology
• ISSN: 1072-0502; 1549-5485; 1549-5485
• DOI: 10.1101/lm.041053.115

We investigated the role of inositol 1,4,5-trisphosphate receptors (IP3Rs) activated by preconditioning low-frequency afferent stimulation (LFS) in the subsequent induction of long-term potentiation (LTP) in CA1 neurons in hippocampal slices from mature guinea pigs. Induction of LTP in the field excitatory postsynaptic potential or the population spike by the delivery of high-frequency stimulation (HFS, a tetanus of 100 pulses at 100 Hz) to the Schaffer collateral-commissural pathway to CA1 neuron synapses was suppressed when group I metabotropic glutamate receptors (mGluRs) were activated prior to the delivery of HFS. LTP induction was also suppressed when CA1 synapses were preconditioned 60 min before HFS by LFS of 1000 pulses at 1 Hz and this effect was inhibited when the test stimulation delivered at 0.05 Hz was either halted or applied in the presence of an antagonist of N-methyl-D-aspartate receptors, group I mGluRs, or IP3Rs during a 20-min period from 20 to 40 min after the end of LFS. Furthermore, blockade of group I mGluRs or IP[subscript 3]Rs immediately before the delivery of HFS overcame the effects of the preconditioning LFS on LTP induction. These results suggest that, in CA1 neurons, after a preconditioning LFS, activation of group I mGluRs caused by the test stimulation results in IP[subscript 3]Rs activation that leads to a failure of LTP induction.