Search

Loss of muscle tone during active (rapid-eye-movement, REM) sleep is due to the inhibition of motoneurons. This inhibition is manifest in high-gain intracellular electrophysiological records as hyperpolarizing synaptic noise, which includes large amplitude active sleep-specific inhibitory postsynaptic potentials (IPSPs). We report here evidence that the large active sleep-specific IPSPs are comprised of a small number of minimal unitary potentials that are characterized by fast rise-times (10–90% rise-times ≤0.75 ms); they are present in high-gain records during quiet sleep or during active sleep where they are intermingled with larger active sleep-specific IPSPs with 10–90% rise-times ≥1.00 ms and amplitudes that are integer multiples of the minimal unitary potentials. In hypoglossal motoneurons, the amplitude of these minimal unitary potentials averaged 0.33±0.04 mV (mean±S.D., n=6). It is concluded that the large IPSPs with slow rise-times that are observed in motoneurons during active sleep are due to the nearly simultaneous arrival of multiple (≤5) minimal unitary potentials. We hypothesize that the same inhibitory interneurons that produce small IPSPs with fast rise-times during quiet sleep are also responsible for the large amplitude active sleep-specific IPSPs. [Copyright &y& Elsevier]

Cholinergic and γ-aminobutyric acid (GABA) mechanisms in the dorsolateral pontomesencephalic tegmentum have been implicated in the control of active (REM) sleep and wakefulness. To determine the relationships between neurons that contain these neurotransmitters in this region of the brainstem in adult cats, combined light and electron microscopic immunocytochemical procedures were employed. Light microscopic analyses revealed that choline acetyltransferase (ChAT) and GABA immunoreactive neurons were distributed throughout the laterodorsal and pedunculopontine tegmental nuclei (LDT and PPT). Surprisingly, approximately 50% of the ChAT immunoreactive neurons in these nuclei also contained GABA. Using electron microscopic pre-embedding immunocytochemistry, GABA immunoreactivity was observed in somas, dendrites and axon terminals in both the LDT and PPT. Most of the GABA immunoreactive terminals formed symmetrical synapses with non-immunolabeled dendrites. Electron microscopic double-immunolabeling techniques revealed that ChAT and GABA were colocalized in axon terminals in the LDT/PPT. Approximately 30% of the ChAT immunoreactive terminals were also GABA immunoreactive, whereas only 6–8% of the GABA immunoreactive terminals were ChAT immunoreactive. Most of the ChAT/GABA immunoreactive terminals formed symmetrical synapses with non-immunolabeled dendrites; however, ChAT/GABA immunoreactive terminals were also observed that contacted ChAT immunoreactive dendrites. With respect to ChAT immunoreactive postsynaptic profiles, approximately 40% of the somas and 50% of the dendrites received synaptic contact from GABA immunoreactive terminals in both the LDT and PPT. These findings (a) indicate that there are fundamental interactions between cholinergic and GABAergic neurons within the LDT/PPT that play an important role in the control of active sleep and wakefulness and (b) provide an anatomical basis for the intriguing possibility that a mechanism of acetylcholine and GABA co-release from the terminals of LDT/PPT neurons is involved in the regulation of behavioral states. [Copyright &y& Elsevier]

The amplitude of electrically-evoked mass action potentials recorded in the spinal cord and brainstem has been reported to decrease only during eye movement events of active sleep. In contrast, we have reported that the response of trigeminal sensory neurons to peripheral stimuli is modulated throughout the behavioral state of active sleep. It is unclear whether eye movement events contribute to the modulation of trigeminal sensory neuron activity during active sleep. In the present study, eye movement events were demarcated in order to investigate how these events affect peripheral input to trigeminal sensory neurons in chronic, intact, behaving cats. When compared with wakefulness, the mean response of 45 trigeminal sensory neurons to low-intensity electrical stimulation of the canine tooth pulp was significantly suppressed by 28% during periods of active sleep where no eye movement activity was present and by 41% during periods of active sleep with eye movement events. Hence, during active sleep, tooth pulp-evoked responses were significantly decreased by 16% during eye movement events when compared with non-eye movement active sleep. To investigate whether presynaptic inhibition played a role in this phenomenon, the excitability of eight individual tooth pulp afferent terminals during eye movement periods was compared with non-eye movement periods of active sleep. No evidence of eye movement-related depolarization of tooth pulp terminals was detected. When compared to wakefulness, the responses of six trigeminal sensory neurons to air puff stimulation of facial hair mechanoreceptors were significantly increased by 96% during periods of active sleep where no eye movement activity was present but were significantly decreased by 15% during eye movement events when compared with non-eye movement active sleep. The results of the present study indicate that neuronal responses to both tooth pulp and facial hair mechanoreceptor stimulation are significantly attenuated during eye movement events of active sleep. [Copyright &y& Elsevier]

The pedunculopontine tegmental nucleus (PPT) has been implicated in the generation and/or maintenance of both active sleep (AS) and wakefulness (W). GABAergic neurons are present within this nucleus and recent studies have shown that these neurons are active during AS . In order to examine the role of mesopontine GABAergic processes in the generation of AS, the GABAA agonist muscimol and the GABAA antagonist bicuculline were microinjected into the PPT of chronic cats that were prepared for recording the states of sleep and wakefulness. Muscimol increased the time spent in AS by increasing the frequency and duration of AS episodes; this increase in AS was at the expense of the time spent in wakefulness. A decrease in PGO density during AS was also observed following the microinjection of muscimol. On the other hand, bicuculline decreased both AS and quiet sleep and increased the time spent in wakefulness. These data suggest that GABA acts on GABAA receptors within the PPT to facilitate the generation of AS by suppressing the activity of waking-related processes within this nucleus. [Copyright &y& Elsevier]