生后早期大鼠初级视皮层Ⅰ层中间神经元电学特性研究

目的:研究视觉发育可塑性关键期内大鼠初级视皮层Ⅰ层中间神经元的电学特性,以期通过分析其电学特性进一步区分神经元的类型。方法:采用脑片膜片钳全细胞记录技术,观察13～15天SD大鼠初级视皮层Ⅰ层单眼反应区(Oc1M)中间神经元的被动、主动电学特性和动作电位的发放特征。结果:大鼠初级视皮层Ⅰ层中间神经元动作电位的后电位表现为后去极化和后超极化两种形式。后去极化的幅度能够达到15.11±3.02 mV;而后超极化的幅度为-6.22±0.53 m V。基于后电位的不同,将Ⅰ层中间神经元分为后去极化神经元(ADPNs)和后超极化神经元(AHPNs)两类。对两类神经元的电学特性进行统计比较发现,ADPNs具有较高的静息电位、较低的阈电位和较高的能障(P<0.05)。此外,两类神经元在动作电位峰幅值、最大下降斜率、峰展宽以及频率适应性上均具有显著性差异(P<0.05)。结论:在视觉发育可塑性关键期内,大鼠初级视皮层Ⅰ层中间神经元可根据其电学特性分为ADPNs和AHPNs两种类型,二者可以进一步通过其被动和主动电学特性以及动作电位发放特性加以区分。     

L—谷氨酸及其拮抗剂对大鼠脑片旁巨细胞外侧核神经元自发放电的影响

作者在大鼠脑干脑片旁巨细胞外侧核（PGCL）区，用多管微电泳技术观察了微电泳谷氨酸（L-Glu)及其拮抗剂DL-2-氨酸-5-磷酸戊酸（AP5）对神经元自发放电的效应及AP5对L-Glu作用的影响。在51片脑片PGCL区共记录136个自发放电稳定的神经元，主要呈重复放电样式，L-Glu和AP5对自发放电均有兴奋，抑制和无影响三种效应，各占所测试神经元的80.65%,8.06%,11.29%(L-Glu)和28.00%,8.00%,64.00%(AP5)。兴奋反应呈量效依赖关系。AP5部分地阻断部分神经元（71.87%)对L-Glu的兴奋作用，结果表明大鼠离体脑片PGCL区神经元自发放电样式主要是重复放电，并从细胞水平上提示PGCL区有起递质作用的内源性兴奋性氨基酸（FAA），其神经元上有N-甲基-D-天冬氨酸（NMDA）和非NMDAEAA受体亚型。     

苯妥英与加巴喷丁对藜芦碱致大鼠海马CA1神经元癫痫样放电的不同影响

目的观察治疗剂量的苯妥英与加巴喷丁对小剂量(0·5μmol/L)藜芦碱诱发大鼠海马神经元癫痫样放电的作用,分析其可能的细胞学机制。方法通过膜片钳全细胞记录技术,胞外灌流0·5μmol/L藜芦碱,制作大鼠海马CA1锥体神经元癫痫样放电模型,如果在灌流30min内出现振荡样放电[长簇(bursting)放电],即认为造模成功。分别在电压钳模式下观察2·5、5、10、15μmol/L苯妥英和2·5、5、10μmol/L加巴喷丁对这种癫痫活动的影响;测定藜芦碱灌流后CA1锥体神经元Ih电流的变化规律。结果藜芦碱(0·5μmol/L)灌流9～16min后,海马CA1锥体神经元出现节律性巨大慢波振荡,100～200Hz的连续高频放电骑跨其上,类似于癫痫生理学中的阵发性去极化漂移(PDS)现象,证明造模成功。苯妥英可阻断藜芦碱诱发的癫痫样活动,且随浓度递增,簇放电间期逐渐延长,但单个簇放电持续时间并不缩短。在藜芦碱致痫过程中,Ih电流并无增大反而明显减小。加巴喷丁不能阻断藜芦碱引起的癫痫样活动。结论在藜芦碱致海马CA1神经元癫痫样活动模型中,苯妥英对藜芦碱致痫的阻断作用具有浓度依赖性,可能通过抑制持续性钠电流的产生而消除癫痫活动。加巴喷丁不能阻断藜芦碱诱发的癫痫样活动,其机制可能与加巴喷丁对持续性钠电流没有作用和藜芦碱致痫并不增加Ih电流有关。     

