Histamine and noradrenaline decrease calcium-activated potassium conductance in hippocampal pyramidal cells

Ample evidence exists for histaminergic and noradrenergic projections to the hippocampus. Both amines exert neurotransmitter or modulator actions on principal neurones in the CA 1 and in the dentate area. A number of mechanisms have been proposed for these actions, including increased potassium conductance, increased chloride conductance and electrogenic pump stimulation, and reduction of the anomalous inward rectification. Action potentials, and particularly bursts of spikes, in CA 1 pyramidal cells, are followed by an afterhyperpolarization (AHP) which consists of two components. The late AHP depends on a calcium-activated potassium conductance gK+ (Ca2+), and has recently been shown to be increased by dopamine. We report here a rapid and reversible decrease of the late AHP component following a burst of sodium spikes or a calcium spike, during perfusion with micromolar concentrations of histamine and noradrenaline. This effect is mediated by H2 receptors and beta-receptors, respectively, and occurred in the absence of changes in the calcium spike. By such a mechanism histamine and noradrenaline can profoundly potentiate the excitatory impact of depolarizing signals.     

Phorbol esters block a voltage-sensitive chloride current in hippocampal pyramidal cells

The importance of second-messenger systems in controlling the excitability of neurones and other cells, through modulation of voltage- and calcium-dependent ionic conductances, has become increasingly clear. Cyclic AMP, acting via protein kinase A, has been identified as the second messenger for several neurotransmitters, and recent studies have suggested that activation of protein kinase C may have similar modulatory actions on neurones. Calcium and potassium currents have so far been shown to be the major ionic conductances modified by kinase activation. We now report that hippocampal pyramidal cells contain a previously undescribed voltage-dependent chloride current which is active at resting potential and is turned off either by membrane depolarization or by activation of protein kinase C by phorbol esters. We propose that this current may reside predominantly in the cell's dendritic membrane and thereby may regulate dendritic excitability.     

Spike train dynamics predicts theta-related phase precession in hippocampal pyramidal cells

According to the temporal coding hypothesis, neurons encode information by the exact timing of spikes. An example of temporal coding is the hippocampal phase precession phenomenon, in which the timing of pyramidal cell spikes relative to the theta rhythm shows a unidirectional forward precession during spatial behaviour. Here we show that phase precession occurs in both spatial and non-spatial behaviours. We found that spike phase correlated with instantaneous discharge rate, and processed unidirectionally at high rates, regardless of behaviour. The spatial phase precession phenomenon is therefore a manifestation of a more fundamental principle governing the timing of pyramidal cell discharge. We suggest that intrinsic properties of pyramidal cells have a key role in determining spike times, and that the interplay between the magnitude of dendritic excitation and rhythmic inhibition of the somatic region is responsible for the phase assignment of spikes.     

Transformation from temporal to rate coding in a somatosensory thalamocortical pathway

The anatomical connections from the whiskers to the rodent somatosensory (barrel) cortex form two parallel (lemniscal and paralemniscal) pathways. It is unclear whether the paralemniscal pathway is directly involved in tactile processing, because paralemniscal neuronal responses show poor spatial resolution, labile latencies and strong dependence on cortical feedback. Here we show that the paralemniscal system can transform temporally encoded vibrissal information into a rate code. We recorded the representations of the frequency of whisker movement along the two pathways in anaesthetized rats. In response to varying stimulus frequencies, the lemniscal neurons exhibited amplitude modulations and constant latencies. In contrast, paralemniscal neurons in both thalamus and cortex coded the input frequency as changes in latency. Because the onset latencies increased and the offset latencies remained constant, the latency increments were translated into a rate code: increasing onset latencies led to lower spike counts. A thalamocortical loop that includes cortical oscillations and thalamic gating can account for these results. Thus, variable latencies and effective cortical feedback in the paralemniscal system can serve the processing of temporal sensory cues, such as those that encode object location during whisking. In contrast, fixed time locking in the lemniscal system is crucial for reliable spatial processing.     

Optical imaging of calcium accumulation in hippocampal pyramidal cells during synaptic activation

The dynamic response of nerve cells to synaptic activation and the spatial distribution of biochemical processes regulated by ion concentration are critically dependent on the cell-surface distribution of ion channels. In the hippocampus, intracellular calcium-ion concentration is thought to influence the biochemical events associated with kindling, excitotoxicity, and long-term potentiation. Computer models of hippocampal pyramidal cells also indicate that calcium-channel location influences dynamic characteristics such as bursting. Here, we have used in situ microfluorometric imaging in brain slices to directly measure the spatial distribution of calcium accumulation in guinea-pig CA1 pyramidal cells during trains of orthodromic synaptic stimulation. Calcium accumulation is substantial throughout the entire proximal section of the apical and basal dendrites. Most of this accumulation results from influx through non-NMDA (N-methyl-D-aspartate) voltage-gated calcium channels, and in the apical dendrite it drops steeply as the dendrite enters stratum moleculare, the termination zone of perforant path afferents. These results demonstrate a marked segregation of calcium-channel activity and directly show a spatial distribution of calcium accumulation during orthodromic synaptic activation.     

