Crosstalk is induced by a reflected wave of a load connected with a transmission line. Thus, analysis of the reflected wave is important. The reflected wave generated from a nonlinear load is complicated. In order to estimate the complicated reflected wave, we measured the reflected and incident waves for the nonlinear load and estimated the dynamic C-V characteristic, which explains the relation between the incident and reflected waves. This paper reports a simple experimental method of extracting reflected waves at a varactor load and presents estimates of the dynamic C-V characteristic of the load. It is shown that the reflected voltage waves simulated using the dynamic C-V characteristic agree with the measured results. (C) 2009 Wiley Periodicals, Inc. Electr Eng Jpn, 167(4): 32-38, 2009; Published online in Wiley InterScience (www. interscience.wiley.corn). DOI 10.1002/eej.20821

Generally, it is difficult to simulate crosstalk due to complicated reflected waves caused by the capacitive nonlinear load. In this letter, a simulation method for the reflected wave and the crosstalk using the V-Q characteristic of the load is described.

In this paper, a new simulation method for crosstalk simulation is described. To simulate the crosstalk accurately, accurate simulation of reflected voltages from loads is required. The authors have studied the simulation method of reflected voltages using a dynamic C-V characteristic. However, this method has a problem that the procedure of calculation becomes complicated. This paper proposes a new simulation method using V-Q characteristic. The proposed method reduces the amount of calculation for the simulation. The simulation accuracy is little lowered though the amount of calculation is much reduced.

Crosstalk analysis is getting more important for avoiding malfunction of circuits. In this paper, crosstalk analysis of parallel microstrip lines with a nonlinear capacitive load is described. A characteristic of the nonlinear capacitive load is changed by a rapidly change of an applied voltage of the load. The change of the characteristic induces a complicated reflected wave that causes complicated crosstalk. To simulate such crosstalk precisely, the dynamic C-V characteristic can be used. However, if the dynamic C-V characteristic is complicated, it takes a long time to simulate the crosstalk by using a conventional method. Thus, a simulation method using a recurrence formula is introduced. The recurrence formula is derived from a function of the dynamic C-V characteristic simply. The calculated results computed by using the introduced method agree with the measured crosstalk and the introduced method is superior in computation time to the conventional method. It is confirmed that the introduced method is effective in crosstalk simulation. (C) 2009 Institute of Electrical Engineers of Japan. Published by John Wiley & Sons, Inc.

In this paper, crosstalk analysis of parallel microstrip lines with a varactor load is described. The varactor load has a transition characteristic. The transition characteristic causes a complicated reflected wave. It is difficult to estimate crosstalk induced by the reflected wave accurately. To estimate the crosstalk, the transition characteristic is investigated. The transition characteristic is expressed as the dynamic C-V characteristic. The crosstalk is simulated using the dynamic C-V characteristic. The result of the simulation agrees with the measured crosstalk. This agreement shows that the dynamic C-V characteristic is effective to estimate crosstalk.

In crosstalk analysis, reflection of a load connected with terminating a transmission line is important. In order to investigate behavior of the reflection, we measured the reflected and the input voltages for the load, and estimated equivalent transition capacitances that explain a relation between the input and the reflected voltages. This paper reports an experimental method to extract reflected voltages at a varactor load and estimated results of the equivalent transition capacitance of the load. It is shown that the reflected voltages simulated using the equivalent capacitance agree with the measured results.

There is an increased incidence of schizophrenia-like psychosis in temporal lobe epilepsy (TLE), and several risk factors have been implicated, including the duration of epilepsy and temporal lobe neuropathology. To investigate the biological mechanism of epileptic psychosis, we examined alterations of central dopaminergic systems in the kainate model of TLE. In adult rats, kainate was microinjected into the left amygdala to induce status epilepticus. An indirect dopamine agonist methamphetamine (MAP, 2 mg/kg, i.p.) was administered before and 1 month after the kainate treatment. MAP-induced locomotor activity was significantly enhanced in the kainate group compared with the baseline (pre-kainate) level, which was antagonized by pretreatment with haloperidol. The enhancement of locomotor activity in the kainate group was significantly correlated with the density of hippocampal CA1 neurons. Although the basal extracellular dopamine concentration was significantly lower in the striatum in the kainate group than in the control group (5.5 vs 39.2 fmol/20-min sample), the maximal concentration following MAP administration did not differ between the two groups. These results clearly demonstrate that hypersensitivity of the dopamine systems develops in the chronic phase of the kainate-induced TLE model, which may be responsible for the mechanism of epileptic psychosis.