小剂量藜芦碱致大鼠海马癫痫样活动的细胞学研究

目的 观察小剂量藜芦碱(Ver)对大鼠海马CA1锥体神经元放电的影响,并对其诱发产生癫痫样放电的离子机制进行初步探讨.方法 应用脑片膜片钳全细胞记录技术,观察小剂量(0.3～0.8μmol/L)Ver灌流后SD大鼠(2～3周龄,共30只)海马CA1锥体神经元的放电特征.通过Schaffer侧支突触前刺激,观察突触受体阻断剂6-氰基-7-硝基喹喔啉-2,3二酮(CNQX,5μmol/L)、2-氨基-5-磷酸基戊酸(AP-5,12.5μmol/L)、牡丹荷包碱(Bic,10μmol/L)以及钠通道阻断剂河鲀毒素(TTX,40～80nmol/L)对藜芦碱致痫的影响,绘制I-V曲线,探讨Ver诱发放电的电生理机制.结果 小剂量Ver灌流后随着膜电位的超极化,大鼠CA1锥体神经元产生模式相对固定的慢波样癫痫样活动.这种放电不被突触阻断剂CNQX AP-5 Bic阻断,但能被小剂量TTX阻断.Ver诱发癫痫样活动后,I-V关系非线性化,去极化矫正增强,小剂量TTX可逆转此改变.Ver灌流可增强TTX敏感的阈下持续性钠电流,并与膜电位水平有关.结论 小剂量Ver可明显改变大鼠海马CA1锥体神经元的放电模式,诱发慢波样癫痫电活动.这种癫痫样放电的产生不受突触传递阻断剂的影响,但与持续性钠电流明显相关.     

力竭运动过程中大鼠苍白球内侧部对皮层的调控作用

目的:探讨力竭运动中大鼠苍白球内侧部对皮层的调控作用。方法:采用皮层脑电(ECoG)及局部场电(LFPs)同步记录技术,动态观察一次性力竭运动中大鼠皮层辅助运动区、苍白球内侧部神经元电活动变化规律。结果:运动开始阶段,大鼠能够自主跟随跑台进行运动,持续约43 min(43±11.8 min)后,大鼠自主运动能力明显降低,此时,皮层神经元功率谱重心频率显著降低(P<0.01),提示神经元兴奋性下降,而苍白球内侧部神经元功率谱重心频率显著升高(P<0.01),提示兴奋性增强;此时给予大鼠一定的外部刺激,大鼠仍可继续运动一段时间直至力竭,皮层神经元功率谱重心频率降至最低(P<0.01),而苍白球内侧部神经元功率谱重心频率达到最高(P<0.01)。力竭运动过程中,苍白球内侧部局部场电活动与皮层脑电活动呈相反变化趋势,且不同阶段两区域神经元在0~30Hz范围内均显著相干。结论:力竭运动过程中苍白球内侧部神经元兴奋性增强经丘脑中继后对皮层神经元产生去兴奋作用,是导致疲劳及运动能力下降的重要因素之一,提示苍白球内侧部-丘脑-皮层通路在运动疲劳产生过程中起重要调控作用。     

多巴胺对猕猴额叶随机延缓反应作业相关神经元活动的影响(英文)

在猕猴执行随机延缓反应作业的同时,观察了微电泳多巴胺及其受体阻断剂氟哌啶醇对额叶作业相关神经元自发放电活动和诱发反应的影响。在该作业中,延缓期在1～4秒之间随机变化,在延缓期动物必须高度注意黄灯信号的出现,如稍不注意就会导致操作错误。在反应期,动物要在1秒钟内作出放开杠杆的反应。在实验中,对109个作业相关神经元观察了多巴胺的效应,这些神经元在作业间期共表现出神经元反应134个。神经元反应多出现在延缓期(48个)和反应期(72个),约占反应总数的90%。有近60%的神经元(61/109)对多巴胺敏感,多巴胺对神经元的自发放电活动既有兴奋效应(21/61),又有抑制效应(40/61),但以抑制效应为主。在延缓期出现反应的神经元中有31个(31/48)对多巴胺敏感,多巴胺对神经元的诱发反应主要起抑制作用(23/31);在反应期出现反应的神经元中有44个(44/72)对多巴胺敏感,多巴胺也以抑制作用为主(32/44),即使神经元的放电活动减弱。对54个(54/61)多巴胺敏感神经元观察了氟哌啶醇的效应,氟哌啶醇的效应与多巴胺相反,并能阻断多巴胺的效应。形态学检查表明,多巴胺敏感性神经元主要分布在大脑额叶弓状沟上支的内侧部。本实验表明,在延缓期和反应期出现放电变化的额叶神经元半数以上都对多巴胺敏感,且以抑制效应为主。由于作业的这两个时期分别与注意和视觉指导下的运动有关,因此,在视-运动耦合以及注意等过程中,在大脑额叶有多巴胺敏感神经元参与,而且主要是参与神经元活动的抑制过程。     

