No abstract

Using microdialysis, we examined the effects of ketamine and pentobarbitone on acetylcholine (ACh) release from the rat hippocampus and striatum. Ketamine 25 and 50 mg kg-1 increased ACh release from the hippocampus to 295% and 353% of basal release, respectively, but not from the striatum. SCH 23390 1 mumol litre-1, a D1 antagonist, significantly inhibited the facilitatory effect of ketamine 50 mg kg-1 on hippocampal ACh release (to 241% of basal level). In contrast, pentobarbitone 20 and 40 mumg kg-1 decreased basal ACh release from both the hippocampus by 41% and 69%, respectively, and the striatum by 37% and 58%, respectively. The results suggest that ketamine and pentobarbitone exert opposite effects on ACh release from the rat hippocampus and that the stimulating effect of ketamine may involve dopamine D1 receptors.

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Using in vivo microdialysis, we have investigated the effects of propofol on acetylcholine (ACh) release from various regions of the rat brain. Propofol 25 and 50 mg kg-1 i.p. decreased basal ACh release from the frontal cortex by 70% and 85%, respectively. Propofol 25 and 50 mg kg-1 i.p. decreased basal ACh release from the hippocampus by 47% and 72%, respectively. However, in rat striatum, propofol 25 mg kg-1 i.p. did not affect basal ACh release and 50 mg kg-1 i.p. produced slight inhibition of basal ACh release (by 19%) only in the second sample after i.p. injection. In addition, we also examined the pharmacological mechanisms mediating the interaction between propofol and a gamma-aminobutyric acid A (GABAA) receptor complex. In the rat hippocampus, local application of bicuculline 1 mumol litre-1, a GABAA receptor antagonist, significantly antagonized the inhibitory effects of propofol 50 mg kg-1 i.p. on basal ACh release. In the rat frontal cortex, local application of bicuculline 1 mumol litre-1 did not antagonize the inhibitory effects of propofol 50 mg kg-1 i.p. on basal ACh release, while systemic application of bicuculline 1 mg kg-1 i.p. significantly antagonized the inhibitory effects of propofol 50 mg kg-1 i.p. These results suggest that propofol has powerful depressant effects on ACh release from the rat frontal cortex and hippocampus but not from the striatum, indicating that propofol has a "region-selective" anaesthetic action. Further, these results suggest that the inhibitory effects of propofol in the rat hippocampus may involve "intra" hippocampal GABAA receptors while the inhibitory effects in the rat frontal cortex may be mediated by GABAA receptors other than "intra" frontal cortex GABAA receptors.

DNA microarrays are routinely used to monitor gene expression profiling and single nucleotide polymorphisms (SNPs). However, for practically useful high performance, the detection sensitivity is still not adequate, leaving low expression genes undetected. To resolve this issue, we have developed a new plastic S-BIO® PrimeSurface® with a biocompatible polymer; its surface chemistry offers an extraordinarily stable thermal property for a lack of pre-activated glass slide surface. The oligonucleotides immobilized on this substrate are robust in boiling water and show no significant loss of hybridization activity during dissociation treatment. This allowed us to hybridize the templates, extend the 3′ end of the immobilized DNA primers on the S-Bio® by DNA polymerase using deoxynucleotidyl triphosphates (dNTP) as extender units, release the templates by denaturalization and use the same templates for a second round of reactions similar to that of the PCR method. By repeating this cycle, the picomolar concentration range of the template oligonucleotide can be detected as stable signals via the incorporation of labeled dUTP into primers. This method of Multiple Primer EXtension (MPEX) could be further extended as an alternative route for producing DNA microarrays for SNP analyses via simple template preparation such as reverse transcript cDNA or restriction enzyme treatment of genome DNA.

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We have studied the effects of ketamine and pentobarbitone on acetylcholine (ACh) release from the rat frontal cortex using microdialysis. Ketamine 25, 50 and 100 mg kg-1 increased ACh release from the frontal cortex to 286%, 253% and 381% of basal release, respectively. In contrast, pentobarbitone 10, 20 and 40 mg kg-1 caused 73%, 78% and 96% inhibition of basal levels, respectively. The results suggest that ketamine and pentobarbitone have opposite effects on ACh release from the rat frontal cortex, as seen previously in the rat hippocampus.

Ketamine has opposite phase-shifting effects on circadian rhythms according to the time of administration, whereas pentobarbital has no effect. Furthermore, both anesthetics decrease the postoperative amplitude of pineal melatonin secretion if administered during the active, but not the resting, phase of the 24-hour rest-activity cycle.