Your browser doesn't support javascript.
loading
G-protein coupled estrogen receptor (GPER1) activation promotes synaptic insertion of AMPA receptors and induction of chemical LTP at hippocampal temporoammonic-CA1 synapses.
Clements, Leigh; Alexander, Amy; Hamilton, Kirsty; Irving, Andrew; Harvey, Jenni.
Afiliación
  • Clements L; Division of Systems Medicine, University of Dundee, Ninewells Hospital and Medical School, Dundee, DD1 9SY, UK.
  • Alexander A; Division of Systems Medicine, University of Dundee, Ninewells Hospital and Medical School, Dundee, DD1 9SY, UK.
  • Hamilton K; Division of Systems Medicine, University of Dundee, Ninewells Hospital and Medical School, Dundee, DD1 9SY, UK.
  • Irving A; Division of Systems Medicine, University of Dundee, Ninewells Hospital and Medical School, Dundee, DD1 9SY, UK.
  • Harvey J; Faculty of Arts, Science and Technology, The University of Northampton, Northampton, NN1 5PH, UK.
Mol Brain ; 16(1): 16, 2023 01 28.
Article en En | MEDLINE | ID: mdl-36709268
It is well documented that 17ß estradiol (E2) regulates excitatory synaptic transmission at hippocampal Shaffer-collateral (SC)-CA1 synapses, via activation of the classical estrogen receptors (ERα and ERß). Hippocampal CA1 pyramidal neurons are also innervated by the temporoammonic (TA) pathway, and excitatory TA-CA1 synapses are reported to be regulated by E2. Recent studies suggest a role for the novel G-protein coupled estrogen receptor (GPER1) at SC-CA1 synapses, however, the role of GPER1 in mediating the effects of E2 at juvenile TA-CA1 synapses is unclear. Here we demonstrate that the GPER1 agonist, G1 induces a persistent, concentration-dependent (1-10 nM) increase in excitatory synaptic transmission at TA-CA1 synapses and this effect is blocked by selective GPER1 antagonists. The ability of GPER1 to induce this novel form of chemical long-term potentiation (cLTP) was prevented following blockade of N-methyl-D-aspartate (NMDA) receptors, and it was not accompanied by any change in paired pulse facilitation ratio (PPR). GPER1-induced cLTP involved activation of ERK but was independent of phosphoinositide 3-kinase (PI3K) signalling. Prior treatment with philanthotoxin prevented the effects of G1, indicating that synaptic insertion of GluA2-lacking α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors underlies GPER1-induced cLTP. Furthermore, activity-dependent LTP occluded G1-induced cLTP and vice versa, indicating that these processes have overlapping expression mechanisms. Activity-dependent LTP was blocked by the GPER1 antagonist, G15, suggesting that GPER1 plays a role in NMDA-dependent LTP at juvenile TA-CA1 synapses. These findings add a new dimension to our understanding of GPER1 in modulating neuronal plasticity with relevance to age-related neurodegenerative conditions.
Asunto(s)
Palabras clave

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Receptores de Estrógenos / Potenciación a Largo Plazo Idioma: En Revista: Mol Brain Asunto de la revista: BIOLOGIA MOLECULAR / CEREBRO Año: 2023 Tipo del documento: Article Pais de publicación: Reino Unido

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Receptores de Estrógenos / Potenciación a Largo Plazo Idioma: En Revista: Mol Brain Asunto de la revista: BIOLOGIA MOLECULAR / CEREBRO Año: 2023 Tipo del documento: Article Pais de publicación: Reino Unido