运动疲劳对大鼠新纹状体神经元电活动的影响

目的:观察运动疲劳大鼠新纹状体神经元自发放电情况,探讨运动疲劳产生的中枢机制.方法:采用胞外玻璃微电极技术,对运动疲劳前后大鼠新纹状体神经元自发放电频率、神经元动作电位时程及动作电位发放形式进行记录,并对放电神经元的分布规律进行分析.结果:(1)在记录到的运动疲劳组大鼠新纹状体神经元中,19%自发放电频率>10Hz,而对照组仅有6%,两组相比存在显著差异(P<0.05);(2)运动疲劳组大鼠新纹状体神经元除观察到规则单脉冲放电、不规则单脉冲放电、单脉冲与爆发式并存的放电形式外,还观察到规则爆发式放电,其串间隔集中在140～210ms;(3)运动疲劳组高频自发放电的神经元主要集中在新纹状体的外侧深部区域. 结论:运动疲劳后新纹状体神经元自发放电频率发生改变,高频放电神经元数量明显增加.结果提示运动疲劳后神经元放电形式发生改变,可能与神经元胞内钙离子浓度升高相关.     

外源性血管内皮生长因子对培养大鼠脊髓神经元缺氧的保护作用

目的 观察血管内皮生长因子(VEGF)对培养大鼠脊髓神经元的缺氧保护作用,并探讨可能的机制.方法 体外原代培养大鼠脊髓神经元细胞,在培养液中加入不同浓度的VEGF164,通过神经元细胞计数、四唑盐染色(MTT)法检测神经元细胞活性,末端脱氧核苷酸介导的X-dUTP缺口末端标记法(TUNEL)观察缺氧后神经元细胞凋亡情况,通过免疫组织化学方法观察缺氧前后大鼠脊髓神经元VEGF及其受体Flk-1/Flt-1表达情况.结果 当细胞培养液中VEGF164终浓度达25 ng/ml时,神经元细胞活性增加11%,细胞计数增加20%,而神经元细胞凋亡指数减少近50%;当培养液中VEGF164浓度达到100 mg/ml时,神经元细胞活性增加近25%,神经元缺氧细胞的凋亡数减少到1/3,而VEGFR2/Flk-1受体抑制剂SU1498可抑制这一作用.结论 VEGF对大鼠脊髓神经元具有缺氧保护作用,可能是通过VEGFR2/FLK-1受体传导途径介导的.     

大鼠海马的神经元构筑

运用Nissl法和Colgi法研究了正常成年SD大鼠海马的神经元构筑。发现大鼠海马内有大锥体细胞、大梭形细胞、小锥体细胞、小梭形细胞和异位颗粒细胞等5种神经元。神经元的类型及分布方式在海马各区之间差别明显。海马内神经元的胞体主要聚集在锥体层。海马各区神经元胞体分布的厚度及密度分别为CA_1区:281.5μm±65.5μm、258.1/mm±84.3/mm;CA_2区:46.6μm±11.5μm、251.0/mm±64.7/mm;CA_3区:61.7μm±16.6μm、201.6/mm±40.5/mm;CA_4区:90.6μm±20.6/μm、196.0/mm±37.3/mm。     

