Redeployment of trigeminal motor axons during metamorphosis.

As a consequence of the degeneration and replacement of the jaw muscle fibers in the leopard frog, Rana pipiens, trigeminal motoneurons innervate different targets before and after metamorphosis. This investigation examined the morphological correlates of the reassignment of trigeminal motoneurons during the initial phases of myofiber turnover. Specifically, silver-cholinesterase histochemistry and electron microscopy were used to 1) identify the fate of motor axons within the neuromuscular junctions (NMJs) applied to degenerating larval myofibers and 2) to determine the origin(s) of the motor axons that innervate the postmetamorphic muscle fibers of the jaw. The results demonstrate that the NMJs are retained on larval myofibers throughout their degeneration and are readily identifiable on the residual larval basal laminae that remain after involution of the sarcoplasm. Light and electron microscopic observations provide evidence that both pre- and post-synaptic elements are present on the degenerating fibers. Furthermore, morphometric analyses indicate that the preponderance (86%) of motor axons supplying adult muscle fibers originates from the larval NMJs. This condition suggests that metamorphic redeployment of trigeminal motoneurons occurs through the resumption of growth at the axon terminal supplying larval muscle rather than through the proximal collateralization of these axons and resorption of larval terminals.     

Short-term brain ‘plasticity’ in humans: transient finger representation changes in sensory cortex somatotopy following ischemic anesthesia

Transient rearrangements of finger representation in primary somatosensory cortex induced by an anesthetic block of the sensory information from adjacent fingers have been shown invasively in animals. Such a phenomenon has been now replicated in seven healthy human volunteers. Somatosensory Evoked Fields (SEFs) have been recorded during separate electrical stimulation of the 1st, 3rd, or 5th finger. Recordings were obtained in control conditions (stage A), following complete ischemic anesthesia of the 4 non-stimulated fingers (stage B), and after regaining sensation (stage C). SEFs were recorded using a 28-channel DC-SQUID magnetometer; a single position of the sensor was enough to identify the source of N20m, P30m and following components using the Equivalent Current Dipole (ECD) model. The amount of afferent input during stages A through C was monitored with surface electrodes placed on the nerve at wrist and elbow. No variation of the nerve compound potential was observed during stages A through C. In stage A, the localizing algorithm was able to discriminate the individual finger representation in accordance with the somatotopic organisation of the sensory homunculus. It was observed that the ECDs responsible for the cortical responses from the unanesthetized finger were significantly changing following a relatively brief period of sensory deprivation from the adjacent fingers. Such changes of the ECDs with respect to the control conditions were characterized by an increase in strength and deepening for the middle finger, and by a shift on the coronal plane for the thumb and the little finger (medial for the former, lateral for the latter). Such changes became progressively evident in stage B, but were persisting in stage C.     

支气管哮喘持续状态下豚鼠气道感觉神经生长相关蛋白43的表达

目的研究支气管哮喘(简称哮喘)过敏性刺激诱发气道感觉神经敏化机制。方法成年雄性豚鼠39只,按随机数字表法分为生理盐水致敏/激发对照组(A组,9只)、卵白蛋白(OVA)致敏/生理盐水激发对照组(B组,9只)、OVA致敏/激发实验组(C组,21只)。A组以生理盐水(0.5ml/只)致敏,B、C组以10%OVA(0.5ml/只)致敏,第10天开始雾化吸入生理盐水(A、B组)或1%OVA(C组)进行激发,每天1次,每次30min,根据实验需要又将C组21只豚鼠分为激发1d组(C1组,6只)、连续激发3d组(C2组,6只)、连续激发5d组(C3组,9只)。利用免疫荧光双标技术结合激光共聚焦扫描显微观察与Westernblot技术,研究生长相关蛋白43(GAP43)在气道神经以及结状神经节、颈静脉神经节内分布与水平及与P物质(SP)和胶质源神经生长因子(GDNF)受体c RET表达神经元关系。结果免疫荧光结果显示,C3组豚鼠气道内GAP43免疫反应阳性神经呈网状分布于大、中支气管内,以黏膜下层为主,部分GAP43阳性神经纤维向黏膜层内延伸;在结状神经节和颈静脉神经节内有大量GAP43免疫阳性神经胞体,在结状神经节内主要与SP免疫阳性胞体共存,在颈静脉神经节内主要与c RET免疫阳性胞体共存。Westernblot结果显示,A、B、C1、C2、C3组GAP43蛋白表达水平吸光度(A)值分别为0.38±0.04、0.41±0.03、0.49±0.05、0.79±0.08、0.76±0.04。C1、C2、C3组分别与A、B组比较差异均有统计学意义(P均0.05);C2组GAP43蛋白表达与C1组比较差异有统计学意义(P<0.01),但与C3组GAP43蛋白表达比较差异无统计学意义(P>0.05)。结论哮喘过敏性刺激能诱发气道感觉神经———SP肽能神经、GDNF敏感性神经纤维与胞体表达GAP43蛋白。     

Synaptic and extrasynaptic NMDA receptors: Problems and prospects

This review is devoted to the problem of induction of differently directed NMDA-dependent longterm plasticity in the central nervous system and their transformation into pathological changes. Their hypothetical mechanisms and the corresponding experimental data are discussed. Special attention is paid to the functional characteristics of synaptic and extrasynaptic NR1/NR2A and NR1/NR2B receptors, their different involvement in the spatiotemporal organization of Ca²⁺ signaling, and peculiarities of biochemical reactions of the cell. The possible structural reorganization of NMDA receptors as one of the kinds of plasticity is also analyzed.     

