THE vesamicol-like compound (+/-)-4-aminobenzovesamicol (ABV) non-comp
etitively inhibits vesicular packaging of acetylcholine (ACh) in presy
naptic terminals. This study tested the hypothesis that microinjection
of ABV into the medial pontine reticular formation (mPRF) of intact,
unanesthetized cats would inhibit rapid eye movement (REM) sleep. Micr
oinjection of ABV alone or before administration of the acetylcholines
terase inhibitor neostigmine was used to evaluate the effects of ABV o
n natural REM sleep and on the neostigmine-induced REM sleep-like stat
e. ABV decreased (24.8%) REM sleep and significantly reduced (33.6%) t
he neostigmine-induced REM sleep-like state. The results show for the
first time that REM sleep generation can be disrupted by blocking a sy
naptic vesicle protein that modulates ACh transport in localized regio
ns of the mPRF.