Protein kinase C injection into hippocampal pyramidal cells elicits features of long term potentiation

Long-term potentiation (LTP) in the hippocampus is an interesting example of synaptic plasticity because of its induction by physiological discharge rates and its long duration. Of the possible biochemical mechanisms that regulate prolonged changes in cell function, protein phosphorylation is a particularly attractive candidate. We have therefore examined the effect of intracellular injection of calcium/diacylglycerol-dependent protein kinase (protein kinase C (PKC] in CA1 pyramidal neurones in hippocampal slices. Injection of the active enzyme elicited long-lasting enhancement of synaptic transmission, similar to LTP, whereas inactivated kinase failed to do so. The observed changes included an increased amplitude of the excitatory post-synaptic potential (e.p.s.p.) and an increased probability of firing and a reduced latency of the associated actin potential.     

Postsynaptic NMDA receptor-mediated calcium accumulation in hippocampal CA1 pyramidal cell dendrites

In the CA1 hippocampal region, intracellular calcium is a putative second messenger for the induction of long-term potentiation (LTP), a persistent increase of synaptic transmission produced by high frequency afferent fibre stimulation. Because LTP in this region is blocked by the NMDA (N-methyl-D-aspartate) receptor antagonist AP5 (DL-2-amino-5-phosphonovaleric acid) and the calcium permeability of NMDA receptors is controlled by a voltage-dependent magnesium block, a model has emerged that suggests that the calcium permeability of NMDA receptor-coupled ion channels is the biophysical basis for LTP induction. We have performed microfluorometric measurements in individual CA1 pyramidal cells during stimulus trains that induce LTP. In addition to a widespread component of postsynaptic calcium accumulation previously described, we now report that brief high frequency stimulus trains produce a transient component spatially localized to dendritic areas near activated afferents. This localized component is blocked by the NMDA receptor antagonist AP5. The results directly confirm the calcium rise predicted by NMDA receptor models of LTP induction.     

Independent evolution of structural and coding regions in a Neurospora mitochondrial intron

The discovery of intervening sequences (introns) in eukaryotic genes has raised questions about the origin and evolution of these sequences. Hypotheses concerning these topics usually consider the intron as a unit that could be lost or gained over time, or as a region within which recombination can occur to facilitate the production of new proteins by exon shuffling. Additional complexities are observed in introns of mitochondrial and chloroplast genes which contain secondary structures required for messenger RNA splicing and open-reading frames encoding proteins. Here we describe differences in the organization of protein-coding sequences in the intron of the mitochondrial ND1 gene in two closely related species of Neurospora. These differences show that intron sequences involved in secondary structure formation and in protein coding can evolve as physically distinct elements. Indeed, the secondary structure elements of the ND1 intron can contain two different coding sequences located at two different positions within the intron.     

基于时序卷积网络的信道编码闭集识别

针对传统识别算法对信号的先验知识要求较高、人工特征提取复杂、低信噪比环境下识别率较低等问题,提出了一种基于时序卷积网络(TCN)的卷积码参数识别方法．引入了深度学习算法处理盲识别问题,依据卷积码的马尔可夫性,将码字作为时间序列处理,把已知类型的编码序列作为时序卷积网络模型的输入进行监督学习,根据训练好的模型对接收端接收到的未知编码信号进行闭集识别分类．实验结果表明：当信噪比大于5 dB时,单一参数类型与混合参数类型平均识别准确率分别大于99.60%和99.50%,且在相关算法对比中有较好的识别表现．     

MBE变速率语音编码研究

变速率、低码率的语音编码技术一直是语音编码中的重要课题，这一研究方向为解决信道带宽相对紧张和信息量日益膨胀的矛盾，显得尤为重要．在介绍了低速率语音编码的基础上，对变速率、低码率的多带激励编码算法进行了深入的研究，形成了2．4KbPs、1．8Kbps 2种码率的语音编码方案．非正式的听音测试显示，该方案具有较好的编码效果．     

Effects of lithium chloride on outward potassium currents in acutely isolated hippocampal CA1 pyramidal neurons

Lithium is best known for its therapeutic efficacy in the treatment of manic-depressive illness. Its clinical profile includes the antimanic and antidepressant ac- tions as well as prophylaxis of both mania and depres- sion. Despite its efficacy, the mole…     

