A randomised comparison of two inactivated hepatitis A vaccines, Avaxim and Vaqta, given as a booster to subjects primed with Avaxim.

To investigate whether Vaqta may be used as a booster in subjects primed with Avaxim, 127 adults primed 6 months previously with Avaxim were randomised to receive either Vaqta or Avaxim as a booster. Prior to the booster all subjects were seropositive. Geometric mean antibody titres increased from 496 to 7262 mIU/mL 1 month after receiving Vaqta as a booster and from 325 to 5131 mIU/mL 1 month after receiving Avaxim as a booster.

NMDA and AMPA receptors evoke transmitter release from noradrenergic axon terminals in the rat spinal cord.

N-methyl-D-aspartate (NMDA) stimulated release of [3H]noradrenaline (NA) from prelabelled rat spinal cord slices. The release was partially insensitive to tetrodotoxin (TTX) and was inhibited by the NMDA antagonist MK-801. Alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionate (AMPA) also evoked release of [3H]NA, which was enhanced by blocking AMPA receptor desensitization with cyclothiazide.

Unique properties of [3H]MK-801 binding in membranes from the rat spinal cord.

In order to investigate possible differences between NMDA receptor-coupled ion channels in the spinal cord and in the cerebral cortex, we have characterized [3H]MK-801 [(+)-5-methyl-10,11-dihydro-5H-dibenzo[a,d]cyclohepten-5,10-imine] binding and its regulation by glutamate and glycine in membrane preparations of the rat spinal cord and cerebral cortex. The K(D) value of [3H]MK-801 binding was higher in the spinal cord than in the cerebral cortex, mainly due to a lower association rate constant. When corrected for the concentrations of residual endogenous amino acids, the EC50 values for glycine were lower at spinal NMDA receptors compared to those in the cerebral cortex, whereas the EC50 values for glutamate were similar in both regions.

Pharmacological characterization of [3H]MK-801 binding in the rat spinal cord.

Using a receptor binding assay for [3H](+)-5-methyl-10,11-dihydro-5H-dibenzo[a,d]cyclohepten-5-10-imi ne (MK-801) the pharmacology of spinal cord NMDA receptors was compared to that of NMDA receptors in the cerebral cortex. The affinities of glutamate site agonists L-glutamate, L-aspartate, ibotenic acid, NMDA and quinolinic acid for stimulation of [3H]MK-801 binding were 6-10 times lower in the spinal cord and the efficacy of quinolinic acid was 50% of that of the other agonists in this region. Also the affinities of glycine site agonists glycine, D-serine, D-alanine and L-serine were lower in the spinal cord as were the affinities of the non-competitive antagonists phencyclidine, (+/-)-cyclazocine and dextromethorphan.

Regional biotransformation of MPTP in the CNS of rodents and its relation to neurotoxicity.

The concentrations of the catecholamine neurotoxin 1-methyl-4-phenyl-1, 2,3,6-tetrahydropridine (MPTP) and its oxidized metabolite 1-methyl-4-phenylpyridine (MPP+) were determined by liquid chromatography in various regions of brains from NMRI and C57 BL/6 mice and from Sprague-Dawley rats after systemic administration of MPTP. Peak levels of MPTP were reached within 5 min after i.v.