Septal myocardial abscess in a male great Anglo-French hound.

We report the diagnosis and follow-up of a septal myocardial abscess in a seven-year-old Anglo-French hound suffering from both renal failure and urinary infection. Serial echocardiography showed the abscess enlarging and progressing into a fistula between the left ventricular outflow tract and the right ventricle. The dog died despite early wide-spectrum intravenous antibiotic therapy. Post-mortem examination confirmed the diagnosis. Bacterial and fungal myocardial abscesses have been described in immunodeficient human beings. To our knowledge, fistulae have rarely been described in dog hearts and only as a consequence of previous valvular endocarditis. In our case, the sigmoid cusps were not involved, so this is the first description of a septal myocardial abscess in a dog.

Spontaneous neuronal activity in organotypic cultures of mouse dorsal root ganglion leads to upregulation of calcium channel expression on remote Schwann cells.

It is well established that neurons regulate the properties of both central and peripheral glial cells. Some of these neuro-glial interactions are modulated by the pattern of neuronal electrical activity. In the present work, we asked whether blocking the electrical activity of dorsal root ganglion (DRG) neurons in vitro by a chronic treatment with tetrodotoxin (TTX) would modulate the expression of the T-type Ca(2+) channel by mouse Schwann cells. When recorded in their culture medium, about one-half of the DRG neurons spontaneously fired action potentials (APs). Treatment for 4 days with 1 microM TTX abolished both spontaneous and evoked APs in DRG neurons and in parallel significantly reduced the percentage of Schwann cells expressing Ca(2+) channel currents. On the fraction of Schwann cells still expressing Ca(2+) channel currents, these currents had electrophysiological parameters (mean amplitude, mean inactivation time constant, steady-state inactivation curve) similar to those of control cultures. Co-treatment for 4 days with 1 microM TTX and 2 mM CPT-cAMP, a cAMP analogue that induces the expression de novo of Ca(2+) channel currents in Schwann cells deprived of neurons, maintained the percentage of Schwann cells expressing Ca(2+) channel currents, showing that TTX does not directly affect the expression of Ca(2+) channel currents by Schwann cell. We conclude that blocking spontaneous activity of DRG neurons in vitro downregulates Ca(2+) channel expression by Schwann cells. These results strongly suggest that DRG neurons upregulate Ca(2+) channel expression by Schwann cells via the release of a diffusible factor whose secretion is dependent on electrical activity.

Functional Ca2+ and Na+ channels on mouse Schwann cells cultured in serum-free medium: regulation by a diffusible factor from neurons and by cAMP.

Regulation of expression of functional voltage-gated ion channels for inward currents was studied in Schwann cells in organotypic cultures of dorsal root ganglia from E19 mouse embryos maintained in serum-free medium. Of the Schwann cells that did not contact axons, 46.5% expressed T-type Ca2+ conductances (ICaT). Two days or more after excision of the ganglia, and consequent disappearance of neurites, ICaT were detectable in only 10.9% of the cells, and the marker 04 disappeared. On Schwann cells deprived of neurons, T- (but not L-) type Ca2+ conductances were re-induced by weakly hydrolysable analogues of cAMP, and by forskolin (an activator of adenylyl cyclase) after long-term treatment (4 days). With CPT cAMP (0.1-2 mM), 8Br cAMP, db cAMP or forskolin (0.01 or 0.1 mM), the proportion of cells with ICaT was not significantly different from the proportion in the cultures with neurons. These agents also induced expression in some cells of tetrodotoxin-resistant Na+ currents, which were rarely induced by neurons, but 04 was not re-induced by cAMP analogue treatments that re-induced ICaT. Inward currents (Ba2+ or Na+) were partly restored (P < 0.05) on Schwann cells cultured for 6-7 days beneath a filter bearing cultured neurons. In contrast, addition of neuron-conditioned medium was ineffective. The results suggest that neurons activate, via diffusible and degradable factors, a subset of Schwann cell cAMP pathways leading to expression of IcaT, and activate additional non-cAMP pathways that lead to expression of 04.

Selective downregulation of an inactivating K+ conductance by analogues of cAMP in mouse Schwann cells.

1. Voltage-dependent K+ conductances on Schwann cells in organotypic cultures of mouse dorsal root ganglia were classified as inactivating or sustained (responsible for currents IA and IK, respectively). IA is known to be much reduced on Schwann cells that contact neurites. 2. In the absence of neurones, IA and IK were present. IA, but not IK, was markedly reduced (by 80% after 105 h of treatment) by 2 mM 8-(4-chlorophenylthio)-cAMP (cpt-cAMP), a weakly hydrolysable analogue of cAMP. The effect did not appear for at least 2 h and was maximal after about 100 h. 3. The effect of 1 mM cpt-cAMP was abolished in the presence of an inhibitor of protein kinases, N-[2-bromocinnamyl(amino)ethyl]-5-isoquinolinesulphonamide (H-89, 10 microM). 4. Other analogues of cAMP, but not an analogue of cGMP (8-bromo-cGMP), also reduced IA. 5. We conclude that IA, but not IK, can be downregulated by activation of the protein kinase A pathway.