Can the theory of "whitening" explain the center-surround properties of retinal ganglion cell receptive fields?

To account for the spatial and temporal response properties of the retina, a number of studies have proposed that these properties serve to "whiten" the visual input. In particular, it has been argued that the sensitivity of retinal ganglion cells is matched to the spatial frequency spectrum of natural scenes, resulting in a flattened or "whitened" response spectrum across a range of frequencies. However, we argue that there are two distinct hypotheses regarding the flattening of the spectrum. The decorrelation hypothesis proposes that the magnitude of each ganglion cell tuning curve rises with spatial frequency, resulting in a flattened response spectrum for natural scene stimuli. With appropriate sampling, this scheme allows neighboring neurons to be uncorrelated with each other. The response equalization hypothesis proposes that the overall response magnitude of neurons increases with spatial frequency. The proposed goal of this model is to allow neurons with different receptive field sizes to produce the same average response to natural scenes. The response equalization hypothesis proposes an explanation for the relative gain of different ganglion cells and we show that this proposal fits well with published data. We suggest that both hypotheses are important in understanding the tuning and sensitivity of ganglion cells. However, using a simulation, both models are shown to be insufficient to explain the center-surround receptive field organization of ganglion cells. We discuss other factors, including representational sparseness, which could be related to the goals of ganglion cell spatial processing. We suggest three constraints needed to describe the basic linear properties of P-type ganglion cells: decorrelation, response equalization, and a minimal wiring or minimal size constraint.     

GABAC receptor-mediated inhibition in the retina

Inhibition at bipolar cell axon terminals regulates excitatory signaling to ganglion cells and is mediated, in part, by GABAC receptors. We investigated GABAC receptor-mediated inhibition using pharmacological approaches and genetically altered mice that lack GABAC receptors. Responses to applied GABA showed distinct time courses in various bipolar cell classes, attributable to different proportions of GABAA and GABAC receptors. The elimination of GABAC receptors in GABAC null mice reduced and shortened GABA-activated currents and light-evoked inhibitory synaptic currents (L-IPSCs) in rod bipolar cells. ERG measurements and recordings from the optic nerve showed that inner retinal function was altered in GABAC null mice. These data suggest that GABAC receptors determine the time course and extent of inhibition at bipolar cell terminals that, in turn, modulates the magnitude of excitatory transmission from bipolar cells to ganglion cells.     

«Cancers du sein»

Résumé: Cet article présente les conclusions d’un groupe de travail appliquant la méthodologie ANAES en ce qui concerne:1. Le traitement de l’aisselle.2. La prise en charge des patientes présentant une tumeur surexprimant HER2.3. L’hormonothérapie adjuvante.4. La chimiothérapie adjuvante.Groupe de travail Liste de médecins référents invités en regard du sujet choisi et répartis sur l’ensemble du territoire français. Fabrice ANDRE (Villejuif) Emmanuel BARRANGER (Paris) Jacques BONNETERRE (Lille) Patricia DE CREMOUX (Paris) Philippe CHOLLET (Clermont-Ferrand) Krishna CLOUGH (Paris) Bruno CUTULI (Reims) Marc DEBLED (Bordeaux) Thierry DELOZIER (Caen) Francette ETTORE (Nice) Pierre FUMOLEAU (Dijon) Jean-Paul GUASTALLA (Lyon) Jean-Marc GUINEBRETIERE (St-Cloud) Michel HERY (Monaco) Louis MAURIAC (Bordeaux) Sylvie MENARD (Milan) Jean-Baptiste MERIC (Paris) Frédérique PENAULT-LLORCA (Clermont-Ferrand) Thierry PETIT (Strasbourg) Henri ROCHE (Toulouse) Jean-Philippe SPANO (Paris) Marc SPIELMANN (Villejuif) Serge UZAN (Paris) Patrice VIENS (Marseille)Groupe de lecture Emmanuel ACHILLE (Strasbourg) Lydie AIMARD (Marseille) Thierry ALTWEGG (Dijon) Eric-Charles ANTOINE (Paris) Bernard ASSELAIN (Paris) François BERTUCCI (Marseille) Laurent CALS (Toulon) Mario CAMPONE (Nantes) Yvan COSCAS (Paris) Paul-Henri COTTU (Paris) Bruno COUDERT (Dijon) Adel COURDI (Nice) Philippe DALIVOUST (Marseille) Véronique DIERAS (Paris) Nadine DOHOLOU (Bordeaux) Marc ESPIE (Paris) Thomas FACCHINI (Reims) Jean-Marc FERRERO (Nice) Joseph GLIGOROV (Paris) Anne-Claire HARDY-BESSARD (Saint-Brieuc) Pierre KERBRAT (Rennes) Anne LESUR (Nancy) Alain LORTHOLARY (Nantes) Jean-Pierre LOTZ (Paris) Elisabeth LUPORSI (Vandœuvre-lès-Nancy) Catherine MAESTRO (Nice) Jean-Pierre MARTIN (Lyon) Jean-Louis MISSET (Paris) Alain MONNIER (Montbéliard) Jean-Marc NABHOLTZ (Paris) Hervé NAMAN (Mougins) Moise NAMER (Nice) Claude NOS (Paris) Raoult PAYAN (Grenoble) Pascal PIEDBOIS (Créteil) Jean-Yves PIERGA (Paris) Xavier PIVOT (Besançon) Pierre POUILLART (Paris) Isabelle RAY-COCQUARD (Lyon) Jacques ROUESSE (St-Cloud) Daniel SERIN (Avignon) Hélène SIMON (Brest) Eric TESSIER (Mougins) Véronique TRILLET-LENOIR (Lyon) Michèle TUBIANA-HULIN (St-Cloud) Jean-Louis WENDLING (Toulon) Laurent ZELEK (Créteil)La présente recommandation a été réalisée avec le soutien des partenaires suivants: – Amgen – AstraZeneca – Chiron – Janssen-Cilag/OBF – Lilly – Novartis – Pfizer – Sanofi-Aventis – Roche     