一种短波通信中基于DSP的低速率语音编码技术

介绍了一种应用在短波通信中的码率为1．5Kbps低速率语音编码算法，此算法基于MELP（mixed excitation linearp rediction）混合激励线性预测语音编码算法的声码器模型，并对算法进行改进，降低复杂度和速率，在DSP芯片的硬件系统中实时运行了该算法，最后给出了算法测试仿真结果。     

Clustering of L-type Ca2+ channels at the base of major dendrites in hippocampal pyramidal neurons

Integration and processing of electrical signals in individual neurons depend critically on the spatial distribution of ion channels on the cell surface. In hippocampal pyramidal neurons, voltage-sensitive calcium channels have important roles in the control of Ca2(+)-dependent cellular processes such as action potential generation, neurotransmitter release, and epileptogenesis. Long-term potentiation of synaptic transmission in the hippocampal pyramidal cell, a form of neuronal plasticity that is thought to represent a cellular correlate of learning and memory, is dependent on Ca2+ entry mediated by synaptic activation of glutamate receptors that have a high affinity for NMDA (N-methyl(-D-aspartate) and are located in distal dendrites. Stimuli causing long-term potentiation at these distal synapses also cause a large local increase in cytosolic Ca2+ in the proximal regions of dendrites. This increase has been proposed to result from activation of voltage-gated Ca2+ channels. At least four types of voltage-gated Ca2+ channels, designated N, L. T and P, may be involved in these processes. Here we show that L-type Ca2+ channels, visualized using a monoclonal antibody, are located in the cell bodies and proximal dendrites of hippocampal pyramidal cells and are clustered in high density at the base of major dendrites. We suggest that these high densities of L-type Ca2+ channels may serve to mediate Ca2+ entry into the pyramidal cell body and proximal dendrites in response to summed excitatory inputs to the distal dendrites and to initiate intracellular regulatory events in the cell body in response to the same synaptic inputs that cause long-term potentiation at distal dendritic synapses.     

实时低速率语音压缩编码的算法研究

针对数字化通信网及多媒体应用中低速率数字语音编码问题，以多带激励（ＭＢＥ）声码器为模型，采用了一些新算法去降低编码速率和改善音质。利用动态规划算法对基音周期进行平滑，去除了声码器中常有的音调噪声。利用ＬＰＣ全极点模型谱逼近ＭＢＥ谱包络，并采用共振峰增强技术来补偿模型误差，有效地降低了编码速率。为了能够实时实现这个编码系统，采用了分裂矢量量化，多级矢量量化和前向多层人工神经网络等技术进行优化和改善，使之在２．４ｋｂｉｔ／ｓ，１．２ｋｂｉｔ／ｓ及８００ｂｉｔ／ｓ等速率上实时实现了较高质量的语音压缩编码。     

多参考预测链的时域可扩展性和抗错性

网络的带宽抖动和数据传输错误是影响视频传输的重要原因。该文提出了一种新的多参考帧图像预测的视频编码算法,即多参考预测链,使视频具有时域可扩展性和抗错性解决网络的这两个潜在问题。该算法中P帧之间的参考预测关系构成多条链状结构,使视频具有时域可扩展性。链间的不相关性使每个链可独立解码,从而增强了码流抗错性。该算法采用R-D框架动态的管理预测关系链,从而适合网络带宽的变化而获得最佳的终端视觉效果。仿真实验表明,采用多参考预测链编码的码流时域可扩展性的应用非常可行,且表现出较高的抗错性。     

H.264视频编码中的快速失真与速率估计算法

H.264视频编码标准采用率失真优化技术追求更高的编码效率。针对每一个宏块,编码器需要遍历多种帧内和帧间模式,复杂度较大,提出了模式选择中速率和失真的快速估计算法。该算法省去了模式判决中的反变换和熵编码过程,利用频域系数来直接估计宏块的编码失真和速率,且失真的估计能适于不同的宏块类型,速率的估计能自适应于视频的内容。仿真结果表明,对于多种类型的视频序列,该算法相对于参考算法能够提供较高的估计准确度,在保持编码率失真性能下降不多的条件下,节省了约35%的模式决定时间。     

移动无线互联网接入中视频编码码率的控制策略

建立了用于接入移动无线互联网的视频编码转换模型,提出了自适应运动矢量估值方法.将编码转换码率控制分为图像层控制和宏块层两级,首先对每帧图像的编码比特数进行预分配,然后采用小波变换系数来表征图像特征,为帧内不同特征的宏块选用不同的量化因子,提出一种新的码率控制策略.模拟实验结果表明该方法在视频图像质量没有明显失真的前提下,提高了视频编码转换速度;编码转换输出码流和编码转换缓冲区占用量较稳定,重建图像的信噪比得到明显的改善.