Avalanches in a Bose-Einstein condensate

Collisional avalanches are identified to be responsible for an 8-fold increase of the initial loss rate of a large 87-Rb condensate. We show that the collisional opacity of an ultra-cold gas exhibits a critical value. When exceeded, losses due to inelastic collisions are substantially enhanced. Under these circumstances, reaching the hydrodynamic regime in conventional BEC experiments is highly questionable.Comment: 4 pages, 2 figures, 1 tabl

Critical collisional opacity in a Bose-Einstein condensate

Summary form only given. In a Bose-Einstein condensate, due to the very low temperature, the s-wave scattering length can be used as a measure for the strength of the atom-atom interaction. Under typical experimental conditions, this interaction is weak and hence can be treated in terms of a mean field. However, when scattering length is large or the density is high, the mean field approximation breaks down. In this collisional (hydrodynamic) regime, effects of the interactions such as quantum depletion or shifts in the frequencies of the elementary excitations become large. It is therefore of great interest to study condensates close to or in the collisional regime. It has been demonstrated in recent experiments that the scattering length and thus the interactions among the atoms can be tuned by means of a Feshbach resonance (Inouye et al, 1998; Courteille et al., 1998; Vuleti et al., 1999; Cornish et al., 2000). In the vicinity of Feshbach resonances, however, the increase of the cross-section for elastic collisions is accompanied by a dramatic increase of particle losses. In this paper we report on the observation of anomalous losses from a 87Rb condensate with a high column density in the absence of an inelastic scattering resonance

Neurotransmitter release and its presynaptic modulation in the rat hippocampus after selective damage to cholinergic or/and serotonergic afferents

Male Long-Evans rats sustained injections of 5,7-dihydroxytryptamine (5,7-DHT) into the fimbria-fornix and the cingular bundle or/and intraseptal injections of 192 IgG-saporin to induce serotonergic or/and cholinergic hippocampal denervations; Sham-operated rats served as controls. Four to ten weeks after lesioning, we measured (i). the electrically evoked release of acetylcholine ([3H]ACh), noradrenaline ([3H]NA) and serotonin ([3H]5-HT) in hippocampal slices in the presence of drugs acting on auto- or heteroreceptors, (ii). the nicotine-evoked release of NA and (iii). the choline acetyltransferase (ChAT) activity and the concentration of monoamines in homogenates. Saporin lesions reduced the accumulation of [3H]choline, the release of [3H]ACh and the ChAT activity, but increased the concentration of NA and facilitated the release of [3H]NA evoked by nicotine. 5,7-DHT lesions reduced the accumulation and the release of [3H]5-HT, the concentration of 5-HT, and also facilitated the release of [3H]NA evoked by nicotine. Accumulation and electrically evoked release of [3H]NA were not altered by either lesion. The combination of both toxins resulted in an addition of their particular effects. The 5-HT(1B) receptor agonist, CP 93129, and the muscarinic agonist, oxotremorine, reduced the release of [3H]ACh in control and 5,7-DHT-lesioned rats; in rats injected with saporin, their effects could not be measured reliably. CP 93129 and the alpha(2)-adrenoceptor agonist, UK 14304, reduced the release of [3H]5-HT in all groups by about 65%. IN CONCLUSION: (i). selective neurotoxins can be combined to enable controlled and selective damage of hippocampal transmitter systems; (ii). 5-HT exerts an inhibitory influence on the nicotine-evoked release of NA, but partial serotonergic lesions do not influence the release of ACh at a presynaptic level and (iii). presynaptic modulatory mechanisms involving auto- and heteroreceptors may be conserved on fibres spared by the lesions

Critical collisional opacity in a Bose-Einstein condensate

Summary form only given. In a Bose-Einstein condensate, due to the very low temperature, the s-wave scattering length can be used as a measure for the strength of the atom-atom interaction. Under typical experimental conditions, this interaction is weak and hence can be treated in terms of a mean field. However, when scattering length is large or the density is high, the mean field approximation breaks down. In this collisional (hydrodynamic) regime, effects of the interactions such as quantum depletion or shifts in the frequencies of the elementary excitations become large. It is therefore of great interest to study condensates close to or in the collisional regime. It has been demonstrated in recent experiments that the scattering length and thus the interactions among the atoms can be tuned by means of a Feshbach resonance (Inouye et al, 1998; Courteille et al., 1998; Vuleti et al., 1999; Cornish et al., 2000). In the vicinity of Feshbach resonances, however, the increase of the cross-section for elastic collisions is accompanied by a dramatic increase of particle losses. In this paper we report on the observation of anomalous losses from a 87Rb condensate with a high column density in the absence of an inelastic scattering resonance

Manual MRI morphometry in Parkinsonian syndromes

Background: Several morphometric magnetic resonance imaging parameters may serve for differential diagnosis of parkinsonism. The objective of this study was to identify which performs best in clinical routine. Methods: We acquired multicentric magnetization-prepared rapid gradient echo sequences in patients with Parkinson's disease (n=204), progressive supranuclear palsy (n=106), multiple system atrophy-cerebellar, (n = 21); multiple system atrophy-parkinsonian (n = 60), and healthy controls (n = 73), performed manual planimetric measurements, and calculated receiver operator characteristics with leave-one-out cross-validation to propose cutoff values. Results: The midsagittal midbrain area was reduced in PSP versus all other groups (P < 0.001). The midsagittal pons area was reduced in MSA-cerebellar, MSA-parkinsonian, and PSP versus PD patients and healthy controls (P < 0.001). The midbrain/pons area ratio was lower in PSP (P < 0.001) and higher in MSA-cerebellar and MSA-parkinsonian versus PD and PSP (P < 0.001). Conclusions: The midsagittal midbrain area most reliably identified PSP, the midsagittal pons area MSA-cerebellar. The midbrain/pons area ratio differentiated MSA-cerebellar and PSP better than the magnetic resonance-Parkinson index. © 2017 International Parkinson and Movement Disorder Society. © 2017 International Parkinson and Movement Disorder Societ

