Aim: In mouse, the administration of 3-iodothyronamine (T1AM) had an antiamnestic and prolearning effect. In addition, T1AM rescued long term potentiation (LTP) in enthorinal cortex exposed to the toxic effect of β-amyloid. In the present study we used a neuronal cell line to evaluate the effects of T1AM on the expression of the calcium calmodulin dependent protein kinase II (CaMKII) and the protein kinase C (PKC), two key players involved in LTP. Methods: A hybrid line of cancer cells of mouse neuroblastoma and rat glioma (NG108-15) was used and treated with 100 nM to 10 μM T1AM for 24 h, alone or in combination with 10 µM resveratrol and/or 10 µM amyloid β peptide (25-35). Protein expression and post-translational modifications were investigated by Western blot technique. Glucose consumption was also measured upon 4 h treatment. Results: NG108-15 express TAAR1, the putative T1AM receptor, as well as AMPA and NMDA receptors, the two main LTP receptors. T1AM (10 μM) induced CaMKII phosphorylation (p<0.001). The response to resveratrol was modified by T1AM, since resveratrol inhibited PKC expression while the association of resveratrol and T1AM (100 nM) produced a remarkable increase vs the baseline (P<0.05). Furthermore an increase in glucose consumption was observed at the highest T1AM concentration (p<0.01). Conclusions: In NG108-15 cells T1AM activated CaMKII and had complex effects on the response to β-amyloid and resveratrol.
Effects of 3-iodothyronamine (T1AM) on long term potentiation (LTP) postsynaptic signaling cascade
Ginevra Sacripanti;Lavinia Bandini;Leonardo Lorenzini;Riccardo Zucchi;Sandra Ghelardoni
2018-01-01
Abstract
Aim: In mouse, the administration of 3-iodothyronamine (T1AM) had an antiamnestic and prolearning effect. In addition, T1AM rescued long term potentiation (LTP) in enthorinal cortex exposed to the toxic effect of β-amyloid. In the present study we used a neuronal cell line to evaluate the effects of T1AM on the expression of the calcium calmodulin dependent protein kinase II (CaMKII) and the protein kinase C (PKC), two key players involved in LTP. Methods: A hybrid line of cancer cells of mouse neuroblastoma and rat glioma (NG108-15) was used and treated with 100 nM to 10 μM T1AM for 24 h, alone or in combination with 10 µM resveratrol and/or 10 µM amyloid β peptide (25-35). Protein expression and post-translational modifications were investigated by Western blot technique. Glucose consumption was also measured upon 4 h treatment. Results: NG108-15 express TAAR1, the putative T1AM receptor, as well as AMPA and NMDA receptors, the two main LTP receptors. T1AM (10 μM) induced CaMKII phosphorylation (p<0.001). The response to resveratrol was modified by T1AM, since resveratrol inhibited PKC expression while the association of resveratrol and T1AM (100 nM) produced a remarkable increase vs the baseline (P<0.05). Furthermore an increase in glucose consumption was observed at the highest T1AM concentration (p<0.01). Conclusions: In NG108-15 cells T1AM activated CaMKII and had complex effects on the response to β-amyloid and resveratrol.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
