抑制性频谱整合对大棕蝠下丘神经元声强敏感性的影响

自由声场条件下 ,采用特定双声刺激方法研究了不同频率通道之间的非线性整合对下丘神经元声强敏感性的调制作用。实验在 1 2只麻醉与镇定的大棕蝠 (Eptesicusfuscus)上进行 ,双电极同步记录 2个配对神经元的声反应动作电位。主要结果如下 :1 )所获 1 1 0个 (5 5对 )配对神经元中 ,85 5 %表现为抑制性频谱整合作用 ,其余 1 4 5 %为易化性频谱整合 ;2 )阈上 1 0dB (SPL)放电率抑制百分比与神经元最佳频率 (BF)及记录深度呈负相关 ;3)抑制效率随声刺激强度升高而逐步下降 ;4 )当掩蔽声分别位于神经元兴奋性频率调谐曲线(FTC)内 (MSin) /外 (MSout)时 ,其抑制效率存在差异。前者的放电率抑制百分比及声反应动力学范围(DR)下降百分比均显著高于后者 ;5 )抑制性频谱整合导致 3类DR改变 :6 1 6 %为下降、 1 0 9%增加、另有2 7 5 %变化小于 1 0 %。本结果进一步支持如下设想 :下丘不同频率通道之间的抑制性频谱整合参与了对强度编码的主动神经调制活动     

弱噪声对小鼠下丘神经元频率调谐的影响

为探讨弱噪声对小鼠 (MusmusculusKm)中脑下丘 (inferiorcolliculus ,IC)神经元声信号提取的影响 ,采用单位胞外记录方法 ,研究了加入弱白噪声 (强度相当于纯音阈强度下 5dB)前后神经元频率调谐曲线的变化。实验共记录到 10 4个下丘神经元 ,测量了 32个神经元的频率调谐曲线。结果显示 :①弱噪声条件下神经元的频率调谐曲线表现出 3种类型 ,即锐化 (34 4 % ,11/ 32 )、拓宽 (18 8% ,6 / 32 )和不受影响 (4 6 9% ,15 / 32 ) ,其中锐化呈现有意义的变化 ;②频率调谐受弱噪声锐化的神经元 ,其Q10 、Q3 0 平均分别增大 (34 4 2±17 0 4 ) % (P =0 0 2 6 ,n =11)和 (4 6 34± 2 2 88) % (P =0 0 0 9,n =7) ,且Q3 0 变化率大于Q10 ;③弱噪声对调谐曲线的高、低频边锐化度不一 ,神经元低频边的反转斜率基本不变 [由 0 16± 0 0 8变为 0 16± 0 0 7kHz/dB (P =0 94 7,n =7) ],而高频边明显下降 [由 0 5 2± 0 2 5下降为 0 2 6± 0 13kHz/dB ,平均减小 (4 3 81±2 4 0 6 ) % ,(P =0 0 4 6 ,n =7) ]。上述结果表明 ,弱噪声可锐化小鼠IC神经元频率调谐 ,并强化神经元的声信号高频分析能力     

大蹄蝠回声定位信号特征与下丘神经元频率调谐

采用超声监测仪录制超声信号和细胞外电生理记录下丘神经元的频率调谐曲线(frequency tuningcurqes,FTCs)的方法,探讨了大蹄蝠(Hipposideros armiger)回声定位信号与下丘(inferior colliculus,IC)神经元频率调谐之间的相关性.结果发现,大蹄蝠回声定位叫声为恒频-调频(consrant frequency-frequenevmodulated,CF-FM)信号,一般含有2-3个谐波,第二谐波为其主频,cF成分频率(Mean±SD,n=18)依次为:(33.3 4±0.2)、(66.5±0.3)、(99.4 4±0.5)kHz;电生理实验共获得72个神经元的频率调谐曲线,Q10-dB值的范围是0.5-95.4(9.2±14.6,rg=72),最佳频率(best frequency,BF)在回声定位主频附近的神经元具有尖锐的频率调谐特性.结果表明,大蹄蝠回声定位信号与下丘神经元频率调谐存在相关性,表现为最佳频率在回声定位信号主频附近的神经元频率调谐曲线的Q10-dB值较大,具有很强的频率分析能力.     