This study aimed at quantitatively evaluating hippocampal central-type benzodiazepine receptors (BZRs) in the kainate model of temporal lobe epilepsy (TLE) by in vitro autoradiography (ARG) using [125I] Iomazenil (IMZ) specific ligand for central-type BZRs. Kainate (1μg/0.5μl) was injected into the left amygdala to induce limbic status epilepticus. One, three, or six months after injection, in vitro ARG with [125I] IMZ and cell counts were performed in the hippocampal CA1–4 regions and dentate gyrus ipsilateral to the kainate injection site, and were compared with the vehicle-injected control group. In all kainate-treated rats, clear pyramidal neuron loss was observed in left hippocampal areas CA1–4. Compared with the control group, progressive reduction of [125I] IMZ binding was also observed. This resulted in a marked binding decrease paralleling pyramidal neuron loss in hippocampal areas CA1 (down to 83% of control), CA2 (76%), CA3 (75%), and CA4 (90%) at 6 months after kainate administration. Conversely, [125I] IMZ binding significantly increased in the dentate gyrus (up to 106% of control) at 1 month, but returned to nearly normal at 3–6 months. These results suggest that central-type BZR neuroimaging is useful in detecting hippocampal sclerosis in the mesial TLE, though central BZR alterations differ depending on hippocampal subfields and post-seizure time-courses.

Kindling of the ventral tegmental area (VTA), a major source of the mesolimbic dopamine pathway, was examined in rats. We applied two quantitative measurements of dopamine sensitivity before and 2 weeks after VTA kindling (20 times electrical stimulations (100 microA at 1 min intervals) delivered once per day for 14 consecutive days): behavioral responses induced by test VTA stimulation and methamphetamine (MAP)-induced locomotor activity. The total amount of MAP-induced locomotor activity was significantly increased after VTA kindling, while the responses to electrical stimulation were unchanged. These results indicate that repeated activation of the mesolimbic dopamine system can produce a neuroplastic change, which results in dopamine supersensitivity.

側頭葉てんかんにおける海馬歯状回顆粒細胞新生の病理学的意義に関して、ラットのカイニン酸扁桃核局所注入モデルを用いて研究した。海馬歯状回顆粒細胞層におけるbromodeoxyuridine陽性細胞数を免疫組織化学法で検出し、CA1、CA3領域における細胞脱落も評価した。カイニン酸投与による辺縁系発作重積の5日後には両側海馬における歯状回前駆細胞の分裂が著明に増加し、その後のシナプス再構成などてんかん原性変化の成因となる可能性が示唆された。NMDA受容体拮抗薬であるMK-801（1mg/kg, i. p.）の単回前処置では、カイニン酸投与後のneurogenesis現象に影響が見られなかった。しかし、MK-801を3回投与した場合には軽度の抑制効果がみられた。一方、MK-801投与がCA1錐体細胞脱落に対して選択的な細胞保護効果を示すことが確認された。以上より、神経細胞脱落は顆粒細胞のneurogenesis促進に必須ではなく、NMDA受容体の活性化が部分的に関与するものと結論された。

Since delusional disorder is characterized by mono-symptomatic paranoid symptoms, it can be a good clinical model for investigating the dopaminergic mechanism responsible for paranoid symptoms. We examined neuroleptic responses, plasma homovanillic acid (pHVA) and genes of the dopamine receptor (DR) and its synthesizing enzyme (tyrosine hydroxylase: TH) in patients with delusional disorder and compared them with those of schizophrenic patients and healthy controls. Results: (1) A relatively small dose of haloperidol was more effective for delusional disorder than for schizophrenia. (2) The pretreatment level of pHVA was higher in patients with persecution-type, but not in those with jealousy-type delusional disorder, compared with age- and sex-matched controls. This increased pHVA level was decreased eight weeks after successful haloperidol treatment. (3) The genotype frequency of the DRD2 gene Ser311Cys was significantly higher in patients with persecution-type delusional disorder (21%), compared with schizophrenic patients (6%) or controls (6%). (4) Patients homozygous for the DRD3 gene Ser9Ser had higher pretreatment levels of pHVA than those heterozygous for Ser9Gly. (v) A significant positive correlation was found between the polymorphic (TCAT) n repeat in the first intron of the TH gene and pretreatment levels of pHVA in delusional disorder. We suggest that delusional disorder, especially the persecution-type, includes a “dopamine psychosis,” and that polymorphism of the DRD2, DRD3 and/or TH gene is part of the genetic basis underlying the hyperdopaminergic state that produces paranoid symptoms. Further studies on a large sample size are required.

The glutamatergic system has been shown to be important for the induction of epileptiform activity and the development of epileptogenesis. To investigate the role of the astroglial glutamate transporter GLAST in epileptogenesis, we examined amygdala (AM)-kindled and pentylenetetrazole (PTZ)-induced seizures in GLAST-deficient mice (GLAST(−/−)) and compared them to those observed in wild-type mice (GLAST(+/+)) and maternal C57Black6/J (C57) mice. AM-kindling resulted in no significant differences in afterdischarge threshold or in the seizure responses induced by first stimulation between these groups. In addition, although no significant differences were seen in kindled seizure development, the generalized seizure duration of AM-kindled seizures in GLAST(−/−) mice was significantly prolonged (approximately 35%) compared with that of C57 mice. Furthermore, GLAST(−/−) mice showed more severe stages of PTZ-induced seizures than GLAST(+/+) mice, and the latency to the onset of seizures was significantly shorter for the mutant mice. These results indicate that GLAST is one of factors determinig seizure susceptibility.