In 70-100-year-old subjects, aortic PWV is a strong independent marker of CVD, a finding that remains to be to confirmed by long-term longitudinal studies.

1 The electroencephalographic (EEG) eects of drugs interacting with dopaminergic and noradrenergic systems were studied in conscious rats. Power spectra (0 ± 30 Hz) were recorded from electrodes implanted bilaterally in the prefrontal cortex. Drug eects on EEG power were calculated as the spectral power following drug administration divided by the spectral power after vehicle administration. were dose-dependently antagonized by coadministration with moda®nil and cirazoline, but not by apomorphine. 4 In conclusion, pharmacological modulation of dopaminergic and noradrenergic transmission may result in consistent EEG changes: decreased dopaminergic or noradrenergic activity induces an increase of EEG spectral power; while increased dopaminergic or noradrenergic activity decreases EEG spectral power.

No abstract

1 The electroencephalographic (EEG) e ects of the propsychotic agent phencyclidine (PCP), were studied in conscious rats using power spectra (0 ± 30 Hz), from the prefrontal cortex or sensorimotor cortex. PCP (0.1 ± 3 mg kg 71 s.c.) caused a marked dose-dependent increase in EEG power in the frontal cortex at 1 ± 3 Hz with decreases in power at higher frequencies (9 ± 30 Hz). At high doses (3 mg kg 71 s.c.) the entire spectrum shifted to more positive values, indicating an increase in cortical synchronization. MK 801 (0.05 ± 0.1 mg kg 71 i.p.) caused similar e ects but with lesser changes in power. 2 In contrast, the non-competitive AMPA antagonists GYKI 52466 and GYKI 53655 increased EEG power over the whole power spectrum (1 ± 10 mg kg 71 i.p.). The atypical antipsychotic clozapine (0.2 mg kg 71 s.c.) synchronized the EEG (peak 8 Hz). The 5-HT 2A -antagonist, M100907, speci®cally increased EEG power at 2 ± 3 Hz at low doses (10 and 50 mg kg 71 s.c.), whereas at higher doses (0.1 mg kg 71 s.c.) the pro®le resembled that of clozapine.

No abstract