Terahertz waves are located in the energy level range of hydrogen bonding and van der Waals forces, and can directly couple with proteins to excite the nonlinear resonance effect of proteins. Therefore, terahertz can affect the conformation of proteins, the structure and function of neurons. Primary cerebral cortex neurons of SD rats were cultured in vitro. Neurons were radiated 3 days by THz with frequency of 0.3-3THz and a power of 100μW; record the growth and development indicators of neurons (Cell body area, total length of process). At the end of a radiation programme, Western blotting was used to detect the protein expressions of GluA1, GluN1, postsynaptic density protein-95(PSD-95) and synaptophysin 38(SYP-38). After the first day of terahertz radiation, the increase in cell area increased by 144.9% (P<0.05); On the second and third days of terahertz radiation, the growth value of the total length of neuronal neurites increased by 65.1% (P<0.05) and 109.4% (P<0.05), respectively; Three days after terahertz irradiation, the protein expressions of GluA1 and SY-38 were increased by 38.1% (P<0.05) and 19.2% (P<0.05), respectively. The results show that (1)The use of Low intensity of broadband terahertz in this study will not cause the death of cortical neurons, and will not affect their growth regularity;(2)Low intensity of broadband terahertz radiation. can promote the growth of cortical neuron cell bodies and processes, but the effects on cortical neuron cell bodies and processes are different. This may be related to the developmental cycle of cultured cortical neurons in vitro, and there is a cumulative effect on the promotion of neuronal processes by low intensity of broadband terahertz;(3) The promotion of neuronal growth and development by low intensity of broadband terahertz radiation may be related to the proportion of AMPA receptor subtypes and the expression of presynaptic specific protein SY-38. These results herald specific frequencies and energies of terahertz radiation as a novel neuromodulation technology for the treatment or intervention of diseases such as neurodevelopmental disorders.
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.
Introduction: Terahertz waves lie within the energy range of hydrogen bonding and van der Waals forces. They can couple directly with proteins to excite non-linear resonance effects in proteins, and thus affect the structure of neurons. However, it remains unclear which terahertz radiation protocols modulate the structure of neurons. Furthermore, guidelines and methods for selecting terahertz radiation parameters are lacking.Methods: In this study, the propagation and thermal effects of 0.3–3 THz wave interactions with neurons were modelled, and the field strength and temperature variations were used as evaluation criteria. On this basis, we experimentally investigated the effects of cumulative radiation from terahertz waves on neuron structure. Results: The results show that the frequency and power of terahertz waves are the main factors influencing field strength and temperature in neurons, and that there is a positive correlation between them. Appropriate reductions in radiation power can mitigate the rise in temperature in the neurons, and can also be used in the form of pulsed waves, limiting the duration of a single radiation to the millisecond level. Short bursts of cumulative radiation can also be used. Broadband trace terahertz (0.1–2 THz, maximum radiated power 100 μW) with short duration cumulative radiation (3 min/day, 3 days) does not cause neuronal death. This radiation protocol can also promote the growth of neuronal cytosomes and protrusions.Discussion: This paper provides guidelines and methods for terahertz radiation parameter selection in the study of terahertz neurobiological effects. Additionally, it verifies that the short-duration cumulative radiation can modulate the structure of neurons.
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.
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