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A K Sundgren

Publications and source records attributed to A K Sundgren.

4 recordsLinked to original sources

Glutamate-evoked currents in acutely dissociated neurons from the rat medial preoptic nucleus.

Membrane currents evoked by glutamate were investigated in acutely dissociated neurons from the medial preoptic nucleus (MPN) of rat. Rapid application of glutamate induced a fast current component in all neurons studied. In addition, in > 50% of the neurons, a slow current component was elicited. The fast and the slow current components were selectively blocked by the AMPA-receptor antagonist NBQX and by the NMDA-receptor channel blocker MK-801, respectively. Rapid application of AMPA induced, in all neurons tested, currents with properties similar to the fast component of the glutamate-evoked currents whereas rapid application of NMDA induced, in approximately 75% of the neurons, currents similar to the slow component of the glutamate-evoked currents. The NMDA-evoked currents showed a marked outward rectification that was attributed to a potential-dependent block by extracellular Mg2+. The NMDA-evoked currents also required the presence of extracellular glycine in the micromolar range. In conclusion, the results show that MPN neurons respond to glutamate with currents that can be attributed to activation of ionotropic glutamate receptors of the AMPA-receptor type as well as of the NMDA-receptor type.

Animals↗

Potential-dependent block of human delayed rectifier K+ channels by internal Na+.

The delayed rectifier K+ currents in differentiated human SH-SY5Y neuroblastoma cells were characterized with tight-seal recording techniques. Activation and inactivation parameters were measured. At high positive potentials, the current showed a marked rectification, causing a region of negative slope conductance in the current vs. potential curve. The rectification depended markedly on the pipette Na+ concentration. Without Na+, no rectification was observed, whereas with high Na+ (20-60 mM), a marked rectification was always observed. Tail current measurements showed a fast ( < 400 microseconds) block of K+ currents in the presence of internal Na+. With 60 mM Na+ in the pipette 8% of the K+ current was blocked at 0 mV, 27% at +20 mV, and 82% at +100 mV. Similar degrees of block were often seen with 30 mM Na+ in the pipette. The submembrane Na+ concentration in intact cells was estimated, on the basis of the reversal of Na+ current, to be approximately 15 mM. Single-channel K+ currents, in the cell-attached configuration, showed a conductance of approximately 20 pS at 40-60 mV above rest but showed rectification at high potentials.

Cobalt↗

Graded action potentials generated by neurons in rat hypothalamic slices.

Preoptic neurons in rat hypothalamic slices were investigated with tight-seal whole-cell recording techniques. The main aim was to investigate the ability to generate graded, stimulus-dependent impulses. In response to rectangular current pulses, all cells generated impulses with an amplitude that to some degree depended on the stimulus strength. Stronger current steps induced impulses of larger amplitude. In 50% of the cells, a systematic variation of impulse amplitude of more than 10 mV (up to 40 mV) was recorded, implying a clear deviation from the 'all-or-nothing' principle. A clear variation in amplitude of spontaneous impulses was also recorded, in the whole-cell mode as well as from intact cells in the cell-attached mode.

Action Potentials↗

Interleukin-1 stimulates the expression of type I and type II interleukin-1 receptors in the rat insulinoma cell line Rinm5F; sequencing a rat type II interleukin-1 receptor cDNA.

The insulin secreting rat Rinm5F cells are often used to study the cytotoxic actions of interleukin-1 (IL-1) on pancreatic beta-cells. We demonstrate here that Rinm5F insulinoma cells express both type I and type II interleukin-1 receptor (IL-1R) mRNAs and gene products. IL-1R agonists, recombinant murine IL-1 alpha (rmIL-1 alpha, 10 ng/ml) and recombinant rat IL-1 beta (rrIL-1 beta, 100 pg/ml or 10 ng/ml) induce the upregulation of mRNA expression for both types of IL-1 receptors (IL-1Rs). This effect of rrIL-1 beta is antagonised by preincubation with recombinant human interleukin 1 receptor antagonist protein (rhIL-1ra, 5 micrograms/ml). Furthermore, this rrIL-1 beta induced upregulation of IL-1R mRNAs is blocked by actinomycin D (7.5 micrograms/ml), whereas cycloheximide (20 micrograms/ml) has no effect. The phorbol ester PMA (20 nM) upregulates the expression of mRNAs both IL-1 receptors, whereas glucose (50 mM) upregulates the expression of the type I IL-1R mRNA only. Pretreatment of cells with pertussis toxin (100 ng/ml) partially blocks the rrIL-1 beta induced expression of mRNA for the type I and, to a lesser extent, the type II IL-1R. Incubation of the cells with rrIL-1 beta also induces a time-dependent expression of c-fos, interleukin-6 (IL-6) and tumour necrosis factor alpha (TNF-alpha) mRNAs. Binding studies with 125I-recombinant human IL-1 beta (125I-rhIL-1 beta) indicate that IL-1R gene products, with the ligand binding characteristics of the type I IL-1R, are constitutively present on Rinm5F cells. Treatment with rrIL-1 beta (6h) increases the number of 125I-rhIL-1 beta binding sites on Rinm5F cells. We have also demonstrated that the number of type II IL-1R binding sites increases after induction with rrIL-1 beta (6h), by indirect immunofluorescence using a monoclonal antibody (ALVA 42) raised against the human type II IL-1R. Furthermore, we have sequenced the type II IL-1R cDNA in the rat insulinoma Rinm5F cells. The comparison of the amino acid sequence of the rat type II IL-1R with that of the mouse and human type II IL-1Rs shows 90% and 62% amino acid identity, respectively. The most important difference between the human and murine type II IL-1Rs, and this rat type II IL-1R cDNA, is an open reading frame coding for a six amino acid longer, strongly charged (QIKEMK), cytosolic domain.(ABSTRACT TRUNCATED AT 400 WORDS)

Amino Acid Sequence↗