Brief Pulses (brief + pulse)

Distribution by Scientific Domains

Selected Abstracts

Nerve growth factor-induced circadian phase shifts and MAP kinase activation in the hamster suprachiasmatic nuclei

Gastón A. Pizzio
Abstract Circadian rhythms are entrained by light and by several neurochemical stimuli. In hamsters housed in constant darkness, i.c.v. administration of nerve growth factor (NGF) at various times in their circadian cycle produced phase shifts of locomotor activity rhythms that were similar in direction and circadian timing to those produced by brief pulses of light. Moreover, the effect of NGF and light were not additive, indicating signalling points in common. These points include the immediate-early gene c-fos and ERK1/2, a component of the mitogen-activated protein kinases (MAPK) family. NGF activates c-FOS and ERK1/2-MAPK in the suprachiasmatic nuclei, the site of a circadian clock in mammals, when administered during the subjective night but not during the day. The effect of NGF on ERK1/2 activation was not inhibited by the administration of MK-801, a glutamate/NMDA receptor antagonist. These results suggest that NGF, acting through MAPK activation, plays a role in photic entrainment of the mammalian circadian clock. [source]

Nutrient cycling efficiency explains the long-term effect of ecosystem engineers on primary production

Summary 1Soil organisms, such as earthworms, accelerate mineralization of soil organic matter and are thought to be beneficial for plant growth. This has been shown in short-term microcosm experiments. It is thus legitimate to ask whether these increases in plant growth are due to brief pulses of mineralization or whether these increases are long-lasting. 2This question was addressed using a system of differential equations modelling the effects of decomposers on nutrient cycling via trophic (nutrient assimilation) and nontrophic effects (through their ecosystem engineering activities). 3The analytical study of this model showed that these processes increase primary production in the long term when they recycle nutrients efficiently, allowing a small fraction of the recycled nutrients to be leached out of the ecosystem. 4Mineralization by the ecosystem engineering activities of decomposers seems to deprive them of a resource. However, it was shown that a decomposer may increase its own biomass, through its ecosystem engineering activities, provided the created recycling loop is efficient enough. 5Mechanisms through which earthworms may modify the efficiency of nutrient cycling are discussed. The necessity of measuring the effect of earthworms on the nutrient input,output balance of ecosystems under field conditions is emphasized. [source]

Spontaneous IPSCs and glycine receptors with slow kinetics in wide-field amacrine cells in the mature rat retina

Margaret Lin Veruki
The functional properties of glycine receptors were analysed in different types of wide-field amacrine cells, narrowly stratifying cells considered to play a role in larger-scale integration across the retina. The patch-clamp technique was used to record spontaneous IPSCs (spIPSCs) and glycine-evoked patch responses from mature rat retinal slices (4,7 weeks postnatal). Glycinergic spIPSCs were blocked reversibly by strychnine (300 nm). Compared to previously described spIPSCs in AII amacrine cells, the spIPSCs in wide-field amacrine cells displayed a very slow decay time course (,fast, 15 ms; ,slow, 57 ms). The kinetic properties of spIPSCs in whole-cell recordings were paralleled by even slower deactivation kinetics of responses evoked by brief pulses of glycine (3 mm) to outside-out patches from wide-field amacrine cells (,fast, 45 ms; ,slow, 350 ms). Non-stationary noise analysis of patch responses and spIPSCs yielded similar average single-channel conductances (,31 and ,34 pS, respectively). Similar, as well as both lower- and higher-conductance levels could be identified from directly observed single-channel gating during the decay phase of spIPSCs and patch responses. These results suggest that the slow glycinergic spIPSCs in wide-field amacrine cells involve ,2, heteromeric receptors. Taken together with previous work, the kinetic properties of glycine receptors in different types of amacrine cells display a considerable range that is probably a direct consequence of differential expression of receptor subunits. Unique kinetic properties are likely to differentially shape the glycinergic input to different types of amacrine cells and thereby contribute to distinct integrative properties among these cells. [source]

Protein kinase C, mediates ethanol withdrawal hyper-responsiveness of NMDA receptor currents in spinal cord motor neurons

Hui-Fang Li
1The present studies were designed to test the hypothesis that neuronal-specific protein kinase C, (PKC,) plays a critical role in acute ethanol withdrawal hyper-responsiveness in spinal cord. 2Patch-clamp studies were carried out in motor neurons in neonatal rat spinal cord slices. Postsynaptic currents were evoked by brief pulses of 2 mMN -methyl- D -aspartic acid (NMDA) in the presence of bicuculline methiodide 10 ,M; strychnine 5 ,M and tetrodotoxin 0.5 ,M. 3Both ethanol depression and withdrawal hyper-responsiveness of NMDA-evoked currents are dependent on increases in intracellular Ca2+. Blocking intracellular increase in Ca2+ by 30 mM 1,2-bis(2-aminophenoxy)-ethane- N,N,N,,N,-tetraacetic acid (BAPTA) not only decreased the ethanol-induced depression of NMDA-evoked currents (33±5% in control vs 20±3% in BAPTA, P<0.05) but also eliminated acute ethanol withdrawal hyper-responsiveness. 4Immunohistochemistry studies revealed that neonatal spinal cord motor neurons contain an abundance of nuclear PKC,. 5Exposure to ethanol (100 mM) induced PKC, translocation from the nucleus to cytoplasm in motor neurons. Pretreatment with the , -isozyme-specific peptide PKC inhibitor, ,V5-3, blocked ethanol-induced translocation and also blocked withdrawal hyper-responsiveness. 6The results show that PKC, mediates ethanol withdrawal hyper-responsiveness in spinal motor neurons; the results may be relevant to some symptoms of ethanol withdrawal in vivo. British Journal of Pharmacology (2005) 144, 301,307. doi:10.1038/sj.bjp.0706033 [source]