普氏蹄蝠下丘CF-CF联合敏感神经元的声反应

为了研究普氏蹄蝠(Hipposideros pratti)下丘(IC)中恒频-恒频(CF-CF)联合敏感神经元声反应特性,以及易化型和抑制型CF-CF联合敏感神经元在IC高频表征区神经元中所占的比例,实验记录了普氏蹄蝠IC神经元在不同频率和声强下的单声反应以及在不同延迟下的双声反应。本实验采用在体细胞内电生理技术从7只听力正常的蝙蝠上共获得77个IC声敏感神经元。所获得的数据经过处理并应用Sigma Plot 10.0软件作图。研究结果显示,77个神经元中37(48.1%)个为CF-CF联合敏感神经元,且多数为抑制型(24/37),少数为(13/37)易化型。实验结果说明普氏蹄蝠IC中既存在易化型也存在抑制型CF-CF联合敏感神经元,其中抑制型CF-CF联合敏感神经元比易化型所占比例更高。这些CF-CF联合敏感神经元有助于蝙蝠在巡航过程中处理回声信息时进行频谱和时相的整合。     

小鼠下丘神经元声反应的性别差异

采用自由声场的纯音短声刺激研究昆明小鼠下丘神经元听反应特征的性别差异。结果表明,①下丘神经元放电形式雌性以相位型为主,雄性以持续紧张型为主,且持续紧张型出现率存在明显的性差(P<005);②最佳频率分布雌雄都主要集中在10～20kHz,而潜伏期分布雌性较雄性集中;③最小阈值分布雌性主要集中于40～63dBSPL,而雄性无明显的集中区;④神经元最大发放雌性明显高于雄性(P<001);⑤脉冲发放函数和潜伏期函数的类型雌雄相同,但非单调型潜伏期函数出现率雄性明显高于雌性(P<001);⑥小鼠下丘神经元频率调谐曲线被分成五类,各类出现率在雌雄间无明显差异,但宽阔型频率调谐曲线百分率雌性明显高于雄性(P<005),且雌性频率调谐曲线高频边反转斜率明显高于雄性(P<005)。因此提示,雌雄小鼠下丘神经元声反应特征存在一定的差异。     

普氏蹄蝠下丘谐波主频神经元的时程选择性

为探讨下丘(Inferior colliculus,IC)回声定位信号主频范围内的神经元的时程选择性,在自由声场刺激条件下,我们在4 只普氏蹄蝠的IC 采用不同时程的声刺激,研究了神经元的时程选择性。通过在体细胞外记录,共获得56 个声敏感下丘神经元,其记录深度、最佳频率和最小阈值的范围分别为1547 - 3967 (2878. 9 ±629.1)μm,20 -68 (49.0 ± 11. 1)kHz 和36.5 -95. 5 (59. 8 ±13. 0)dB SPL。根据所记录到的下丘神经元对不同时程的声刺激的反应,即对不同时程的选择性(Duration selectivity),将其分为6 种类型:短通型(Short-pass,SP,n = 11/56)、带通型(Band-pass,BP,n = 1/56)、长通型(Long-pass,LP,n = 5 /56)、反带通型(Band-reject,BR,n = 3 /56)、多峰型(Multi-peak,MP,n =6 /56)和全通型(All-pass,AP,n =30 /56)或非时程选择型(Nonduration-selective,NDS)。通过比较普氏蹄蝠下丘谐波主频内和主频外神经元的时程选择性,我们发现处于回声定位信号主频范围内神经元(n =32)比主频外神经元(n = 24)具有更短的最佳时程和更高的时程选择性。结果提示,在普氏蹄蝠回声定位过程中谐波主频内神经元较谐波主频外神经元发挥了更为重要的作用。     

