| Home > Publications Database > Gamma oscillation plasticity is mediated via parvalbumin interneurons. |
| Journal Article | DZNE-2024-00105 |
; ; ; ;
2024
Assoc.
Washington, DC [u.a.]
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Please use a persistent id in citations: doi:10.1126/sciadv.adj7427
Abstract: Understanding the plasticity of neuronal networks is an emerging field of (patho-) physiological research, yet the underlying cellular mechanisms remain poorly understood. Gamma oscillations (30 to 80 hertz), a biomarker of cognitive performance, require and potentiate glutamatergic transmission onto parvalbumin-positive interneurons (PVIs), suggesting an interface for cell-to-network plasticity. In ex vivo local field potential recordings, we demonstrate long-term potentiation of hippocampal gamma power. Gamma potentiation obeys established rules of PVI plasticity, requiring calcium-permeable AMPA receptors (CP-AMPARs) and metabotropic glutamate receptors (mGluRs). A microcircuit computational model of CA3 gamma oscillations predicts CP-AMPAR plasticity onto PVIs critically outperforms pyramidal cell plasticity in increasing gamma power and completely accounts for gamma potentiation. We reaffirm this ex vivo in three PVI-targeting animal models, demonstrating that gamma potentiation requires PVI-specific signaling via a Gq/PKC pathway comprising mGluR5 and a Gi-sensitive, PKA-dependent pathway. Gamma activity-dependent, metabotropically mediated CP-AMPAR plasticity on PVIs may serve as a guiding principle in understanding network plasticity in health and disease.
Keyword(s): Animals (MeSH) ; Parvalbumins: metabolism (MeSH) ; Hippocampus: metabolism (MeSH) ; Long-Term Potentiation: physiology (MeSH) ; Signal Transduction (MeSH) ; Interneurons: physiology (MeSH) ; Neuronal Plasticity: physiology (MeSH) ; Parvalbumins
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