Exogenous AMPA downregulates gamma-frequency network oscillation in CA3 of rat hippocampal slices.

Pharmacologically-induced persistent hippocampal γ oscillation in area CA3 requires activation of α-Amino-3-hydroxy-5-methyl-4-isoxazolepropionate receptors (AMPARs). However, we demonstrated that exogenous AMPA dose-dependently inhibited carbachol (CCH)-induced γ oscillation in the CA3 area of rat hippocampal slices, but the underlying mechanism is not clear. Application of AMPARs antagonist NBQX (1 µM) did not affect γ oscillation power (γ power), nor AMPA-mediated γ power reduction. At 3 µM, NBQX had no effect on γ power but largely blocked AMPA-mediated γ power reduction. Ca2+-permeable AMPA receptor (CP-AMPAR) antagonist IEM1460 or CaMKK inhibitor STO-609 but not CaMKIIα inhibitor KN93 enhanced γ power, indicating that activation of CP-AMPAR or CaMKK negatively modulated CCH-induced γ oscillation. Either CP-AMPAR antagonist or CaMKK inhibitor alone did not affected AMPA-mediated γ power reduction, but co-administration of IEM1460 and NBQX (1 µM) largely prevented AMPA-mediated downregulation of γ suggesting that CP-AMPARs and CI-AMPARs are involved in AMPA downregulation of γ oscillation. The recurrent excitation recorded at CA3 stratum pyramidale was significantly reduced by AMPA application. Our results indicate that AMPA downregulation of γ oscillation may be related to the reduced recurrent excitation within CA3 local neuronal network due to rapid CI-AMPAR and CP-AMPAR activation.

High Frequency Electromagnetic Radiation Stimulates Neuronal Growth and Hippocampal Synaptic Transmission.

Terahertz waves lie within the rotation and oscillation energy levels of biomolecules, and can directly couple with biomolecules to excite nonlinear resonance effects, thus causing conformational or configuration changes in biomolecules. Based on this mechanism, we investigated the effect pattern of 0.138 THz radiation on the dynamic growth of neurons and synaptic transmission efficiency, while explaining the phenomenon at a more microscopic level. We found that cumulative 0.138 THz radiation not only did not cause neuronal death, but that it promoted the dynamic growth of neuronal cytosol and protrusions. Additionally, there was a cumulative effect of terahertz radiation on the promotion of neuronal growth. Furthermore, in electrophysiological terms, 0.138 THz waves improved synaptic transmission efficiency in the hippocampal CA1 region, and this was a slow and continuous process. This is consistent with the morphological results. This phenomenon can continue for more than 10 min after terahertz radiation ends, and these phenomena were associated with an increase in dendritic spine density. In summary, our study shows that 0.138 THz waves can modulate dynamic neuronal growth and synaptic transmission. Therefore, 0.138 terahertz waves may become a novel neuromodulation technique for modulating neuron structure and function.