Vitamin B6 protects primate retinal neurons from ischemic injury

Vitamin B6 derivatives protect the retinal neurons from excitotoxic injury in vitro. However, their in vivo role in a process involving excitotoxicity, such as ischemia, remains unknown. We studied potential protective effects of pyridoxal 5′-phosphate (PLP) and pyridoxal hydrochloride (pyridoxal) on the retinal neurons in a monkey model of transient global ischemia. Daily intravenous injections (15 mg/kg) of pyridoxal and PLP were performed for consecutive 10 days. On the sixth day, whole brain complete ischemia was produced by clipping the innominate and the left subclavian arteries for 20 min. The monkeys were sacrificed 5 days after ischemia and their retinas were processed for histological analysis. The ischemia induced a marked cellular injury in the retina as shown by the loss of ganglion cells and the reduction of thickness of the ganglion cell, inner plexiform, and inner nuclear layers. PLP significantly prevented the ganglion cell loss and the reduction of thickness of the ganglion cell layer. Pyridoxal significantly prevented the ganglion cell loss as well as the reduction of thickness of ganglion cell, inner plexiform and inner nuclear layers. These results suggest that PLP and pyridoxal counteract the postischemic neuronal death in the adult primate retina, offering a potential for a novel pharmacotherapy of retinal ischemic injury.     

电刺激蝶腭神经节对鼻粘膜血流的调控作用

为了解蝶腭神经节在鼻粘膜血流调节中的作用，应用激光多普勒血流仪观察刺激蝶腭神经节对猫鼻粘膜血流变化的调控作用。结果表明，电刺激一侧蝶腭神经节可以引起双侧鼻粘膜血管扩张，血流增加，并产生喷嚏反射，这种反应依电刺激的强度、频率而异，且与刺激时间有关。电刺激一侧副交感神经（切除颈上交感神经节的翼管神经）远侧游离端，只引起同侧血管反应。提示刺激蝶腭神经节引起的血管反应可能是通过中枢反射机制起作用。实验还显示刺激蝶腭神经节具有“反向血流调节作用”，这种调节作用的机制有待于进一步研究。     

Limit of spared pattern vision following lesions of the immature visual cortex

Lesions of primary visual cortex sustained early in life spare certain aspects of visual processing that can be linked to expansions of bypass pathways to extrastriate cortex. They also trigger, in an age-dependent way, partial or complete transneuronal retrograde degeneration of β (X) retinal ganglion cells, which are implicated in visual processing under conditions of low contrast. We used two-dimensional geometric patterns whose saliency was reduced by gradually increasing levels of superimposed masking lines, and by reductions in spatial contrast. Normative data were collected from intact cats, and baseline lesion data were collected from cats with lesions sustained as young adults (postnatal day 180, P180). Experimental data were collected from cats that sustained lesions on P1–3 or P26–30. For high contrast patterns, the adult group was impaired at both acquisition (sequential progressive levels of masking) and concurrent (parallel high and low levels of masking) performance, whereas the early-lesioned groups were impaired only at concurrent performance. All lesion groups were equally impaired when contrast was reduced to modest or lower levels. These results show that sparing of masked-pattern learning is limited to the high end of the spatial contrast domain. Electronic Publication     