菲菊头蝠的下丘神经元基本声反应特性

自由声场刺激条件下,采用单单位胞外微电极记录方法,研究了一种未被研究过的恒频/调频(CF/FM)蝙蝠———菲菊头蝠(Rhinolophuspusillus)的下丘神经元基本声反应特性,其结果发现,在所得的110个下丘神经元中,发放类型包括相位型(54·5%)、紧张型(25·5%)、持续型(7·3%)、梳齿型(7·3%)和暂停型(5·4%)等5种类型。记录深度在208~1855(829·0±328·1)μm之间,最佳频率在16·7~75·6(38·9±15·7)kHz之间,最小阈值在5~74(34·7±13·6)dBSPL之间,阈上10dBSPL潜伏期在5·0~27·5(15·2±3·9)ms之间。最佳频率随记录深度的增加而增大(r=0·9578,P<0·001);记录的54个频率调谐曲线(FTCs)均为开放型,其中52个为单峰型,2个为双峰型。52个单峰型FTC的Q10-dB值介于1·56~31·61之间,并且大部分是狭窄型(Q10-dB值>5),占69·2%(36/52),少部分为宽阔型(Q10-dB值<5),占30·8%(16/52)。2个双峰型神经元FTC在低频处为宽阔型,高频处为狭窄型,Q10-dB值分别为1·95、8和2·89、6·51。共获得34个神经元的强度-发放率函数(RIFs),可分为单调型、非单调型和饱和型。结合先前所研究的FM蝙蝠———普通伏翼蝠(Pipistrellusabramus)下丘神经元的基本声反应特性,比较分析了CF/FM蝙蝠与FM蝙蝠下丘神经元的声反应差异及其行为学意义。     

偏离最佳频率的声信号对几内亚长翼蝠下丘神经元的前掩蔽

为探讨偏离神经元最佳频率(best frequency,BF)的声刺激对下丘神经元的前掩蔽效应,实验选用5只听力正常的几内亚长翼蝠(Miniopterus magnater),记录它们的下丘神经元对偏离BF的掩蔽声和探测声(BF)的反应.结果发现,当掩蔽声向高或低频方向偏离神经元的BF时,掩蔽效应逐渐降低.根据计算出的...     

调频声的调制范围和刺激呈现率对小鼠下丘神经元听反应的影响(英文)

在自然声环境中,多数与生命活动相关的声音都包含有调频声成分,这些调频声往往都具有不同的调制范围和重复率。本研究采用常规电生理技术检测小鼠下丘神经元对具有不同调制范围和刺激呈现率声信号的反应情况。在所记录的90 个下丘神经元中,超过60% 的神经元对较窄的调制范围有最好的反应(窄通型,上扫:60.00%, 54/90;下扫:63.33%,57/90),其它少部分的反应类型有带通型(上扫:16.67%,15/90;下扫:18.89%,17/90)、宽通型(上扫:4.44%, 4/90;下扫:4.44%, 4/90)和全通型(上扫:18.89%, 17/90;下扫:13.33%, 12/90)。当使用不同的刺激呈现率后(从0.5 次 /s 到10 次 /s),神经元的发放率和发放时程随着刺激呈现率的升高而缩短,而潜伏期则逐渐增加。另外,调制范围和刺激呈现率都会影响下丘神经元对调频声上下扫的方向选择性。以上结果表明小鼠中脑下丘神经元对调频声刺激反应的时相特征可受到调制范围和刺激呈现率的调制,其神经机制可能与下丘神经元的频谱以及时相整合有关。     

