输出高重复频率脉冲列的全固态激光器

报道了利用声光振幅调制锁模的方法，在激光二极管端面抽运Nd：YVO4激光器上获得320MHz高重复频率脉冲列的实验结果。实验采用平一平腔结构，腔长452mm，耦合输出镜透过率为3．6％。所用声光介质为熔融石英晶体，以铌酸锂作换能器，在驱动功率4．5W时，对1064nm波长衍射效率为50，相应的调制深度为0．31。在最佳锁模状态下，激光二极管抽运功率为3．5W，此时激光平均输出功率为15mw。示波器记录脉冲宽度680ps，实测光束质量因子M^2小于1．5。并在实验基础上对激光器工作的稳定性进行了分析，结果表

激光尘埃粒子计数器微型光学传感器的研究

研制成功便携式激光尘埃粒子计数器的核心部件——微型光学传感器。该传感器采用直角散射光收集形式。以高功率半导体激光器作为光源，同时采用高性能的PIN型光电二极管作为光电探测器。散射光收集系统为单一大数值孔径的球面反射镜，其对粒子散射光的收集角范围从20°到160°。粒子散射光信号是脉冲信号，其频谱成份主要在高频段，所以在PIN型光电二极管后用一个带通式前置放大器来消除外界的低频噪声．根据米氏散射理论计算了该光学传感器的光散射响应特性，并用聚苯乙烯标准粒子实测了该光学传感器的性能。结果表明，该系统具有高的信噪

Subsurface damage in optical substrates

The origin, character, analysis and treatment of subsurface damage (SSD) were summarized in this paper. SSD, which was introduced to substrates by manufacture processes, may bring about the decrease of laser-induced damage threshold (LIDT) of substrates and thin films. Nondestructive evaluation (NDE) methods for the measurement of SSD were used extensively because of their conveniences and reliabilities. The principle, experimental setup and some other technological details were given for total internal reflection microscopy (TIRM), high-frequency scanning acoustic microscopy (HFSAM) and laser-modulated scattering (LMS). However, the spatial resolution, probing depth and theoretic models of these NDE methods demanded further studies. Furthermore, effective surface treatments for minimizing or eliminating SSD were also presented in this paper. Both advantages and disadvantages of ion beam etching (IBE) and magnetorheological finishing (MRF) were discussed. Finally, the key problems and research directions of SSD were summarized. (c) 2005 Elsevier GmbH. All rights reserved.

Stress-facilitated LTD induces output plasticity through a synchronized-spikes and spontaneous unitary discharges the CA1 region of the hippocampus

Long-term potentiation (LTP) and long-term depression (LTD) of the excitatory synaptic inputs plasticity in the hippocampus is believed to underlie certain types of learning and memory. Especially, stressful experiences, well known to produce long-lasting strong memories of the event themselves, enable LTD by low frequency stimulation (LFS, 3 Hz) but block LTP induction by high frequency stimulation (HFS, 200 Hz). However, it is unknown whether stress-affected synaptic plasticity has an impact on the output plasticity. Thus, we have simultaneously studied the effects of stress on synaptic plasticity and neuronal output in the hippocampal CA1 region of anesthetized Wistar rats. Our results revealed that stress increased basal power spectrum of the evoked synchronized-spikes and enabled LTD induction by LFS. The induction of stress-facilitated LTD but not LFS induced persistent decreases of the power spectrum of the synchronized-spikes and the frequency of the spontaneous unitary discharges; However, HFS induced UP in non-stressed animals and increased the power spectrum of the synchronized-spikes, without affecting the frequency of the spontaneous unitary discharges, but HFS failed to induce UP in stressed animals without affecting the power spectrum of the synchronized-spikes and the frequency of the spontaneous unitary discharges. These observations that stress-facilitated LTD induces the output plasticity through the synchronized-spikes and spontaneous unitary discharges suggest that these types of stress-related plasticity may play significant roles in distribution, amplification and integration of encoded information to other brain structures under stressful conditions. (C) 2004 Elsevier Ireland Ltd and The Japan Neuroscience Society. All rights reserved.

Spatial exploration induces a persistent reversal of long-term potentiation in rat hippocampus

Experience-dependent long-lasting increases in excitatory synaptic transmission in the hippocampus are believed to underlie certain types of memory(1-3). Whereas stimulation of hippocampal pathways in freely moving rats can readily elicit a long-term potentiation (LTP) of transmission that may last for weeks, previous studies have failed to detect persistent increases in synaptic efficacy after hippocampus-mediated learning(4-6). As changes in synaptic efficacy are contingent on the history of plasticity at the synapses(7), we have examined the effect of experience-dependent hippocampal activation on transmission after the induction of LTP, We show that exploration of a new, non-stressful environment rapidly induces a complete and persistent reversal of the expression of high-frequency stimulation-induced early-phase LTP in the CA1 area of the hippocampus, without affecting baseline transmission in a control pathway. LTP expression is not affected by exploration of familiar environments. We found that spatial exploration affected LTP within a defined time window because neither the induction of LTP nor the maintenance of long-established LTP was blocked. The discovery of a novelty-induced reversal of LTP expression provides strong evidence that extensive long-lasting decreases in synaptic efficacy may act in tandem with enhancements at selected synapses to allow the detection and storage of new information by the hippocampus.

Glucocorticoid receptor and protein/RNA synthesis-dependent mechanisms underlie the control of synaptic plasticity by stress

Learning and memory are exquisitely sensitive to behavioral stress, but the underlying mechanisms are still poorly understood. Because activity-dependent persistent changes in synaptic strength are believed to mediate memory processes in brain areas such as the hippocampus we have examined the means by which stress affects synaptic plasticity in the CA1 region of the hippocampus of anesthetized rats, Inescapable behavioral stress (placement on an elevated platform for 30 min) switched the direction of plasticity, favoring low frequency stimulation-induced decreases in synaptic transmission (long-term depression, LTD), and opposing the induction of long-term potentiation by high frequency stimulation, We have discovered that glucocorticoid receptor activation mediates these effects of stress on LTD and longterm potentiation in a protein synthesis-dependent manner because they were prevented by the glucocorticoid receptor antagonist RU 38486 and the protein synthesis inhibitor emetine. Consistent with this, the ability of exogenously applied corticosterone in non-stressed rats to mimic the effects of stress on synaptic plasticity was also blocked by these agents, The enablement of low frequency stimulation-induced LTD by both stress and exogenous corticosterone was also blocked by the transcription inhibitor actinomycin D, Thus, naturally occurring synaptic plasticity is liable to be reversed in stressful situations via glucocorticoid receptor activation and mechanisms dependent on the synthesis of new protein and RNA, This indicates that the modulation of hippocampus-mediated learning by acute inescapable stress requires glucocorticoid receptor-dependent initiation of transcription and translation.

N-methyl-D-aspartate receptor-dependent long-term potentiation in CA1 region affects synaptic expression of glutamate receptor subunits and associated proteins in the whole hippocampus

Long term potentiation in hippocampus, evoked by high-frequency stimulation, is mediated by two major glutamate receptor subtypes, alpha-amino-3-hydroxyl-5-methyl-4-isoxazole propionate receptors and N-methyl-D-aspartate receptors. Receptor subunit compos