Olanzapine Sensitization and Clozapine Tolerance: From Adolescence to Adulthood in the Conditioned Avoidance Response Model

Disruption of conditioned avoidance response (CAR) in rodents is one trademark feature of many antipsychotic drugs. In adult rats, repeated olanzapine (OLZ) treatment causes an enhanced disruption of avoidance response (sensitization), whereas repeated clozapine (CLZ) treatment causes a decreased disruption (tolerance). The present study addressed (1) whether OLZ sensitization and CLZ tolerance can be induced in adolescent rats, and (2) the extent to which OLZ sensitization and CLZ tolerance induced in adolescence persists into adulthood. Male adolescent Sprague–Dawley rats (approximate postnatal days (BP) 43–47) were first treated with OLZ (1.0 or 2.0 mg/kg, subcutaneously (sc)) or CLZ (10 or 20 mg/kg, sc) daily for 5 consecutive days in the CAR model. They were then tested for the expression of OLZ sensitization or CLZ tolerance either in adolescence (BP 50) or after they matured into adults (BP 76 and 92) in a challenge test during which all rats were injected with either a lower dose of OLZ (0.5 mg/kg) or CLZ (5.0 mg/kg). When tested in adolescence, rats previously treated with OLZ showed a stronger inhibition of CAR than those previously treated with vehicle (ie, sensitization). In contrast, rats previously treated with CLZ showed a weaker inhibition of CAR than those previously treated with vehicle (ie, tolerance). When tested in adulthood, the OLZ sensitization was still detectable at both time points (BP 76 and 92), whereas the CLZ tolerance was only detectable on BP 76, and only manifested in the intertrial crossing. Performance in the prepulse inhibition and fear-induced 22 kHz ultrasonic vocalizations in adulthood were not altered by adolescence drug treatment. Collectively, these findings suggest that atypical antipsychotic treatment during adolescence can induce a long-term specific alteration in antipsychotic effect that persists into adulthood despite the brain maturation. As antipsychotic drugs are being increasingly used in children and adolescents in the past two decades, findings from this study are important for understanding the impacts of adolescent antipsychotic treatment on the brain and behavioral developments. This work also has implications for clinical practice involving adolescence antipsychotic treatments in terms of drug choice, drug dose, and schedule

Structural and Resting State Functional Connectivity of the Subthalamic Nucleus: Identification of Motor STN Parts and the Hyperdirect Pathway

Contains fulltext : 109610.pdf (publisher's version ) (Open Access)Deep brain stimulation (DBS) for Parkinson's disease often alleviates the motor symptoms, but causes cognitive and emotional side effects in a substantial number of cases. Identification of the motor part of the subthalamic nucleus (STN) as part of the presurgical workup could minimize these adverse effects. In this study, we assessed the STN's connectivity to motor, associative, and limbic brain areas, based on structural and functional connectivity analysis of volunteer data. For the structural connectivity, we used streamline counts derived from HARDI fiber tracking. The resulting tracks supported the existence of the so-called "hyperdirect" pathway in humans. Furthermore, we determined the connectivity of each STN voxel with the motor cortical areas. Functional connectivity was calculated based on functional MRI, as the correlation of the signal within a given brain voxel with the signal in the STN. Also, the signal per STN voxel was explained in terms of the correlation with motor or limbic brain seed ROI areas. Both right and left STN ROIs appeared to be structurally and functionally connected to brain areas that are part of the motor, associative, and limbic circuit. Furthermore, this study enabled us to assess the level of segregation of the STN motor part, which is relevant for the planning of STN DBS procedures

Regulation of the common carotid arterial blood flow by nicotinic receptors in the medulla of cats

Background and purpose: Actions of glutamate and serotonin on their respective receptors in the dorsal facial area (DFA) of the medulla are known to regulate common carotid arterial (CCA) blood flow in cats. Less is known about acetylcholine action on its nicotinic receptor (nAChR) subtypes in the DFA for regulation of CCA blood flow and this aspect was investigated. Experimental approach: Nicotinic and muscarinic agonists and antagonists were microinjected into the DFA through a three-barrel tubing in anesthetized cats. Results: CCA blood flow was dose-dependently increased by nicotine (a non-selective nAChR agonist) and choline (a selective alpha 7-nAChR agonist). These effects of nicotine were attenuated by alpha-bungarotoxin (an alpha 7-nAChR antagonist), methyllycaconitine (an alpha 7-nAChR antagonist), mecamylamine (a relatively selective alpha 3 beta 4-nAChR antagonist) and dihydro-beta-erythroidine (a relatively selective alpha 4 beta 2-nAChR antagonist). The choline-induced flow increase was attenuated by alpha-bungarotoxin and mecamylamine, but not by dihydro-beta-erythroidine. Muscarinic agonists (muscarine and methacholine) and antagonist (atropine) affected neither the basal nor the nicotine-induced increase in the CCA blood flow. Conclusions and implications: Functional alpha 7, alpha 4 beta 2, and alpha 3 beta 4 subunits of the nAChR appear to be present on the DFA neurons. Activations of these receptors increase the CCA blood flow. The present findings do not preclude the presence of other nAChRs subunits. Muscarinic receptors, if any, on the DFA are not involved in regulation of the CCA blood flow. Various subtypes of nAChRs in the DFA may mediate regulation of the CCA and cerebral blood flows