Neutralisation of intense ion beams at JET
Neutralization is an important issue in the design of neutral beam injection (NBI) systems for heating and fueling fusion plasmas. It has long been established that the neutralization efficiency of the JET injectors falls short of the theoretical value as determined by the expected gas target thickness and the well-known reaction cross-sections. This problem is even more acute in the recently upgraded 130 kV/60 Amp injectors at JET. An illustration shows the measured deuterium power delivered to JET as a function of extracted beam power. It has been proposed that the efficiency deficit is caused by a reduction in the line integrated gas density in the injector's neutralizer. This density reduction could be due to a number of factors including wall pumping and modification of the flow regime, but recent spectroscopic measurements of the neutralization system suggest that the density depletion is due to heating of the neutralizer gas. The mechanism responsible for this is thought to be indirect energy transfer from the beam to the neutral gas via the low temperature plasma that is formed in the neutralization process inside the neutralizer cell. This paper presents measurements of neutralization efficiency based on calorimetric data from the JET injectors. We also present some results from an experimental investigation at the JET Neutral Beam Test Bed including measurements of the low temperature neutralizer plasma. The plasma measurements are used as input parameters for a gas heating model and the outputs of this model are compared to a spectroscopic measurement of the neutralizer gas temperature. Overall, the results support hypothesis that the neutralization deficit is caused by gas density depletion due to indirect heating of the neutralizer gas.
A new hydrogen particle source
• A submitted manuscript is the author's version of the article upon submission and before peer-review. There can be important differences between the submitted version and the official published version of record. People interested in the research are advised to contact the author for the final version of the publication, or visit the DOI to the publisher's website. • The final author version and the galley proof are versions of the publication after peer review. • The final published version features the final layout of the paper including the volume, issue and page numbers.
Alterations in spontaneous single unit activity of striatal subdivisions during ontogenesis in mutant dystonic hamsters
The pathophysiology of idiopathic dystonia, characterized by sustained twisting movements and postures, is still unknown. Clinically, however, the basal ganglia are thought to be the main causative origin of idiopathic dystonia. In the dtsz hamster, a genetic animal model for idiopathic paroxysmal dystonia, the attacks occur in response to mild stress and the severity of dystonia is age-dependent. Previous autoradiographic studies in the dtsz hamster revealed a decreased dopamine D1 and D2 receptor binding and an increased [3H]-2-deoxyglucose uptake in the dorsomedial caudate-putamen (CPu), a region supposed to be critically involved in dystonia. Therefore, we were interested whether the spontaneous firing rate of dorsomedial striatal neurons is age-dependently altered in comparison to age-matched non-dystonic control hamsters. Extracellular recordings of spontaneous single unit activity of dorsomedial and ventromedial Type II striatal neurons, i.e., biphasic positive-negative action potentials, from fentanyl anesthetized animals revealed a drastically increased firing rate in the dorsomedial CPu of mutants during age of maximum severity of dystonia. In post-dystonic dtsz hamsters, i.e., after remission of stress-inducible dystonia, no significant differences regarding the dorsomedial CPu could be obtained. We conclude that the dorsomedial subregion of the CPu seems to be critically involved in the dystonic syndrome of dtsz hamsters and that a transiently reduced inhibitory control over excitatory cortico-striatal processes, possibly due to an altered development of GABAergic inhibition, occurs during ontogenesis in dtsz hamsters.