大鼠红核和颈段皮质脊髓背侧束联合损伤模型的建立

目的　为研究脊髓损伤后的可塑性变化 ,建立大鼠红核和皮质脊髓背侧束 (dCST)联合损伤模型。方法　立体定位仪下 ,致伤颈 3dCST和双侧红核 ,甲苯胺蓝染色显示损伤范围。示踪剂观测皮质脊髓腹侧束 (vCST)的出芽情况 ;同时 ,评定大鼠前肢功能的变化情况。结果　精确地致伤红核和dCST后 ,vCST的出芽数量和大鼠前肢功能评分成显著负相关 (P <0 0 1)。结论　大鼠红核和dCST联合损伤模型是研究脊髓损伤后可塑性变化的良好模型     

AMPA受体介导的突触可塑性与药物依赖

突触可塑性改变是形成药物依赖长期效应的病理基础,兴奋性氨基酸受体在其中起十分重要的作用。近年来的研究表明,多种药物依赖过程与AMPA受体有关。联系药物依赖所致的AMPA受体的变化与神经元的可塑性改变,探讨AMPA受体介导药物依赖的形成机制,可为进一步理解AMPA受体在药物依赖中的作用提供帮助。     

Long-Term Depression in Rat Cerebellum Requires both NO Synthase and NO-sensitive Guanylyl Cyclase

Long-term depression (LTD) of synaptic transmission between parallel fibres and Purkinje cells is a well-known example of synaptic plasticity taking place in the cerebellum. Nitric oxide (NO) has been implicated in synaptic plasticity in other brain areas, but its function in cerebellar LTD is controversial. Even when an involvement is suggested, the NO signal transduction pathway is unclear. One candidate is the cyclic GMP-synthesizing enzyme, soluble guanylyl cyclase, whose activity in the brain and elsewhere is powerfully stimulated by NO. By recording intracellularly from Purkinje cells in cerebellar slices, we demonstrate that blockade of NO synthase completely inhibits LTD induced by pairing parallel fibre stimulation with postsynaptic Ca²⁺ spike firing. LTD was also blocked by intracellular application of 1H-[1, 2, 4]oxadiazolo[4, 3-a]quinoxalin-1-one, a recently identified potent and selective inhibitor of soluble guanylyl cyclase. These findings indicate that soluble guanylyl cyclase is required for cerebellar LTD and suggest that this enzyme, located within Purkinje cells, transduces the NO signal in this form of synaptic plasticity.     

Transmitter Release Associated with Long-term Synaptic Depression in Rat Corticostriatal Slices

Using a corticostriatal slice preparation, we have recently shown that tetanic stimulation of the corticostriatal pathway produces long-term depression (LTD) of striatal excitatory synaptic transmission. In the present study we have analysed the relationship between LTD and the striatal release of different endogenous transmitters. Samples of perfusate were collected via a small cannula placed just above the surface of the striatal slice close to the recording electrode, and were analysed by HPLC. The high-frequency stimulation (100 Hz, three trains, 3 s duration, 20 s intervals) used to induce LTD caused a significant but transient increase in the release of both excitatory (aspartate and glutamate) and inhibitory (glycine and GABA) amino acid transmitters. Tetanic stimulation also produced a significant, but transient increase in the release of endogenous dopamine. We conclude that the tetanic stimulation of the corticostriatal pathway is able to induce a large but transient release of excitatory amino acids and of dopamine, whose participation in the induction of striatal LTD has been demonstrated previously. Moreover, the maintenance of this form of synaptic plasticity does not seem to require a sustained change in transmitter release.     

Cytochemical Redistribution of 5'-Nucleotidase in the Developing Cat Visual Cortex

The adenosine-producing ectoenzyme 5'-nucleotidase has recently been shown to undergo a marked redistribution during development of the cat visual cortex and to be involved in the remodelling of ocular dominance columns (Schoen et al., J. Comp. Neurol. , 296 , 379 – 392, 1990). Using an enzyme-cytochemical technique, we now investigate the developmental redistribution of 5'-nucleotidase activity in area 17 of kittens at the ultrastructural level. Between postnatal days 35 and 42, when 5'-nucleotidase is concentrated in layer IV, enzyme reaction product occupies the clefts of asymmetrical synapses within the neuropil. During later development (9th and 13th postnatal weeks), when 5'-nucleotidase spreads over all cortical laminae, the enzyme disappears from its synaptic localization and becomes increasingly associated with astrocytic membranes. The transient appearance of 5'-nucleotidase at synapses parallels the time-course and laminar profile of the synaptic remodelling which takes place during the critical period of visual cortex development. This suggests that synapse-bound 5'-nucleotidase activity plays a role in synaptic malleability, whereas its later association with glial profiles is likely to reflect other functions of the enzyme.     

The aging brain

A recent interest in aging of the nervous system is related to the remarkable increase in the numbers of elderly persons throughout the world. As a reflection of the added years, pathologies in the older person have also increased. Primary among those which affect the activities and behavior of these people are the dementias, especially Alzheimer's Disease. To focus on such problems, however, requires an understanding of the changes which take place in the normal aging nervous system. This paper reviews some of the accepted criteria for these changes as well as the possible attempts by the nervous system to alter its structure in response to these changes.