地塞米松对大鼠背根神经节细胞ATP激活电流的快速抑制作用

目的探讨地塞米松对大鼠背根神经节(DRG)神经元ATP激活电流的快速调节作用及其相关信号机制。方法采用酶加机械法分离、培养大鼠DRG神经元,全细胞膜片钳法记录ATP激活电流及地塞米松对ATP激活电流的影响。结果细胞外给予ATP(100μmol/L)在大鼠DRG神经元可引起3种内向电流,即快速脱敏感反应电流(快反应电流)、慢速脱敏感反应电流(慢反应电流)及混合电流。预先给予地塞米松(0.01~10μmol/L)可剂量依赖性地抑制ATP快反应电流及混合电流中的快反应电流成分,而对慢反应电流及混合电流中的慢反应电流成分无明显影响。地塞米松对ATP激活电流的快速抑制作用可被糖皮质激素受体拮抗剂RU38486(10μmol/L)、蛋白激酶A抑制剂H-89(10μmol/L)阻断,而G蛋白激活抑制剂GDP-β-S(0.2mmol/L)、蛋白激酶C抑制剂Chelerythrine chloride(10μmol/L)对地塞米松的快速抑制作用无明显影响。结论地塞米松通过糖皮质激素受体激活细胞内PKA信号途径可选择性地抑制大鼠DRG神经元中由P2X3受体介导的ATP快反应电流,提示糖皮质激素可能通过非基因组作用影响初级感觉神经元的ATP/P2X3受体功能而参与痛觉的调制。     

体力活动对小白鼠大脑皮质躯体感觉区与尾壳核神经元形态学的影响

18～20日龄昆明种雄性同源小鼠,经配对,随机分配于运动组与对照组,运动组小鼠进行体力活动。对两组小鼠大脑组织进行制片,光学显微镜观察。结果表明,体力活动能促进小白鼠大脑皮质感觉区Ⅴ层大锥体细胞核仁增大、Ⅵ层中等锥体细胞和尾壳核中等星形细胞树突棘增多。     

MR volumetric analysis of the human entorhinal,perirhinal, and temporopolar cortices.

PURPOSEOur purpose was to investigate the normal volumes of the human entorhinal, perirhinal, and temporopolar cortices on MR imaging studies using a customized program.METHODSWe designed a protocol in which the volumes of the entorhinal, perirhinal, and temporopolar cortices were determined from coronal MR images using anatomic landmarks defined on the basis of cytoarchitectonic analyses of 49 autopsy cases. MR volumetry of these cortical areas was performed in 52 healthy volunteers.RESULTSThe overall mean volumes were 1768 +/- 328 mm3/1558 +/- 341 mm3 (right/left) for the entorhinal cortex, 2512 +/- 672 mm3/2572 +/- 666 mm3 for the perirhinal cortex, and 2960 +/- 623 mm3/3091 +/- 636 mm3 for the temporopolar cortex. The right entorhinal cortex was 12% larger than the left. The volume of the temporopolar cortex was reduced bilaterally by 13% in the older age group compared with younger subjects, while the volumes of the entorhinal and perirhinal cortices were unaffected by age. There were no differences between men and women in the volumes of any of the three cortices.CONCLUSIONOur method provides a tool by which to measure volumes of the entorhinal, perirhinal, and temporopolar cortices on coronal MR images.     

PYK2在海人酸癫痫大鼠海马神经元及小胶质细胞中的表达变化

目的 观察海人酸癫痫大鼠海马内神经元和小胶质细胞中PYK2的表达并探讨其意义。方法 建立海人酸大鼠癫痫模型，大鼠癫痫发作后8、24、72h后处死大鼠，采用免疫组化方法观察大鼠海马内小胶质细胞的活化状况，以及海马神经元和活化后小胶质细胞中PYK2的表达变化。结果 与正常大鼠相比，癫痫大鼠中PYK2的表达在癫痫发作8h后急剧下降，并随时间推移继续下降。癫痫发作24h后，海马中出现大量呈阿米巴形状、强烈表达活化型PYK2的活化型小胶质细胞；癫痫后72h，海马中出现大量有活化型PYK2强表达的“杆”状活化型小胶质细胞。结论 癫痫可致海马神经元及小胶质细胞PYK2表达变化；小胶质细胞中活化型PYK2的表达可能与小胶质细胞活化有关。     

Functional interactions of the entorhinal cortex: an 18F-FDG PET study on normal aging and Alzheimer's disease.

