Involvement of postsynaptic G proteins in hippocampal long-term potentiation

Katsuki, Hiroshi; Kaneko, Shuji; Satoh, Masamichi

doi:10.1016/0006-8993(92)90349-e

Cited by 11 publications

(2 citation statements)

References 17 publications

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“…In contrast to the weak TBS, a conventional LTP induction protocol, such as TBS with 10 burst trains, can produce full-size LTP in both G␣qand G␣11deficient mice that is indistinguishable from LTP in wild-type mice. In other studies, postsynaptic injection of GTP␥S, a nonhydrolyzable guanine nucleotide analog, does not occlude LTP in area CA1 (Goh and Pennefather, 1989;Katsuki et al, 1992). These results suggest that the signal transduction pathway involving G␣q or G␣11 is not essential but has a significant modulatory effect in the induction of LTP.…”

Section: Role Of Signal Transduction Pathway Via G␣q/g␣11 In Ltp Indumentioning

confidence: 65%

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Group I Metabotropic Glutamate Receptor Signaling via Gαq/Gα11 Secures the Induction of Long-Term Potentiation in the Hippocampal Area CA1

et al. 2002

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Heterotromeric G-proteins of the Gq family are thought to transduce signals from group I metabotropic glutamate receptors (mGluRs) in central neurons. We investigated roles of this cascade in hippocampal long-term potentiation (LTP) by using null-mutant mice lacking the alpha subunit of Gq (Galphaq) or G11 (Galpha11). We found no obvious abnormalities in the morphology, layer structure, expression of NMDA receptors, and basic parameters of excitatory synaptic transmission in the hippocampus of Galphaq mutant mice. We used theta burst stimulation (TBS) (3-10 burst trains at 5 Hz; each train consisted of five stimuli at 100 Hz) to induce LTP at Schaffer collateral to CA1 pyramidal cell synapses. Conventional TBS with 10 burst trains induced robust LTP in wild-type, Galphaq mutant, and Galpha11 mutant mice. Weak TBS with three burst trains consistently induced LTP in wild-type mice. In contrast, the same weak TBS was insufficient to induce LTP in Galphaq and Galpha11 mutant mice. In wild-type mice, the LTP by weak TBS was abolished by inhibiting group I mGluR or protein kinase C (PKC) but not by blocking muscarinic acetylcholine receptors. Prior activation of group I mGluR by an agonist significantly enhanced the LTP by weak TBS in wild-type mice. However, this priming effect was absent in Galphaq mutant mice. These results indicate that the signaling from group I mGluR to PKC involving Galphaq/Galpha11 does not constitute the main pathway for LTP, but it secures LTP induction by lowering its threshold in the hippocampal area CA1.

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Section: Role Of Signal Transduction Pathway Via G␣q/g␣11 In Ltp Indumentioning

confidence: 65%

“…Furthermore, LTP is impaired in PKC␥ mutant mice (Abeliovich et al, 1993). However, maximal activation of postsynaptic G-protein does not occlude the induction of LTP in area CA1 (Goh and Pennefather, 1989;Katsuki et al, 1992).…”

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confidence: 95%