| First Author | Grigoryan G | Year | 2023 |
| Journal | Proc Natl Acad Sci U S A | Volume | 120 |
| Issue | 51 | Pages | e2312752120 |
| PubMed ID | 38091292 | Mgi Jnum | J:352515 |
| Mgi Id | MGI:7568757 | Doi | 10.1073/pnas.2312752120 |
| Citation | Grigoryan G, et al. (2023) Synaptic plasticity at the dentate gyrus granule cell to somatostatin-expressing interneuron synapses supports object location memory. Proc Natl Acad Sci U S A 120(51):e2312752120 |
| abstractText | Somatostatin-expressing interneurons (SOMIs) in the mouse dentate gyrus (DG) receive feedforward excitation from granule cell (GC) mossy fiber (MF) synapses and provide feedback lateral inhibition onto GC dendrites to support environment representation in the DG network. Although this microcircuitry has been implicated in memory formation, little is known about activity-dependent plastic changes at MF-SOMI synapses and their influence on behavior. Here, we report that the metabotropic glutamate receptor 1alpha (mGluR1alpha) is required for the induction of associative long-term potentiation (LTP) at MF-SOMI synapses. Pharmacological block of mGluR1alpha, but not mGluR5, prevented synaptic weight changes. LTP at MF-SOMI synapses was postsynaptically induced, required increased intracellular Ca(2+), involved G-protein-mediated and Ca(2+)-dependent (extracellular signal-regulated kinase) ERK1/2 pathways, and the activation of NMDA receptors. Specific knockdown of mGluR1alpha in DG-SOMIs by small hairpin RNA expression prevented MF-SOMI LTP, reduced SOMI recruitment, and impaired object location memory. Thus, postsynaptic mGluR1alpha-mediated MF-plasticity at SOMI input synapses critically supports DG-dependent mnemonic functions. |