Alzheimer's disease (AD) is a brain disorder characterized by reduced cerebral glucose metabolism (CMRgl) in several cortical regions. Evidence from neuropathology studies, animal models of AD, and (18)F-FDG PET studies on cognitive impairment suggest that disrupted connections with the entorhinal cortex (EC) could be implicated in the emergence of the cortical hypometabolism. This (18)F-FDG PET study assessed the functional interactions-that is, the intercorrelations between the EC and the whole brain in vivo-in normal aging and AD. METHODS: Eighty-seven consecutive clinical AD patients underwent (18)F-FDG PET scanning at rest. Thirty-five sex- and age-matched healthy elderly subjects were studied as controls (NC). A voxel-based correlation analysis was performed with statistical parametric mapping to assess significant correlations between relative CMRgl (rCMRgl) in the EC and the rest of the brain, for NC and AD patients. Results were considered significant at P < 0.001. RESULTS: The pattern of EC functional interactions varies between normal aging and AD patients. In NC, the left and right EC were bilaterally correlated with several cortical and limbic regions, in accord with the major anatomic pathways identified in nonhuman primates. Alternatively, in AD patients, the EC correlations with the contralateral hemisphere were entirely lost, whereas those within the ipsilateral hemisphere were preserved only with the inferior temporooccipital (T-O) areas. CONCLUSION: This (18)F-FDG PET correlation study indicates that AD-related processes lead to an altered functional relationship between the EC and several cortical and limbic regions, with respect to normal aging. Our results suggest that the assessment of coupled rCMRgl reductions between the EC and the ipsilateral T-O cortex, besides the typical pattern of cortical reduction, could increase (18)F-FDG PET diagnostic sensitivity and further motivate its inclusion in the clinical assessment of AD.     

Functional interactions between entorhinal cortex and posterior cingulate cortex at the very early stage of Alzheimer's disease using brain perfusion single-photon emission computed tomography

OBJECTIVE: The cause of the reduced regional cerebral blood flow (rCBF) in the posterior cingulate cortex in the early stage of Alzheimer's disease has not been clarified. In Alzheimer's disease, the posterior cingulate cortex itself shows little neuropathologic degeneration, and a hypothesis explaining such a discrepancy is that the functional impairment in the posterior cingulate cortex reflects remote effects caused by degeneration in distant but connected areas, such as the entorhinal cortex. To test the hypothesis, we investigated the functional connectivity between the entorhinal cortex and posterior cingulate cortex. METHODS: Sixty-one patients with probable Alzheimer's disease at a very early stage and 61 age-matched healthy controls underwent both brain structural magnetic resonance imaging (MRI) and single-photon emission computed tomography (SPECT). Voxel-based morphometry was performed on MRI data to identify clusters of significantly reduced grey matter concentration in patients with Alzheimer's disease relative to controls, which were set as volumes of interest (VOIs) for correlation analyses of SPECT images. We then used adjusted rCBF values in the VOIs as covariates of interest in statistical parametric mapping. RESULTS: Voxel-based morphometry demonstrated a significant reduction in grey matter concentration in the bilateral entorhinal cortex in Alzheimer's disease. A positive correlation between rCBF in the entorhinal cortex as VOI and that in the limbic and paralimbic systems, including the posterior cingulate cortex, anterior cingulate cortex, lingual gyri and left middle temporal gyrus (P<0.001), was observed in Alzheimer's disease. Control subjects also showed a similar correlation in the limbic and paralimbic systems, but not in the posterior cingulate cortex. CONCLUSION: These results indicate that rCBF changes in the posterior cingulate cortex may be closely related to those in the entorhinal cortex in patients with Alzheimer's disease, thereby supporting the 'remote effect' hypothesis.     

MR volumetry of the entorhinal, perirhinal, and temporopolar cortices in drug-refractory temporal lobe epilepsy

BACKGROUND AND PURPOSE: The occurrence of damage in the entorhinal, perirhinal, and temporopolar cortices in unilateral drug-refractory temporal lobe epilepsy (TLE) was investigated with quantitative MR imaging. METHODS: Volumes of the entorhinal, perirhinal, and temporopolar cortices were measured in 27 patients with unilateral drug-refractory TLE, 10 patients with extratemporal partial epilepsy, and 20 healthy control subjects. All patients with TLE were evaluated for epilepsy surgery and underwent operations. RESULTS: In left TLE, the mean volume of the ipsilateral entorhinal cortex was reduced by 17% (P <.001 compared with control subjects) and that of the ipsilateral temporopolar cortex by 17% (P <.05). In right TLE, the mean ipsilateral entorhinal volume was reduced by 13% (P < or =.01), but only in patients with hippocampal atrophy. Asymmetry ratios also indicated ipsilateral cortical atrophy. When each patient was analyzed individually, the volume of the ipsilateral hippocampus was reduced (> or = 2 SD from the mean of controls) in 63% and that of the entorhinal cortex in 52% of patients with TLE. Furthermore, ipsilateral entorhinal (left: r = 0.625, P <.001; right: r = 0.524, P < or =.01), perirhinal (left: r = 0.471, P <.05), and temporopolar (right: r = 0.556, P <.01) volumes correlated with ipsilateral hippocampal volumes. There was no association, however, with clinically or pathologically identified causes of epilepsy, duration of epilepsy, or age at onset of epilepsy. Mean cortical volumes were unaffected in extratemporal partial epilepsy. CONCLUSION: Subpopulations of patients with unilateral TLE have ipsilateral damage in the entorhinal and temporopolar cortices. The damage is associated with hippocampal damage.     

