Benzodiazepine receptor agonists cause drug-specific and state-specific alterations in EEG power and acetylcholine release in rat pontine reticular formation.

摘要: INSOMNIA IS THE MOST COMMON SLEEP DISORDER AND HAS A DIRECT IMPACT ON PUBLIC HEALTH QUALITY OF LIFE.1–3 BENZODIAZEPINE (BDZ) non-benzodiazepine (NBDZ) hypnotics are commonly used to treat insomnia. These have specific binding sites on the ionotropic γ-aminobutyric acid type (GABAA) receptor complex, and they decrease neuronal excitability by enhancing inhibitory effect of endogenous GABA.4 Different BDZ NBDZ show different affinities for various GABAA subtypes. Although these improve total sleep time,2,3,5–7 some drugs associated with risk tolerance dependence can cause next-day drowsiness, impaired memory, or rebound insomnia.8–10 Despite widespread use, mechanisms which alter chemical neurotransmission in brain regions regulating remain poorly understood. Cholinergic transmission pontine reticular formation (PRF) contributes generation rapid eye movement (REM) activation11 cortical electroencephalogram (EEG), is characteristic both wakefulness REM sleep.12,13 Acetylcholine (ACh) release PRF greater during than non-REM (NREM) wakefulness.14 Enhancing cholinergic increases cat,15 rat,16–19 mouse.20–22 GABAergic inhibits sleep23–25 ACh release,26 but no previous vivo studies characterized effects PRF. The present study had 2 goals. first was test hypothesis that microdialysis delivery diazepam zolpidem eszopiclone differentially alters EEG delta power. second goal intravenous (IV) administration PRF, sleep, Portions data been presented as abstracts.27,28