Histamine prevents polyamine accumulation in mouse C57.1 mast cell cultures.

The effects of histamine on polyamine uptake and metabolism was studied in a mouse mast cell line (C57.1), as a cell model in which both biogenic amines are important for maintaining cell function and viability. Results obtained after incubations with exogenous histamine indicated that histamine prevents polyamine accumulation by affecting polyamine uptake. A plasma membrane transport system for polyamines has been also studied in mast cells. It seems to be a Na(+)-dependent uptake with high affinity for both spermine and spermidine and lower affinity for putrescine and agmatine. Polyamine uptake was reduced in both cells treated with exogenous histamine and histamine-preloaded cells. However, ornithine decarboxylase activity and cell proliferation were not affected by histamine. Incubation with histamine enhanced the spermidine/spermine acetyl transferase induction caused by N(1)-ethyl-N(11)-[(cyclopropyl)methyl]-4,8-diazaundecane, suggesting that polyamine acetylation could be another mechanism by which histamine prevents polyamine accumulation in C57.1 mast cells.

Agmatine uptake by cultured hamster kidney cells.

Agmatine, the product of arginine decarboxylation, has been recently found in a wide variety of animal tissues. In spite of the emergent interest on agmatine in animals, the mechanism of agmatine uptake in mammalian cells has been scarcely studied. An analysis of radiolabeled agmatine uptake was carried out by using a classical, kinetic approach with BHK-21 hamster kidney cells in culture. A high affinity, temperature- and energy-dependent agmatine transport system in BHK-21 kidney cells is here kinetically characterized which seems to be a "general" transporter shared by di- and triamines and different to a highly specific carrier for the tetraamine spermine.

Characterization of spermine uptake by Ehrlich tumour cells in culture.

Spermine is taken up by Ehrlich ascites tumour cells through a specific, saturable, temperature and energy-dependent transport system with a remarkably low affinity constant for spermine (around 1 microM). In the absence of a potassium ion gradient through the plasma membrane, spermine uptake remains saturable but the value of the Km for spermine is much higher (153 microM). Difluormethylornithine treatment (3 mM for 48h) induces significant increases in Vmax values (up to 9-fold) and changes in the Km values with scarce statistical significance. Among the biogenic amines tested, only spermidine and, partly, agmatine seem to share the same transport system with spermine. No difference is observed in the rate of spermine transport when assays are carried out in the presence of 50-fold excess of ornithine or calcium, or 100-fold excess of glutamine.

Fluid percussion injury causes disruption of the septohippocampal pathway in the rat.

Fluid percussion injury (FPI) causes memory deficits, loss of hippocampal neurons, and basal forebrain cholinergic immunoreactivity in rats. Basal forebrain septohippocampal projections terminate in specific hippocampal regions. The purpose of this study was to examine the effects of FPI on the septohippocampal pathway (SHP). Halothane-anesthetized rats received either a sham injury or a parasagittal FPI. To characterize the anatomical effects of FPI on the SHP, silver stains were performed on brains of animals at 1, 5, and 10 days following FPI and were compared to sham-injured preparations. To characterize the effects of FPI on retrograde transport in the SHP, a separate group of FPI and sham-injured animals with survival times of 2, 5, and 10 days received bilateral WGA-HRP injections into the hippocampal formation 24 h prior to sacrifice. Argyrophilic CA3 neurons were present 1 day following FPI. Five days following FPI, terminal degeneration was present in the inner third of the molecular layer of the dentate gyrus bilaterally that was not present 1 day after injury. Fiber and terminal degeneration was not observed in the basal forebrain until 10 days after FPI. WGA-HRP-labeled septal neurons decreased significantly (P < 0.05) ipsilateral to injury in animals sacrificed 5 and 10 days following FPI but not 2 days after injury. This investigation demonstrated that FPI produces focal injury in the hippocampal formation. In addition, the appearance of terminal degeneration in the dentate molecular layer correlated with the significant reduction in axonal transport 5 days following injury. This correlation illustrates the secondary processes that structurally damage the SHP up to 10 days after injury.