[A rare cause of acute heart failure? : Aorto-right atrial fistula!] / Eine seltene Ursache für akute Herzinsuffizienz? : Aorta-rechtsatriale Fistel!

BACKGROUND: Acute heart failure with symptoms such as dyspnea and edema has various causes. In rare cases cardiac fistulas can cause acute heart failure. Herein we present a case of subacute heart failure due to an acquired fistula between the aorta and right atrium. CASE REPORT: A 48-year-old male was referred to the emergency room with increasing dyspnea on exercise and pitting edema of the lower extremities starting approximately 4 weeks previously. Echocardiographic workup showed an aorta-to-right atrium fistula. The patient was referred to a cardiothoracic surgery center for closure of the fistula.

NMDA and benzodiazepine receptors have synergistic and antagonistic effects on precursor cells in adult hippocampal neurogenesis.

We studied how the noncompetitive NMDA receptor antagonist MK801 affected different stages of adult hippocampal neurogenesis in mice, and investigated how the activation of benzodiazepine receptors with diazepam interacted with the effects of MK801 on the precursor cells in the adult dentate gyrus. Our findings were: (i) one single MK801 application increased precursor cell proliferation and adult neurogenesis but not gliogenesis 4 weeks later; (ii) the number of label-retaining precursor cells decreased after MK801 (with P = 0.06); (iii) the pro-neurogenic effect included increased cell cycle entry of precursor cells as well as completed cell divisions, except in type-2a cells; (iv) NMDA receptor blockade also increased the number of nestin-GFP-expressing cells expressing calretinin; (v) diazepam alone had a very similar effect on overall precursor cell proliferation to that of MK801 alone; and (vi) diazepam, when co-applied with MK801, abolished the suppression of divisions of type-2a cells induced by MK801 alone, suppressed the MK801-induced effect on proliferation of type-2b cells and had no influence on the effects of MK801 on type-3 cells, but did suppress the increased number of nestin-GFP-positive cells expressing calretinin. From these results we hypothesize that, depending on the precursor cell stage, NMDA-dependent neurotransmission has distinct effects that are partly antagonized and partly enhanced by GABAergic input. We propose that NMDA receptor-dependent signalling maintains the precursor cells in the dentate gyrus while blocking initial stages of development and promoting more advanced stages.

Lesions of dopaminergic neurons in the substantia nigra pars compacta and in the ventral tegmental area enhance depressive-like behavior in rats.

Depression is the most common psychiatric complication in Parkinson's disease (PD). The pathophysiological events leading to PD-associated depression, however, remain largely unknown. The present study tested the differential implication of dopaminergic systems in depressive-like behavior in rats and its response to l-Dopa and the selective serotonin reuptake inhibitor citalopram. The learned helplessness model was used as a behavioral paradigm. Rats were lesioned in the substantia nigra pars compacta (SNc) and the ventral tegmental area (VTA) and assigned to subgroups with respect to the stereologically verified extent of the nigral and/or VTA degeneration. Both lesions increased depressive-like behavior in rats, which was reduced by both citalopram and l-Dopa treatment. We conclude that dopaminergic lesions of either the SNc or the VTA contribute to the manifestation of depressive-like behavior in rats. The effects of citalopram administration on depressive behavior induced by lesions of dopaminergic brain regions furthermore suggest an involvement of serotonergic pathways in dopaminergic cell loss-induced depression.

Enriched environment induces cellular plasticity in the adult substantia nigra and improves motor behavior function in the 6-OHDA rat model of Parkinson's disease.

The adult substantia nigra bears the capacity to generate new neural cells throughout adulthood. The mechanisms of cellular plasticity in this brain region remain unknown. In the adult dentate gyrus, dopamine was suggested to be one of the key players in neurogenesis. We therefore investigated nigral cellular plasticity in the 6-OHDA rat model of Parkinson's disease. The absolute numbers of newborn cells in the SN were not affected by dopamine depletion. Interestingly, we found a specific downregulation of generation of newborn nigral astrocytic cells. As enriched environment with physical activity are robust inducers of neuro- and gliogenesis in the adult DG, we investigated the role of these physiological stimuli in nigral cellular plasticity and in motor behavior of 6-OHDA lesioned rats. We describe a significant increase in numbers of newborn NG2-positive and GFAP-positive cells in the SN. Moreover, 6-OHDA lesioned animals living in enriched environment with physical activity for 7 weeks showed improved motor behavior compared to controls under standard conditions. Thus, physiological neurogenic and gliogenic stimuli induce significant microenvironmental changes in the adult SN and improve motor behavior in the 6-OHDA lesion model of PD.