Gamma band activity in the RAS-intracellular mechanisms

Abstract

Gamma band activity participates in sensory perception, problem solving, and memory. This review considers recent evidence showing that cells in the reticular activating system (RAS) exhibit gamma band activity, and describes the intrinsic membrane properties behind such manifestation. Specifically, we discuss how cells in the mesopontine pedunculopontine nucleus (PPN), intralaminar parafascicular nucleus (Pf), and pontine Subcoeruleus nucleus dorsalis (SubCD) all fire in the gamma band range when maximally activated, but no higher. The mechanisms involve high threshold, voltage-dependent P/Q-type calcium channels or sodium-dependent subthreshold oscillations. Rather than participating in the temporal binding of sensory events as in the cortex, gamma band activity in the RAS may participate in the processes of preconscious awareness, and provide the essential stream of information for the formulation of many of our actions. We address three necessary next steps resulting from these discoveries, an intracellular mechanism responsible for maintaining gamma band activity based on persistent G-protein activation, separate intracellular pathways that differentiate between gamma band activity during waking vs during REM sleep, and an intracellular mechanism responsible for the dysregulation in gamma band activity in schizophrenia. These findings open several promising research avenues that have not been thoroughly explored. What are the effects of sleep or REM sleep deprivation on these RAS mechanisms? Are these mechanisms involved in memory processing during waking and/or during REM sleep? Does gamma band processing differ during waking vs REM sleep after sleep or REM sleep deprivation?

Gamma band directional interactions between basal forebrain and visual cortex during wake and sleep states

“…One factor contributing to the prominent BF gamma oscillations may be the presence of gap junctions, which have been reported in BF populations (McKenna et al, 2013) and which can synchronize temporal neural activity (Gibson et al, 1999;Deans et al, 2001), thus enhancing the overall LFP amplitude. Certain membrane characteristics, by which neurons can generate intrinsic gamma oscillations (Garcia-Rill et al, 2014) without the need of excitatory-inhibitory coupling, could also be at work in BF to generate the observed large gamma power. Regardless of the mechanism of generation, BF LFPs and in particular their gamma components are highly sensitive to brain state, and in fact allow more accurate decoding of the WAKE state than visual cortical LFPs.…”

Modulation of gamma oscillations in the pedunculopontine nucleus by neuronal calcium sensor protein-1: relevance to schizophrenia and bipolar disorder

“…Such a mechanism would help explain the decrease in gamma-band activity seen in schizophrenia and bipolar disorder. We described preliminary data for this project in a recent poster and review Garcia-Rill et al 2014).…”

Continuous stimulation of the pedunculopontine tegmental nucleus at 40Hz affects preparative and executive control in a delayed sensorimotor task and reduces rotational movements induced by apomorphine in the 6-OHDA parkinsonian rat

“…The mechanisms underlying the action of PPTg-DBS on motor signs are not well understood, possibly involving a remodulation of neuronal activity in both the basal ganglia-cortical circuits and brainstem descending pathways. In addition to improving the initiation of gait, freezing of gait and axial disabilities, PPTg-DBS has been reported to affect sleep and cognitive functions likely through modulation of the reticulo-thalamo-cortical network [5,7,8]. Accordingly, a significant increase of cerebral blood was observed in several cortical and subcortical areas [50,51].…”