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  • We described the presence of dye

    2018-11-13

    We described the presence of dye and electrical coupling in the RAS, specifically in the intralaminar parafascicular nucleus (Pf), the PPN, and the subcoeruleus dorsalis (SubCD), which modulates REM sleep [42–44]. We also found that the stimulant modafinil decreased the resistance of PPN, Pf, and SubCD neurons [42], in keeping with results in the cortex, reticular thalamus, and inferior olive [45].
    Pedunculopontine physiology and gamma frequency activity Neuronal and synaptic properties of thalamocortical networks [34]. Cortical gamma band generation can be influenced by subcortical Dig-11-ddUTP structures like the hippocampus and Dig-11-ddUTP [46,47]. The neuronal networks behind such activity include inhibitory cortical interneurons with intrinsic membrane potential oscillatory activity in the gamma band range [30,48,49], many of which are electrically coupled [50], as well as rhythmically bursting pyramidal neurons (also electrically coupled) [51]. At the thalamic level, thalamocortical excitatory neurons have intrinsic properties needed to generate subthreshold gamma band membrane potential oscillations [52]. Cortical interneurons can generate membrane potential gamma oscillations through the activation of voltage-dependent, persistent sodium channel-dependent subthreshold oscillations [51], and metabotropic glutamate receptors [53]. In thalamocortical neurons, the mechanism responsible for gamma band activity involves high threshold P/Q-type voltage-gated calcium channels located in the dendrites [52]. In addition to the cortex and thalamus, the hippocampus, cerebellum, and basal ganglia have all been described as manifesting gamma band activity [54–59]. It was reported that gamma band activity in the motor cortex lags behind coherent activity in subcortical structures [60,61]. This led to the suggestion that motor cortex gamma synchronization reflects a momentary arousal-related event for enabling the initiation of movement [62–64]. That is, structures such as the RAS and thalamus may play an early permissive role in the control of movement. The PPN is most active during waking and REM sleep [65], and modulates ascending projections through the thalamus (modulating arousal), and descending projections through the pons and medulla (modulating REM sleep and posture and locomotion). The PPN is made up of non-overlapping populations of cholinergic, glutamatergic, and GABAergic neurons [66]. The PPN contains three cell types based on in vitro intrinsic membrane properties [67–69]. Recordings of PPN neurons in vivo identified multiple types of thalamic-projecting PPN cells distinguished by their firing properties relative to ponto-geniculo-occipital (PGO) wave generation [70]. Some neurons exhibited low spontaneous firing frequencies (<10Hz), but most showed high rates of tonic firing in the beta/gamma range (20–80Hz). In other in vivo studies, PPN neurons increased firing during REM sleep and were labeled “REM-on” cells, or during both waking and REM sleep and were called “Wake/REM-on” cells, and also during waking only and were called “Wake-on” cells [71–73]. Stimulation of the PPN will potentiate the manifestation of fast (20–40Hz) oscillations in the cortical EEG, outlasting stimulation by 10–20s [74]. These results suggest that PPN cells do fire at gamma band frequencies in vivo, and that its outputs can indirectly induce gamma band activity in its targets. We were the first to report that all PPN cells fired maximally at gamma band frequency when depolarized using current steps [75]. This is the only property shared by every cell in the PPN, regardless of transmitter type or electrophysiological type. Further results demonstrated that both voltage-dependent N- and P/Q-type calcium channels mediate the depolarizing phase of gamma band oscillations in the PPN. Voltage clamp results suggested that calcium channels are located distally to the cell body, probably in PPN dendritic compartments [76], as has been determined in thalamic neurons [52]. We then confirmed using fast imaging techniques that PPN calcium channel-mediated oscillations are due to P/Q- and N-type channels, and revealed the fact that these channels are distributed along the dendrites of PPN cells [77].