鸡投射视顶盖视网膜节细胞的形态学分类

目的　研究鸡视网膜 视顶盖投射系母体———视网膜节细胞 (RGCs)的形态学类型。方法　用逆行追踪法标记鸡投射至视顶盖的RGCs,再用细胞内注射法将标记的RGCs的全树突可视化 ,根据其细胞体和树突野的大小和树突分支特征进行形态学分类。　结果　鸡投射至视顶盖的RGCs可分为 3群、5亚群 ,即小细胞体和小树突野的I群细胞 ,包括简单型的Is亚群和复杂型的Ic亚群 ;中等细胞体和树突野的II群细胞 ,包括IIs和IIc两亚群 ;具有巨大的细胞体和树突野的IV群细胞 ,仅见IVc亚群。各亚群的比例分别是 :Ic 2 7 7%、Is 33 6 %、IIc 2 5 %、IIs 2 4 4 %、IVc 11 8%。　结论　投射至鸡视顶盖的RGCs以中小型细胞为主 (约占 88 2 % )和一部分大型细胞 (占11 8% ) ,其中Ic亚群细胞类似于哺乳动物的 β节细胞 ,而Is和IIs亚群细胞在哺乳动物尚未见报道 ,在鸡RGCs高密度区存在的Ⅲ群细胞没有投射至视顶盖     

In situ hybridization analysis of substance P receptor in the rat retina

Substance P receptor is known to provide a principal interface between tachykinin peptides and tachykinin-sensitive cells in retinal circuitry and to produce several physiological functions such as excitation of ganglion cells. We reported results of in situ hybridization analysis of substance P receptor in rat retina using digoxigenin-labeled RNA probes to yield discrete cell labeling. Distinct hybridization signal was present in a great majority of ganglion cells that provide retinal fibers to a central target. It was also present in a subpopulation of amacrine cells. Following optic nerve crush, ganglion cells lost their hybridization signal in a time-dependent manner, while hybridization-positive amacrine cells were persistently seen. From the results, we identified the hybridization message as distinctly localized to two systems, output cells and intrinsic cells in retinal circuitry.     

Displaced retinal ganglion cells in normal frogs and those with regenerated optic nerves

Summary We have analysed the number and spatial distribution of displaced retinal ganglion cells in the frog Litoria (Hyla) moorei. A series of normal animals was compared with one in which the optic nerve was crushed and allowed to regenerate. Ganglion cells were labelled with horseradish peroxidase (HRP) applied to the optic nerve, and retinae were examined as sections or whole mounts. We analysed separately ganglion cells with somata displaced to the inner nuclear (Dogiel cells, DGCs) and to the inner plexiform layer (IPLGCs). These findings were related to data for the orthotopic ganglion cells (OGCs). The mean number of DGCs in the normal series was 2,550 (±281) and fell to 1,630 (±321) after regeneration, representing a mean loss of 36%. This reduction was not significantly different from the mean loss of 43% from the OGC population in which mean values fell from 474,700 (±47,136) to 268,700 (±54,395). In both the normal and the regenerate series, DGCs were estimated to represent means of only 0.6% of the OGC population. Densities of DGCs were highest in the nasoventral and temporo-dorsal peripheries; densities of both DGCs and OGCs were lower after optic nerve regeneration. We conclude that the factors which affect ganglion cell death during optic nerve regeneration, do so to similar extents amongst the DGC and the OGC populations. The IPLGCs were very rare in normal animals with a mean of 420 (±95). However, their numbers increased after regeneration to a mean of 3,350 (±690), estimated to be 1.2% of the OGC population. These cells normally favoured peripheral retina but became pan-retinal after regeneration. The primary dendrites of the majority of IPLGCs were oriented in the same direction as those of OGCs. We conclude that most IPLGCs were OGCs which had relocated their somata to the inner plexiform layer.     

培养猴颈交感神经节脑内移植治疗帕金森病的实验研究

目的探索帕金森病外科治疗的移植方法，并为培养交感神经节移植脑内能否长期存活寻找组织学证据。方法用１甲基－４苯基－１，２，３，６－四氢吡啶（ＭＰＴＰ）诱发猴帕金森病模型１１只，将自体腓神经培养２４～２８天所得的雪旺细胞与神经节组织共同培养后行脑尾状核移植，观察２年后取标本，用乙醛酸诱发多巴胺荧光和免疫组织化学方法检测。结果猴帕金森病症状明显好转，移植２年后脑尾状核仍可见存活的神经节细胞，移植物与脑组织间有轴、树突联系，多巴胺荧光及神经丝蛋白、突触素、铬粒素等染色阳性。结论神经节与雪旺细胞共同培养后移植脑内可存活２年，是治疗帕金森病的较好方法。组织学观察结合荧光及免疫组织化学染色结果是判定移植物存活与否的重要手段。