后掩蔽效应对大棕蝠下丘神经元声反应的影响

以回声定位蝙蝠为模式动物,采用在体动物细胞外单位记录法,研究了后掩蔽效应对下丘神经元声反应的影响。结果显示,部分神经元(38％,12／31)对测试声刺激的反应明显受到掩蔽声的抑制,其后掩蔽效应强弱与掩蔽声和测试声的相对强度差(inter-stimulus level difference,SLD),以及测试声与掩蔽声之间的间隔时间(inter-stimulus onset asynchrony,SOA)有关：当掩蔽声强度升高或测试声强度降低时,后掩蔽效应增强;而SOA的缩短,亦可见后掩蔽效应增强。另外,相当数量的神经元(52%,16／31)对测试声刺激的反应并不受掩蔽声的影响,其中有的神经元只有在特定SLD和SOA时,才表现出后掩蔽效应。而少数下丘神经元(10％,3／31)在特定SLD和SOA时,掩蔽声对测试声反应有易化作用。上述结果表明,部分下丘神经元参与了声认知活动中的后掩蔽形成过程,推测下丘神经元在定型声反应特性中,对掩蔽声诱导的兴奋前抑制性输入与测试声诱导的兴奋性输入之间的时相性动态整合起关键作用。     

幼小蝙蝠下丘神经元的听反应特性

实验在出生6—8天的8只幼龄鲁氏菊头蝠(Rhinolophus rouxi)上进行。使用玻璃微电极记录中脑下丘听神经元对超声信号的反应。共观察了162个听单位,它们对超声反应的最佳频率分布范围为25.8—60.9千赫,多数集中在43.0—47.0千赫。反应的潜伏期在6.0—38.0毫秒,平均为15.4±5.2毫秒。反应的最低阈值在25—84dB,平均为69.8±10.3dB.这些神经元对超声刺激的调谐曲线都较宽阔,故Q10-dB值都较小。当微电极由下丘表面垂直下插时,所记录到的神经元的最佳频率与记录深度之间不存在相关关系,即没有音调筑构现象。听神经元的这些特性与同种成年动物构成显著差异。     

Frequency tuning, latencies, and responses to frequency-modulated sweeps in the inferior colliculus of the echolocating bat, Eptesicus fuscus

Neurons in the inferior colliculus (IC) of the awake big brown bat, Eptesicus fuscus, were examined for joint frequency and latency response properties which could register the timing of the bat's frequency-modulated (FM) biosonar echoes. Best frequencies (BFs) range from 10 kHz to 100 kHz with 50% tuning widths mostly from 1 kHz to 8 kHz. Neurons respond with one discharge per 2-ms tone burst or FM stimulus at a characteristic latency in the range of 3–45 ms, with latency variability (SD) of 50 μs to 4–6 ms or more. BF distribution is related to biosonar signal structure. As observed previously, on a linear frequency scale BFs appear biased to lower frequencies, with 20–40 kHz overrepresented. However, on a hyperbolic frequency (linear period) scale BFs appear more uniformly distributed, with little overrepresentation. The cumulative proportion of BFs in FM₁ and FM₂ bands reconstructs a scaled version of the spectrogram of FM broadcasts. Correcting FM latencies for absolute BF latencies and BF time-in-sweep reveals a subset of IC cells which respond dynamically to the timing of their BFs in FM sweeps. Behaviorally, Eptesicus perceives echo delay and phase with microsecond or even submicrosecond accuracy and resolution, but even with use of phase-locked FM and tone-burst stimuli the cell-by-cell precision of IC time-frequency registration seems inadequate by itself to account for the temporal acuity exhibited by the bat. Accepted: 21 June 1997     

电刺激蝙蝠中脑上丘对下丘听神经元电活动的影响

实验在24只鲁氏菊头蝠(Rhinolophus rouxi)上进行.使用玻璃微电极在中脑下丘中央核记录听神经元电反应.刺激点位于上丘核.共观察了294个对超声刺激产生反应的下丘听单位.当电刺激上丘时,有122个听单位的反应受到影响,占所观察总数的41.5%.其中96个单位表现为抑制性影响(占32.65%),26个单位表现为易代性效应(占8.84%).其余172个单位不受上丘刺激的影响(58.50%).实验中发现,上述抑制潜伏期一般在5毫秒以上,抑制时程较长.抑制程度与上丘刺激电流强度呈相关关系(r=0.99).实验中还发现,刺激上丘同样可抑制部分下丘神经元的自发放电活动,其抑制后效应相当长,有的可达120毫秒以上.     

