LONG-TERM INCREASE OF REM-SLEEP AND PONTO GENICULOOCCIPITAL POTENTIALS (PGO) PROVOKED BY CHOLINERGIC ACTIVATION OF THE TEMPORAL-LOBE AMYGDALA IN THE CAT

The rapid eye movements (REM) sleep is always preceded and accompanied by the occurrence of ponto-geniculo-occipital (PGO) waves. This fact has prometed several authors to consider the PGO mechanisms as a key c omponent for the onset of REM sleep. It has been found that a single c arbachol microinjection in the parabraquial region (PBL), induces the occurrence of PGO waves, and that this phenomenon is always followed b y a significant and prolonged (8 days) increase of REM sleep and its p receding slow wave sleep episodes with PGO waves (SPHOL). This finding s strongly suggest the participation of PBL region in PGO wave generat ion and in the onset of REM sleep. through a cholinergic mechanism. On the other hand, these findings further allow to analyze the role in R EM sleep induction of prosencephalic structures physiologically and an atomically related to the PBL region. Reciprocal anatomical projection s exist between the PBL region and the central amygdaloid nucleus (CN) , which also contains cholinergic neurons. it has been shown that PGO waves propagate from the pontine region to the temporal lobe amygdala (AMG), and that electrical stimulation of the AMG during REM sleep pro duces a significant Increase of PGO waves density. These results suppo rt that the AMG facilitates the occurrence of PGO waves. Recently, we have demonstrated that carbachol microinjection into the CN induces a significant and prolonged (five days) enhancement of REM sleep and SPH OL episodes. Thus it can be hypothesized that the cholinergic activati on of CN facilitates the occurrence of PGO waves and consequently the enhancement of SPHOL and REM sleep. The aim of the present study was t o test these hypothesis, by evaluating the PGO wave density during the enhancement of SPHOL and REM sleep episodes induced by carbachol micr oinjection into the CN. Twelve adult male cats were prepared with chro nically implanted electrodes for monitoring wakefulness, sleep stages (EEG, EOG and EMG) and PGO waves, For microinjection of different dose s of carbachol (4 mu g/0.25 mu l, 8 mu g/0.50 mu l and 16 mu g/1.0 mu l) into the CN, animals were also prepared with bilaterally implanted stainless guide tube cannulae. Animals underwent three consecutive 8h control sleep recordings. Recordings of the same duration were perform ed during the subsequent five days following a unilateral or bilateral carbachol microinjection Sleep recordings were visually scored for wa king, slow wave sleep I, slow wave sleep II, SPHOL episodes and REM sl eep Statistical analysis of the percentage number and the mean duratio n of waking and sleep stages were calculated by a computational progra m for sleep scoring in cats. PGO waves were tape recorded and analyzed by a computational software for calculating the PGO density. The patt ern of PGO waves occurrence was also evaluated by determining the PGO waves burst density during central and after carbachol (4 mu g) microi njection into the CN. Variables were average for all cats under contro l condition and for each of the five days following a carbachol microi njection. The difference between the mean values obtained during contr ol and after carbachol application, was statistically evaluated by ANO VA and Student ''t'' test. The cholinergic activation of the CN induce d a prolonged and significant enhancement of PGO waves density. This e nhancement was due to a progressive and significant increase of PGO bu rst density beginning on the first day of carbachol administration. Re sults also showed that PGO enhancement is followed and accompanied by increased amounts of REM sleep and SPHOL episodes. These results confi rm our previous study and further show that cholinergic activation oi the CN facilitates the occurrence of PGO waves. Our findings support t he hypothesis that CN participates in REM sleep induction by facilitat ing the generation of PGO waves, which are a component of its onsettin g mechanism. We now propose that the amygdaloid CN exerts an stimulati ng effect on the PBL region, which in turn activates the pontine choli noceptive zone for REM sleep induction.