Benzodiazepine binding sites in the cingulate cortex after lesion of the noradrenaline and dopamine containing afferents

The distribution of benzodiazepine binding sites was analysed in the cingulate cortex of the rat brain by quantitative radioautography of brain sections incubated with a full agonist benzodiazepine ligand, 3H-flunitrazepam (3H-FLU), or with a partial agonist with non benzodiazepine structure, (7-3H)-4hydroxy-N(4,5-dihydroxy-2-thiazolyl)-6 methoxy-3-quinoline (3H-RU 43028), after lesion of noradrenaline (NA) and dopamine (DA) containing afferents to this structure. NA denervation was obtained by systemic administration of N-(2-chlorethyl)-N ethyl-2-bromobenzylamine (DSP4) and destruction of both NA and DA containing afferents was induced by unilateral injection of 6-hydroxydopamine (6-OHDA) in the middle forebrain bundle (MFB). A similar caudo-rostral pattern of distribution was found in the cingulate cortex after incubation with these two ligands which bound a greater number of sites in the anterior portion of the structure. In spite of a very precise anatomical sampling (200 micron intervals along the postero-anterior axis) no significant difference was observed when intact and lesioned brains were compared. It is concluded that benzodiazepine binding sites eventually localized on catecholaminergic afferents to the cingulate cortex do not represent a significant proportion of the total population of these sites in this structure.     

Neurosarcoidosis: evaluation using computed tomography and magnetic resonance imaging

Two patients with unusual central nervous system sarcoid were investigated using computed tomography and magnetic resonance imaging, as well as other x-ray studies. A patient with intramedullary involvement of the spinal cord as well as nerve root involvement was examined. Follow-up examination after treatment with steroids showed a return to normal. The second patient had optic nerve involvement as well as two intracranial parenchymal lesions and granulomatous arachnoiditis. In this patient magnetic resonance imaging offered no advantages over computed tomography in the orbit but was significantly more accurate intracranially.     

Hyperalgesic pseudothrombophlebitis. New syndrome in male homosexuals

Five male homosexuals, four of whom had Kaposi's sarcoma, presented with painful swelling of the lower extremity. The overlying skin was erythematous and exquisitely tender. Deep vein thrombosis was strongly suspected in all patients. Venography, however, revealed no evidence of venous occlusion. This condition, which in this report is termed the hyperalgesic pseudothrombophlebitis syndrome, appears to be another unusual manifestation of the acquired immune deficiency syndrome. It should be considered among the entities known to mimic deep vein thrombosis and must be recognized in order to prevent unnecessary anticoagulation in these patients.     

The prostaglandin paradox: additive inhibition of neutrophil function by aspirin-like drugs and the prostaglandin E1 analog misoprostol.

Nonsteroidal antiinflammatory drugs (NSAID) are thought to act in part by inhibiting prostaglandin H (PGH) synthase which diminishes release of inflammatory prostaglandins (PG). Paradoxically, PG of the E series also have antiinflammatory properties. We therefore studied the combined effects of NSAID and PGE1 on neutrophil activation. Incubation of neutrophils with a PGE1 analog, misoprostol (miso; 1 microM; 5 min, 37 degrees), reduced superoxide anion generation in response to the chemoattractant fmet-leu-phe (FMLP) to 70.7 +/- 7% of control (p less than 0.01). Piroxicam (10 microM) independently reduced FMLP dependent superoxide anion generation to 63.7 +/- 7.4% (p less than 0.01) of control. Addition of miso to piroxicam reduced superoxide anion production to 37.4 +/- 1.9%, an inhibition that exceeded that observed with either drug alone. Similarly, the addition of miso enhanced the inhibitory effects of indomethacin and sodium salicylate on superoxide anion generation, and of all 3 NSAID on other neutrophil functions (degranulation, aggregation and global rises in cytosolic calcium). Miso (1 microM) and NSAID, alone or in combination, did not inhibit superoxide anion generation in response to the calcium ionophore A23187 or phorbol myristate acetate, agents that bypass G protein depending signaling pathways, and that do not induce a rise in cytosolic cyclic AMP (cAMP). Therefore, our data clearly show that miso at micromolar concentrations, augments the inhibitory effects of NSAID on neutrophil activation via a mechanism dependent upon signal transduction across the plasma membrane.     

Variation of tryptophan-5-hydroxylase concentration in the rat raphe dorsalis nucleus afterp-chlorophenylalanine administration. II. Anatomical distribution of the tryptophan-5-hydroxylase protein and regional variation of its turnover rate

Distribution of tryptophan-5-hydroxylase (TpOH)-containing cells and TpOH protein tissue concentrations were evaluated in the nucleus raphe dorsalis (NRD) of rat brain by immunocytochemistry and direct transfer onto nitrocellulose filters of unfixed adjacent brain sections. This work has demonstrated that: (1) the direct transfer onto nitrocellulose filters could be easily used for the quantitative analysis of TpOH protein distribution; (2) the origin of the TpOH in this brain nucleus was preferentially cellular; (3) classical subdivisions, qualtitatively defined from morphometric and topographic observations could be precisely described in terms of cellular density, tissue and cellular concentrations and turnover of TpOH protein. Such differences could imply a physiological control of TpOH gene expression in the serotoninergic neurons.     

Prion Strain Discrimination Based on Rapid In Vivo Amplification and Analysis by the Cell Panel Assay

Prion strain identification has been hitherto achieved using time-consuming incubation time determinations in one or more mouse lines and elaborate neuropathological assessment. In the present work, we make a detailed study of the properties of PrP-overproducing Tga20 mice. We show that in these mice the four prion strains examined are rapidly and faithfully amplified and can subsequently be discriminated by a cell-based procedure, the Cell Panel Assay.