Chengbiao Lu

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.

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.

Summary: Normal aging is characterized with a decline in hippocampal memory functions that is associated with changes in long‐term potentiation (LTP) of the CA3‐to‐CA1 synapse. Age‐related deficit of the dopaminergic system may contribute to impairment of CA1 LTP. Here we assessed how the modulation of CA1 LTP by dopamine is affected by aging and how it is dependent on the Ca²⁺ source. In slices from adult mice, the initial slope of the field potential showed strong LTP, but in slices from aged mice LTP was impaired. Dopamine did not affect LTP in adult slices, but enhanced LTP in aged slices. The dopamine D1/D5 receptor (D1R/D5R) agonist SKF‐81297 did not affect LTP in adult but caused a relative small increase in LTP in aged slices; however, although there was no difference in dopamine D4 receptor (D4R) expression, the D4R agonist PD168077 increased LTP in aged slices to a magnitude similar to that in adult slices. The N‐Methyl‐D‐aspartate receptor antagonist D‐AP5 reduced LTP in adult slices, but not in aged slices. However, in the presence of D‐AP5, PD168077 completely blocked LTP in aged slices. The voltage‐dependent calcium channel (VDCC) blocker nifedipine reduced LTP in adult slices, but surprisingly enhanced LTP in aged slices. Furthermore, in the presence of nifedipine, PD168077 caused a strong enhancement of LTP in aged slices to a magnitude exceeding LTP in adult slices. Our results indicate that the full rescue of impaired LTP in aging by the selective D4R activation and that a large potentiation role on LTP by co‐application of D4R agonist and VDCC blocker may provide novel strategies for the intervention of cognitive decline of aging and age‐related diseases.