Development Of Dendritic Morphology Research Articles

Ammonium and Tetraalkylammonium Salts as Additives for Li Metal Electrodes

Lithium metal batteries are considered a promising technology to implement high energy density rechargeable systems beyond lithium-ion batteries. However, the development of dendritic morphology is the basis of safety and performance issues and represents the main limiting factor for using lithium anodes in commercial rechargeable batteries. In this study, the electrochemical behaviour of Li metal has been investigated in organic carbonate-based electrolytes by electrochemical impedance spectroscopy measurements and deposition/stripping galvanostatic cycling. Low amounts of tetraalkylammonium hexafluorophosphate salts have been added to the electrolytes with the aim of regulating the lithium deposition/stripping process through the electrostatic shielding effect that improves the lithium deposition. The use of NH4PF6 also determined good lithium deposition/stripping performance due to the chemical modification of the native solid electrolyte interphase via direct reaction with lithium.

Bisphenol A Promotes Dendritic Development and Changes the Expressions of RhoA and Rac1/Cdc42 of Hippocampal Neurons

Bisphenol A(BPA),an environmental endocrine disruptor widely used in plastic production,has attracted high attention to its adverse effects on brain developmental process.The purpose of the study was to investigate the effects of exposure to BPA for 24 h on dendritic morphological development and the underlying mechanisms.The results demonstrated that cultured hippocampal neurons exposed to BPA(10,100 nmol/L) or 17β-estradiol(17β-E2,10 nmol/L) for 24 h significantly increased the total length of dendrite,motility and density of dendritic filopodia,as well as the expression of F-actin(filamentous actin).These changes were suppressed by an ERs antagonist ICI182780,a non-competitive NMDA receptor antagonist MK-801,and a mitogen-activated ERK1/2-activating kinase(MEK1/2) inhibitor U0126.Furthermore,exposure to BPA(100 nmol/L) promoted the expression of Rac1/Cdc42 but inhibited that of RhoA,which were completely blocked by ICI182780,and partially suppressed by U0126.The results reveal that BPA changes upstream regulatory molecules of dendritic development through ERK1/2 signaling pathway mediated by estrogen receptor,and then affects the development of dendritic morphology in hippocampus neurons.

Structural factors of dendritic segregation in aluminum alloys

The effect of cooling rate in the solidification range and the development of the dendritic structure on the formation of nonequilibrium eutectics in Al-Cu alloys is investigated experimentally and by computer simulation. It is shown that 1D models cannot predict the experimentally observed dependences adequately since they do not take into account the development of the dendritic structure during solidification. The 2D models allow one to describe the process of solidification and the development of dendritic morphology more exactly and, as a result, predict dendritic liquation satisfactorily. It is revealed that a coarsening of the dendritic structure at the last stages of solidification in the rate range up to 20 K/s exerts the strongest effect on the formation of nonequilibrium eutectics.

NMDA receptor binding declines differentially in three spinal motor nuclei during postnatal development

The NMDA subtype of glutamate receptors mediates a variety of neuronal processes involved in the development of dendritic morphology. For example, NMDA receptor antagonism during the early postnatal period attenuates dendritic growth in spinal motoneurons. NMDA receptors are present in high levels in the spinal cord early in the postnatal period and decline during development, a period of extensive dendritic plasticity in the spinal cord. Previous studies have suggested that an adult pattern of distribution of NMDA receptors is established as early as postnatal day (P)21 (day of birth = P1). However, given that dendritic growth in spinal motoneurons is not complete by this age and that NMDA receptor activation is necessary for dendritic growth, we assessed NMDA receptor binding in specific spinal motor nuclei during normal development. NMDA receptors were labeled with [ 3H]MK-801 at P7, P14, P28, P49, and in adult male rats. Receptor binding in the spinal nucleus of the bulbocavernosus (SNB), dorsolateral nucleus (DLN) and retrodorsolateral nucleus (RDLN) was measured using in vitro quantitative autoradiography. NMDA receptor binding over the SNB, DLN and RDLN in intact males was initially high, and declined to adult levels. However, the time course of the decline differed across nuclei. The local decline in NMDA receptor binding observed in the SNB and DLN is coincident with the periods of dendritic growth in these nuclei, further supporting a role for NMDA receptors in the development of motoneuron dendritic morphology.