Synthesis of rat hepatic zinc thionein in response to the stress of sham operation

Following sham operation for adrenalectomy, a dramatic 30-fold increase in rat hepatic zinc thionein occurs, peaking at 18 hours after surgery. Hepatic cytosolic and serum zinc levels rise concomitantly with zinc thionein. Copper in hepatic thionein and cytosol rises only slightly and serum copper not at all during the period of observation. In the period 18 to 48 hours after surgery the content of hepatic zinc thionein decreases with a $\text{t}\text{1}\text{2}$ of 16.4 hours.Pretreatment with cycloheximide (1 mg/kg b.w.) two hours before surgery inhibits the rise in zinc thionein by 52%, the rise in cytosolic zinc by 56%, and actually causes a decrease in serum zinc by 33%. Pretreatment with the α-adrenergic receptor blocker, phetolamine (10 mg/kg b.w.), or the β-adrenergic receptor blocker, propranolol (10 mg/kg b.w.), 30 minutes before surgery also inhibited the rise in zinc thionein (82% and 60%, respectively) and cytosolic zinc (75% and 47%, respectively), and decreased serum zinc (38% and 44%, respectively) 19 hours after surgery.Treatment with corticosterone (40 mg/kg b.w.) alone or epinephrine (1–20 μg/kg b.w.) alone did not alter hepatic zinc thionein levels 18 hours late, although they each caused hypozincemia and epinephrine raised cytosolic zinc levels. Treatment with corticosterone and epinephrine together did, however, raise zinc thionein levels 3.2-fold (P<0.02).These experiments are consistent with the hypothesis that adrenal hormones are involved in the regulation of zinc metabolism, and, hence, zinc thionein in levels in rat liver following the stress of sham operation.     

Fate of DNA lesions that elicit sister-chromatid exchanges

Using 3-way differential staining (TWD) of sister chromatids, the fate of DNA lesions involved in sister-chromatid exchange (SCE) formation was determined in murine bone marrow cells in vivo, after treatment with either mitomycin C (MMC) or cyclophosphamide (CP). Both MMC (2.6 mg/kg b.w.) and CP (7 mg/kg b.w.) induced an SCE frequency near the expected in the 2 subsequent cell divisions, but the frequency of SCE occurring at the same locus in successive cell divisions was substantially lower than expected. The results are compared with previous data obtained after exposure to gamma-rays. A model of SCE induction is proposed.     

菊头幅出生后下丘听神经元反应特性的演化

实验在出生后1周到6周的幼年和成年鲁氏菊头蝠(Rhinolophusrouxi)上进行。结果发现,出生第1周的动物下丘听神经元对超声刺激反应的最佳频率低,潜伏期长,阈值高。它们的平均值分别为:31.24±14.08千赫,16.56±3.83毫秒和74.24±6.22dB。同时,调谐曲线宽阔,Q10-dB值小,其均值为2.34±0.96。随着周令增长,上述特性逐渐改变。到第6周时,最佳频率的均值发展到70.16±19.16千赫,最佳频率分布峰值也移至75—85千赫的高频段,反应潜伏期均值降至8.12±1.86毫秒,阈值均值降至32.82±26.36dB,已出现相当多具有非常陡削调谐曲线的神精元,Q10-dB值在20以上者占到80％,有的高达100以上,已接近成年动物。     

Induction of chromosome aberrations, micronucleus formation and sperm abnormalities in mouse following carbofuran exposure