4D deformation modeling of cortical disease progression in Alzheimer's dementia.

This work describes the development of a model of cerebral atrophic changes associated with the progression of Alzheimer's disease (AD). Linear registration, region-of-interest analysis, and voxel-based morphometry methods have all been employed to elucidate the changes observed at discrete intervals during a disease process. In addition to describing the nature of the changes, modeling disease-related changes via deformations can also provide information on temporal characteristics. In order to continuously model changes associated with AD, deformation maps from 21 patients were averaged across a novel z-score disease progression dimension based on Mini Mental State Examination (MMSE) scores. The resulting deformation maps are presented via three metrics: local volume loss (atrophy), volume (CSF) increase, and translation (interpreted as representing collapse of cortical structures). Inspection of the maps revealed significant perturbations in the deformation fields corresponding to the entorhinal cortex (EC) and hippocampus, orbitofrontal and parietal cortex, and regions surrounding the sulci and ventricular spaces, with earlier changes predominantly lateralized to the left hemisphere. These changes are consistent with results from post-mortem studies of AD.     

光动力疗法治疗鲜红斑痣的基础研究—血啉甲醚与血卟啉衍生物吸收特性的比较

目的　观察新型光敏剂——血啉甲醚(HMME)在鸡冠皮肤组织和血管内皮细胞(EC)的吸收特点。 方法　莱亨鸡12只,分为HMME组和血卟啉衍生物(HpD)组,每组6只。分别静脉注射HMME或HpD10mg/kg,每隔10min取血2.5ml和鸡冠皮肤组织2.5g。培养新生儿脐带EC,培养液中加入HMME或HpD,孵育浓度分别为20、40、60、80和100 μg/ml,孵育时间为即刻、15、30、60、120、180和240min。采用荧光分析法测定光敏剂含量,并绘制EC吸收光敏剂的浓度—含量和时间—含量关系曲线。 结果　静脉注射HMME或HpD后,其血清浓度的峰值出现在注射后10min,以后随时间迅速下降,二者的曲线形态基本一致。HMME在鸡冠组织中的含量于注射后10min显著高于HpD（P＜0.01）,以后虽然下降速率较快,但在注射后80min仍显著高于HpD（P＜0.05）。培养EC可迅速吸收HMME和HpD,30min达峰值的89%以上;其吸收量与孵育浓度呈线性关系,对HMME的吸收量显著高于HpD（P＜0.01）。 结论　HMME较HpD更容易被皮肤微血管EC摄取,这将有利于鲜红斑痣的治疗。     

Different physiological MRI noise between cortical layers.

Significantly higher temporal fluctuations of the blood oxygenation level-dependent (BOLD) signal in the living rat group compared to that in the dead rat group were observed in the cortex, suggesting the existence of physiological information in the signal fluctuations. A similar analysis shows significantly different fluctuations between visual cortical layers. The highest fluctuations were observed in layers 4 and 5 and the lowest in layer 1. Given the consistency with published electrophysiology studies anticipating high spontaneous activity in the deeper layers (particularly layer 4), and low activity in superficial layers, we hypothesize that the BOLD signal temporal fluctuations may reflect cortical neuronal activity. Temporal fluctuations in ultrahigh spatial resolution data of the rat brain were measured in two ways. In the first, analyses were performed according to known layer widths, and in the second equal lines of 117 micro along the cortex were selected. The second approach yielded temporal fluctuations along the cortex that resemble known neuronal density distributions including the intralayer structure, particularly within layer 5.     

Superficial siderosis in the central nervous system

We describe a rare entity, superficial siderosis of the central nervous system, due to multiple small episodes of subarachnoid haemorrhage from any source. Non-specific neurological findings are associated with deposition of ironcontaining pigments in the leptomeninges and superficial layers of the cortex. T2-weighted magnetic resonance imaging demonstrates characteristic low signal in the meninges.