Anti-tumour activity in vitro and in vivo of selective differentiating agents containing hydroxamate.

A series of hydroxamates, which are not metalloprotease inhibitors, have been found to be selectively toxic to a range of transformed and human tumour cells without killing normal cells (fibroblasts, melanocytes) at the same concentrations. Within 24 h of treatment, drug action is characterized by morphological reversion of tumour cells to a more normal phenotype (dendritic morphology), and rapid and reversible acetylation of histone H4 in both tumour and normal cells. Two hydroxamates inhibited growth of xenografts of human melanoma cells in nude mice; resistance did not develop in vivo or in vitro. A third hydroxamate, trichostatin A, was active in vitro but became inactivated and had no anti-tumour activity in vivo. Development of dendritic morphology was found to be dependent upon phosphatase activity, RNA and protein synthesis. Proliferating hybrid clones of sensitive and resistant cells remained sensitive to ABHA, indicating a dominant-negative mechanism of sensitivity. Histone H4 hyperacetylation suggests that these agents act at the chromatin level. This work may lead to new drugs that are potent, and selective anti-tumour agents with low toxicity to normal cells. © 1999 Cancer Research Campaign

Influence of the neuropeptide somatostatin on the development of dendritic morphology: a cysteamine-depletion study in the rat auditory brainstem

We investigated the functional role of somatostatin during early ontogeny of the brain, when the neuropeptide as well as its receptors are heavily expressed in the auditory brainstem. Rat pups received a daily injection of cysteamine which, when applied at low concentrations, most selectively depletes somatostatin. Neurons from the lateral superior olive, an auditory brainstem nucleus which transiently receives a dense somatostatinergic input, were intracellularly labeled at postnatal day 14 or 18. The dendritic morphology of these neurons was then analyzed quantitatively and compared with neurons from controls. Cysteamine treatment induced a reduction of the number of dendritic end points by more than 50%. At postnatal day 14, for example, controls and somatostatin-depleted animals had an average of 58 and 28 end points, respectively. The number of primary dendrites was also significantly reduced by cysteamine. In contrast, the size of the somata, the orientation of the dendritic trees within the lateral superior olive, the dendritic areas, and the cross-sectional size of the lateral superior olive were not altered. These results indicate that somatostatin depletion during early development has profound effects on the maturation of dendritic morphology. The selective influence on the dendritic trees suggests that somatostatin acts as an endogenous trophic peptide and promotes the achievement of dendritic complexity.

Neonatal adrenalectomy alters dendritic branching of hippocampal granule cells

Alterations in glucocorticoid hormones are known to affect the development of brain and behavior, but the details of these effects at the cellular level are unclear. The present study was undertaken to determine whether dendritic growth and branching in glucocorticoid target neurons, the granule neurons of the hippocampal dentate gyrus, are affected by glucocorticoid hormones. Computerized morphometric analysis of Golgi impregnated granule cells showed that adrenalectomy on Postnatal Day 21 resulted in a small decrease in dendritic branching of lower order dendrites in both male and female rats at 42 days of age, while branching of distal dendrites was left unaffected. Conversely, dendritic branching in rats treated daily with hydrocortisone acetate (5 mg/kg) during the same period was not significantly different from that of untreated rats. Total dendritic length was unaffected by either treatment. These results suggest that relatively minor alterations may occur in the circuitry in the inner molecular layer of the dentate gyrus, a region involving intrahippocampal connections, in the absence of physiological levels of glucocorticoid hormones. Whether these effects are mediated via glucocorticoid hormone effects on the presynaptic afferent neurons or via granule cell metabolic pathways remains to be determined. The most surprising result, given the presence of glucocorticoid receptors in granule cells and the relatively dramatic effects of glucocorticoid manipulations on whole brain that have been reported, is that the effects of these manipulations on dendritic morphology are minimal. While effects upon other aspects of hippocampal circuitry may have occurred, these results suggest that either the hormonal milieu may have already had its principal effects on dendritic branching patterns prior to the time that these manipulations were begun or that the hormonal milieu has very little effect upon the development of dendritic morphology in the dentate gyrus.