Carbofuran was tested to study in vivo cytogenetic effects in mouse bone marrow cells and morphological alterations in sperms. The acute oral and intraperitoneal (i.p.) LD(50) of carbofuran was determined to be 9.5 or 2.0 mg/kg b.w. in mice, respectively. The animals were orally administered 1.9, 3.8 or 5.7 mg/kg b.w. (20, 40 and 60% of LD(50)) of carbofuran for 24 h or 1.9 mg/kg b.w. for 4 consecutive days (cumulative 7.6 mg/kg or 80% of LD(50)) to analyse chromosome aberrations (CAs). For micronucleus test (MT) animals were orally exposed to 5.7 mg/kg b.w. for 24 and 48 h or 1.9 mg/kg b.w. for 4 consecutive days. For reference mice were exposed to peanut oil (negative control) and cyclophosphamide (20 mg/kg) or ethyl methanesulfonate (EMS: 100 mg/kg) positive control for CAs and MT respectively. To analyse the effect on sperm morphology mice were exposed to single i.p. dose of 1 and 2 mg/kg b.w. of carbofuran and repeatedly to 0.5 mg/kg for 5 consecutive days. Cytogenetic analysis revealed that all the test doses induced mitotic inhibition, CAs, micronucleus (MN) formation and sperm abnormalities in a dose dependent manner. Present observations concurrent with earlier reports substantiate the genotoxic potential of carbofuran and possible risk to human beings.     

Subclinic effect of the administration of T-2 Toxin and Nivalenol in mice

Four experiments using T-2 toxin and nivalenol at different dosage, which represented the 25% and 40% of the LD50 (experiment A: 1.04 mg of T-2 toxin per kilogram of body weight, experiment B: 2.34 mg of T-2 toxin/kg b.w., experiment C: 1.04 mg of T-2 toxin/kg b. w. and 2.34 mg of T-2 toxin/kg b.w.; experiment D: 0.82 mg of nivalenol/kg b.w. and 1.845 mg of nivalenol/kg b.w.) were conducted on 400 mice. Both toxins were administered to mice of different ages (experiments A and B were adults, experiment C and D were young) by intraperitoneal single injection, and the clinical signs, hematological variables and histoanatomo pathological changes were studied. All animals survived. No changes anatomo-histopathological nor significative differences in weight gain were observed. Different behaviors were found for nivalenol and T-2 toxin. The most significant change was the increase in the level of monocytes in old animals, so this could be a biological indicator for T-2 toxin subclinical intoxication.     

Short-term oral exposure to aluminium decreases glutathione intestinal levels and changes enzyme activities involved in its metabolism

To study the effects of aluminium (Al) on glutathione (GSH) metabolism in the small intestine, adult male Wistar rats were orally treated with AlCl3.6H2O at doses of 30, 60, 120 and 200 mg/kg body weight (b.w.) per day, during seven days. Controls received deionized water. At doses above 120 mg/kg b.w., Al produced both a significant reduction of GSH content and an increase of oxidized/reduced glutathione ratio (P < 0.05). The index of oxidative stress of the intestine mucosa in terms of lipid peroxidation evaluated by thiobarbituric acid reactive substances was significantly increased (52%) at higher Al dose used. The duodenal expression of the multidrug resistance-associated protein 2 in brush border membranes, determined by Western blot technique, was increased 2.7-fold in rats treated with 200mg AlCl3/kg b.w (P < 0.01). Intestine activities of both GSH-synthase (from 60 mg/kg b.w.) and GSSG-reductase (from 120 mg/kg b.w.) were significantly reduced (26% and 31%, respectively) while glutathione-S-transferase showed to be slightly modified in the Al-treated groups. Conversely, gamma-glutamyltranspeptidase activity was significantly increased (P < 0.05) due to the Al treatment. Al reduced in vitro mucosa-to-lumen GSH efflux (P < 0.05). A positive linear correlation between the intestine GSH depletion and reduction of in situ 45Ca intestinal absorption, both produced by Al, was found (r = 0.923, P = 0.038). Taking as a whole, these results show that Al would alter GSH metabolism in small intestine by decreasing its turnover, leading to an unbalance of redox state in the epithelial cells, thus contributing to deteriorate GSH-dependent absorptive functions.