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The European Space Agency Rosetta Spacecraft, launched on March 2, 2004 toward Comet 67P/Churyumov-Gerasimenko, carries a relatively small and lightweight millimeter-submillimeter spectrometer instrument, the first of its kind launched into deep space. The instrument will be used to study the evolution of outgassing water and other molecules from the target comet as a function of heliocentric distance. During flybys of the asteroids (2867) Steins and (21) Lutetia in 2008 and 2010 respectively, the instrument will measure thermal emission and search for water vapor in the vicinity of these asteroids.The instrument, named MIRO (Microwave Instrument for the Rosetta Orbiter), consists of a 30-cm diameter, offset parabolic reflector telescope followed by two heterodyne receivers. Center-band operating frequencies of the receivers are near 190 GHz (1.6 mm) and 562 GHz (0.5 mm). Broadband continuum channels are implemented in both frequency bands for the measurement of near surface temperatures and temperature gradients in Comet 67P/Churyumov-Gerasimenko and the asteroids (2867) Steins and (21) Lutetia. A 4096 channel CTS (Chirp Transform Spectrometer) spectrometer having 180 MHz total bandwidth and 44 kHz resolution is, in addition to the continuum channel, connected to the submillimeter receiver. The submillimeter radiometer/spectrometer is fixed tuned to measure four volatile species – CO, CH3OH, NH3 and three, oxygen-related isotopologues of water, H216O, H217O and H218O. The basic quantities measured with the MIRO instrument are surface temperature, gas production rates and relative abundances, and velocity and excitation temperature of each species, along with their spatial and temporal variability. This paper provides a short discussion of the scientific objectives of the investigation, and a detailed discussion of the MIRO instrument system.

Although kainate receptor activation has been known to evoke epileptiform activity, little is known about the role of kainate receptors in synaptic transmission. Here we report that kainate (KA) receptors are present on interneurons and, when activated, cause a large increase in the frequency of spontaneous inhibitory postsynaptic currents (IPSCs) driven by action potentials. Stimulation of excitatory afferents generates a pharmacologically identifiable synaptic current mediated by KA receptors in interneurons. This synaptic current is similar to that mediated by AMPA receptors in its response to short stimulus trains, current–voltage relations and coefficient of variation, but it is much smaller in peak amplitude and much slower. KA application also considerably depresses evoked IPSCs. This depression seems to be in large part an indirect consequence of the repetitive firing evoked by the activation of the interneuronal somatic/dendritic KA receptors.

Kainate (KA) receptor activation depresses stimulus-evoked γ -aminobutyric acid (GABA-mediated) synaptic transmission onto CA1 pyramidal cells of the hippocampus and simultaneously increases the frequency of spontaneous GABA release through an increase in interneuronal spiking. To determine whether these two effects are independent, we examined the mechanism by which KA receptor activation depresses the stimulus-evoked, inhibitory postsynaptic current (IPSC). Bath application of the α -amino-3-hydroxy-5-methyl-4-isoxazole proprionic acid (AMPA)/KA receptor agonist KA in the presence of the AMPA receptor antagonist GYKI 53655 caused a large increase in spontaneous GABA release and a coincident depression of the evoked IPSC. The depressant action on the evoked IPSC was reduced, but not abolished, by the GABAB receptor antagonist SCH 50911, suggesting that the KA-induced increase in spontaneous GABA release depresses the evoked IPSC through activation of presynaptic GABAB receptors. KA had no resolvable effect on the potassium-induced increase in miniature IPSC frequency, suggesting that KA does not act through a direct effect on the release machinery or presynaptic calcium influx. KA caused a decrease in pyramidal cell input resistance, which was reduced by GABAA receptor antagonists. KA also caused a reduction in the size of responses to iontophoretically applied GABA, which was indistinguishable from the SCH 50911-resistant, residual depression of the evoked IPSC. These results suggest that KA receptor activation depresses the evoked IPSC indirectly by increasing interneuronal spiking and GABA release, leading to activation of presynaptic GABAB receptors, which depress GABA release, and postsynaptic GABAA receptors, which increase passive shunting.

Bortolotto et al. report that the kainate subtype of glutamate receptor is essential for the plasticity of certain types of synaptic transmission in the brain, which is of interest as these receptors were previously not thought to initiate plastic processes. In particular, a new antagonist (LY382884) was shown to act selectively against the GluR5 type of kainate receptor: in the presence of LY382884, which reduces kainate-receptor-mediated postsynaptic responses by ∼40%, long-term potentiation (LTP) at hippocampal mossy-fibre synapses could no longer be induced. Here we argue that the available evidence does not support a major role for kainate receptors in the induction of mossy-fibre LTP.

Hippocampal mossy fibers, which are the axons of dentate granule cells, form powerful excitatory synapses onto the proximal dendrites of CA3 pyramidal cells. It has long been known that high-affinity binding sites for kainate, a glutamate receptor agonist, are present on mossy fibers. Here we summarize recent experiments on the role of these presynaptic kainate receptors (KARs). Application of kainate has a direct effect on the amplitude of the extracellularly recorded fiber volley, with an enhancement by low concentrations and a depression by high concentrations. These effects are mediated by KARs, because they persist in the presence of the α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor-selective antagonist GYKI 53655, but are blocked by the α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid/KAR antagonist 6-cyano-7-nitroquinoxaline-2,3-dione and the KAR antagonist SYM2081. The effects on the fiber volley are most likely caused by a depolarization of the fibers via the known ionotropic actions of KARs, because application of potassium mimics the effects. In addition to these effects on fiber excitability, low concentrations of kainate enhance transmitter release, whereas high concentrations depress transmitter release. Importantly, the synaptic release of glutamate from mossy fibers also activates these presynaptic KARs, causing an enhancement of the fiber volley and a facilitation of release that lasts for many seconds. This positive feedback contributes to the dramatic frequency facilitation that is characteristic of mossy fiber synapses. It will be interesting to determine how widespread facilitatory presynaptic KARs are at other synapses in the central nervous system.

There is still a long way, to put it mildly, from redefining glia as the center of cognition. However, it is increasingly apparent that glia play a more influential role in the brain than previously imagined and that some of the most central assumptions about the division of labor in the brain are due for revision.

Bortolotto et al . 1 report that the kainate subtype of glutamate receptor is essential for the plasticity of certain types of synaptic transmission in the brain, which is of interest as these receptors were previously not thought to initiate plastic processes. In particular, a new antagonist (LY382884) was shown to act selectively against the GluR5 type of kainate receptor: in the presence of LY382884, which reduces kainate-receptor-mediated postsynaptic responses by ∼40%, long-term potentiation (LTP) at hippocampal mossy-fibre synapses could no longer be induced 1 . Here we argue that the available evidence does not support a major role for kainate receptors in the induction of mossy-fibre LTP.

Satake et al . show that glutamate release in the cerebellum causes heterosynaptic depression of GABA release and that AMPA receptors act presynaptically to mediate this phenomenon.